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Boundless Biology: 12.2: Patterns of Inheritance

Boundless Biology
12.2: Patterns of Inheritance
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table of contents
  1. 1: The Study of Life
    1. 1.1: The Science of Biology
      1. 1.1.0: Introduction to the Study of Biology
      2. 1.1.1: Scientific Reasoning
      3. 1.1.2: The Scientific Method
      4. 1.1.3: Basic and Applied Science
      5. 1.1.4: Publishing Scientific Work
      6. 1.1.5: Branches and Subdisciplines of Biology
    2. 1.2: Themes and Concepts of Biology
      1. 1.2.0: Properties of Life
      2. 1.2.1: Levels of Organization of Living Things
      3. 1.2.2: The Diversity of Life
  2. 2: The Chemical Foundation of Life
    1. 2.1: Atoms, Isotopes, Ions, and Molecules
      1. 2.1.0: Overview of Atomic Structure
      2. 2.1.1: Atomic Number and Mass Number
      3. 2.1.2: Isotopes
      4. 2.1.3: The Periodic Table
      5. 2.1.4: Electron Shells and the Bohr Model
      6. 2.1.5: Electron Orbitals
      7. 2.1.6: Chemical Reactions and Molecules
      8. 2.1.7: Ions and Ionic Bonds
      9. 2.1.8: Covalent Bonds and Other Bonds and Interactions
      10. 2.1.9: Hydrogen Bonding and Van der Waals Forces
    2. 2.2: Water
      1. 2.2.0: Water’s Polarity
      2. 2.2.1: Water’s States: Gas, Liquid, and Solid
      3. 2.2.2: Water’s High Heat Capacity
      4. 2.2.3: Water’s Heat of Vaporization
      5. 2.2.4: Water’s Solvent Properties
      6. 2.2.5: Water’s Cohesive and Adhesive Properties
      7. 2.2.6: pH, Buffers, Acids, and Bases
    3. 2.3: Carbon
      1. 2.3.0: The Chemical Basis for Life
      2. 2.3.1: Hydrocarbons
      3. 2.3.2: Organic Isomers
      4. 2.3.3: Organic Enantiomers
      5. 2.3.4: Organic Molecules and Functional Groups
  3. 3: Biological Macromolecules
    1. 3.1: Synthesis of Biological Macromolecules
      1. 3.1.0: Types of Biological Macromolecules
      2. 3.1.1: Dehydration Synthesis
      3. 3.1.2: Hydrolysis
    2. 3.2: Carbohydrates
      1. 3.2.0: Carbohydrate Molecules
      2. 3.2.1: Importance of Carbohydrates
    3. 3.3: Lipids
      1. 3.3.0: Lipid Molecules
      2. 3.3.1: Waxes
      3. 3.3.2: Phospholipids
      4. 3.3.3: Steroids
    4. 3.4: Proteins
      1. 3.4.0: Types and Functions of Proteins
      2. 3.4.1: Amino Acids
      3. 3.4.2: Protein Structure
      4. 3.4.3: Denaturation and Protein Folding
    5. 3.5: Nucleic Acids
      1. 3.5.0: DNA and RNA
      2. 3.5.1: The DNA Double Helix
      3. 3.5.2: DNA Packaging
      4. 3.5.3: Types of RNA
  4. 4: Cell Structure
    1. 4.1: Studying Cells
      1. 4.1.0: Cells as the Basic Unit of Life
      2. 4.1.1: Microscopy
      3. 4.1.2: Cell Theory
      4. 4.1.3: Cell Size
    2. 4.2: Prokaryotic Cells
      1. 4.2.0: Characteristics of Prokaryotic Cells
    3. 4.3: Eukaryotic Cells
      1. 4.3.0: Characteristics of Eukaryotic Cells
      2. 4.3.1: The Plasma Membrane and the Cytoplasm
      3. 4.3.2: The Nucleus and Ribosomes
      4. 4.3.3: Mitochondria
      5. 4.3.4: Comparing Plant and Animal Cells
    4. 4.4: The Endomembrane System and Proteins
      1. 4.4.0: Vesicles and Vacuoles
      2. 4.4.1: The Endoplasmic Reticulum
      3. 4.4.2: The Golgi Apparatus
      4. 4.4.3: Lysosomes
      5. 4.4.4: Peroxisomes
    5. 4.5: The Cytoskeleton
      1. 4.5.0: Microfilaments
      2. 4.5.1: Intermediate Filaments and Microtubules
    6. 4.6: Connections between Cells and Cellular Activities
      1. 4.6.0: Extracellular Matrix of Animal Cells
      2. 4.6.1: Intercellular Junctions
  5. 5: Structure and Function of Plasma Membranes
    1. 5.1: Components and Structure
      1. 5.1.0: Components of Plasma Membranes
      2. 5.1.1: Fluid Mosaic Model
      3. 5.1.2: Membrane Fluidity
    2. 5.2: Passive Transport
      1. 5.2.0: The Role of Passive Transport
      2. 5.2.1: Selective Permeability
      3. 5.2.2: Diffusion
      4. 5.2.3: Facilitated transport
      5. 5.2.4: Osmosis
      6. 5.2.5: Tonicity
      7. 5.2.6: Osmoregulation
    3. 5.3: Active Transport
      1. 5.3.0: Electrochemical Gradient
      2. 5.3.1: Primary Active Transport
      3. 5.3.2: Secondary Active Transport
    4. 5.4: Bulk Transport
      1. 5.4.0: Endocytosis
      2. 5.4.1: Exocytosis
  6. 6: Metabolism
    1. 6.1: Energy and Metabolism
      1. 6.1.0: The Role of Energy and Metabolism
      2. 6.1.1: Types of Energy
      3. 6.1.2: Metabolic Pathways
      4. 6.1.3: Metabolism of Carbohydrates
    2. 6.2: Potential, Kinetic, Free, and Activation Energy
      1. 6.2.0: Free Energy
      2. 6.2.1: The First Law of Thermodynamics
      3. 6.2.2: The Second Law of Thermodynamics
      4. 6.2.3: Activation Energy
    3. 6.3: ATP: Adenosine Triphosphate
      1. 6.3.0: ATP: Adenosine Triphosphate
    4. 6.4: Enzymes
      1. 6.4.0: Enzyme Active Site and Substrate Specificity
      2. 6.4.1: Control of Metabolism Through Enzyme Regulation
  7. 7: Cellular Respiration
    1. 7.1: Energy in Living Systems
      1. 7.1.0: Transforming Chemical Energy
      2. 7.1.1: Electrons and Energy
      3. 7.1.2: ATP in Metabolism
    2. 7.2: Glycolysis
      1. 7.2.0: Importance of Glycolysis
      2. 7.2.1: The Energy-Requiring Steps of Glycolysis
      3. 7.2.2: The Energy-Releasing Steps of Glycolysis
      4. 7.2.3: Outcomes of Glycolysis
    3. 7.3: Oxidation of Pyruvate and the Citric Acid Cycle
      1. 7.3.0: Breakdown of Pyruvate
      2. 7.3.1: Acetyl CoA to CO2
      3. 7.3.2: Citric Acid Cycle
    4. 7.4: Oxidative Phosphorylation
      1. 7.4.0: Electron Transport Chain
      2. 7.4.1: Chemiosmosis and Oxidative Phosphorylation
      3. 7.4.2: ATP Yield
    5. 7.5: Metabolism without Oxygen
      1. 7.5.0: Anaerobic Cellular Respiration
    6. 7.6: Connections of Carbohydrate, Protein, and Lipid Metabolic Pathways
      1. 7.6.0: Connecting Other Sugars to Glucose Metabolism
      2. 7.6.1: Connecting Proteins to Glucose Metabolism
      3. 7.6.2: Connecting Lipids to Glucose Metabolism
    7. 7.7: Regulation of Cellular Respiration
      1. 7.7.0: Regulatory Mechanisms for Cellular Respiration
      2. 7.7.1: Control of Catabolic Pathways
  8. 8: Photosynthesis
    1. 8.1: Overview of Photosynthesis
      1. 8.1.0: The Purpose and Process of Photosynthesis
      2. 8.1.1: Main Structures and Summary of Photosynthesis
      3. 8.1.2: The Two Parts of Photosynthesis
    2. 8.2: The Light-Dependent Reactions of Photosynthesis
      1. 8.2.0: Introduction to Light Energy
      2. 8.2.1: Absorption of Light
      3. 8.2.2: Processes of the Light-Dependent Reactions
    3. 8.3: The Light-Independent Reactions of Photosynthesis
      1. 8.3.0: CAM and C4 Photosynthesis
      2. 8.3.1: The Calvin Cycle
      3. 8.3.2: The Carbon Cycle
  9. 9: Cell Communication
    1. 9.1: Signaling Molecules and Cellular Receptors
      1. 9.1.0: Signaling Molecules and Cellular Receptors
      2. 9.1.1: Forms of Signaling
      3. 9.1.2: Types of Receptors
      4. 9.1.3: Signaling Molecules
    2. 9.2: Propagation of the Cellular Signal
      1. 9.2.0: Binding Initiates a Signaling Pathway
      2. 9.2.1: Methods of Intracellular Signaling
    3. 9.3: Response to the Cellular Signal
      1. 9.3.0: Termination of the Signal Cascade
      2. 9.3.1: Cell Signaling and Gene Expression
      3. 9.3.2: Cell Signaling and Cellular Metabolism
      4. 9.3.3: Cell Signaling and Cell Growth
      5. 9.3.4: Cell Signaling and Cell Death
    4. 9.4: Signaling in Single-Celled Organisms
      1. 9.4.0: Signaling in Yeast
      2. 9.4.1: Signaling in Bacteria
  10. 10: Cell Reproduction
    1. 10.1: Cell Division
      1. 10.1.0: The Role of the Cell Cycle
      2. 10.1.1: Genomic DNA and Chromosomes
      3. 10.1.2: Eukaryotic Chromosomal Structure and Compaction
    2. 10.2: The Cell Cycle
      1. 10.2.0: Interphase
      2. 10.2.1: The Mitotic Phase and the G0 Phase
    3. 10.3: Control of the Cell Cycle
      1. 10.3.0: Regulation of the Cell Cycle by External Events
      2. 10.3.1: Regulation of the Cell Cycle at Internal Checkpoints
      3. 10.3.2: Regulator Molecules of the Cell Cycle
    4. 10.4: Cancer and the Cell Cycle
      1. 10.4.0: Proto-oncogenes
      2. 10.4.1: Tumor Suppressor Genes
    5. 10.5: Prokaryotic Cell Division
      1. 10.5.0: Binary Fission
  11. 11: Meiosis and Sexual Reproduction
    1. 11.1: The Process of Meiosis
      1. 11.1.0: Introduction to Meiosis
      2. 11.1.1: Meiosis I
      3. 11.1.2: Meiosis II
      4. 11.1.3: Comparing Meiosis and Mitosis
    2. 11.2: Sexual Reproduction
      1. 11.2.0: Advantages and Disadvantages of Sexual Reproduction
      2. 11.2.1: Life Cycles of Sexually Reproducing Organisms
  12. 12: Mendel's Experiments and Heredity
    1. 12.1: Mendel’s Experiments and the Laws of Probability
      1. 12.1.0: Introduction to Mendelian Inheritance
      2. 12.1.1: Mendel’s Model System
      3. 12.1.2: Mendelian Crosses
      4. 12.1.3: Garden Pea Characteristics Revealed the Basics of Heredity
      5. 12.1.4: Rules of Probability for Mendelian Inheritance
    2. 12.2: Patterns of Inheritance
      1. 12.2.0: Genes as the Unit of Heredity
      2. 12.2.1: Phenotypes and Genotypes
      3. 12.2.2: The Punnett Square Approach for a Monohybrid Cross
      4. 12.2.3: Alternatives to Dominance and Recessiveness
      5. 12.2.4: Sex-Linked Traits
      6. 12.2.5: Lethal Inheritance Patterns
    3. 12.3: Laws of Inheritance
      1. 12.3.0: Mendel's Laws of Heredity
      2. 12.3.1: Mendel's Law of Dominance
      3. 12.3.2: Mendel's Law of Segregation
      4. 12.3.3: Mendel's Law of Independent Assortment
      5. 12.3.4: Genetic Linkage and Violation of the Law of Independent Assortment
      6. 12.3.5: Epistasis
  13. 13: Modern Understandings of Inheritance
    1. 13.1: Chromosomal Theory and Genetic Linkage
      1. 13.1.0: Chromosomal Theory of Inheritance
      2. 13.1.1: Genetic Linkage and Distances
      3. 13.1.2: Identification of Chromosomes and Karyotypes
    2. 13.2: Chromosomal Basis of Inherited Disorders
      1. 13.2.0: Disorders in Chromosome Number
      2. 13.2.1: Chromosomal Structural Rearrangements
      3. 13.2.2: X-Inactivation
  14. 14: DNA Structure and Function
    1. 14.1: Historical Basis of Modern Understanding
      1. 14.1.0: Discovery of DNA
      2. 14.1.1: Modern Applications of DNA
    2. 14.2: DNA Structure and Sequencing
      1. 14.2.0: The Structure and Sequence of DNA
      2. 14.2.1: DNA Sequencing Techniques
    3. 14.3: DNA Replication
      1. 14.3.0: Basics of DNA Replication
      2. 14.3.1: DNA Replication in Prokaryotes
      3. 14.3.2: DNA Replication in Eukaryotes
      4. 14.3.3: Telomere Replication
    4. 14.4: DNA Repair
      1. 14.4.0: DNA Repair
  15. 15: Genes and Proteins
    1. 15.1: The Genetic Code
      1. 15.1.0: The Relationship Between Genes and Proteins
      2. 15.1.1: The Central Dogma: DNA Encodes RNA and RNA Encodes Protein
    2. 15.2: Prokaryotic Transcription
      1. 15.2.0: Transcription in Prokaryotes
      2. 15.2.1: Initiation of Transcription in Prokaryotes
      3. 15.2.2: Elongation and Termination in Prokaryotes
    3. 15.3: Eukaryotic Transcription
      1. 15.3.0: Initiation of Transcription in Eukaryotes
      2. 15.3.1: Elongation and Termination in Eukaryotes
    4. 15.4: RNA Processing in Eukaryotes
      1. 15.4.0: mRNA Processing
      2. 15.4.1: Processing of tRNAs and rRNAs
    5. 15.5: Ribosomes and Protein Synthesis
      1. 15.5.0: The Protein Synthesis Machinery
      2. 15.5.1: The Mechanism of Protein Synthesis
      3. 15.5.2: Protein Folding, Modification, and Targeting
  16. 16: Gene Expression
    1. 16.1: Regulation of Gene Expression
      1. 16.1.0: The Process and Purpose of Gene Expression Regulation
      2. 16.1.1: Prokaryotic versus Eukaryotic Gene Expression
    2. 16.2: Prokaryotic Gene Regulation
      1. 16.2.0: The trp Operon: A Repressor Operon
      2. 16.2.1: Catabolite Activator Protein (CAP): An Activator Regulator
      3. 16.2.2: The lac Operon: An Inducer Operon
    3. 16.3: Eukaryotic Gene Regulation
      1. 16.3.0: The Promoter and the Transcription Machinery
      2. 16.3.1: Transcriptional Enhancers and Repressors
      3. 16.3.2: Epigenetic Control: Regulating Access to Genes within the Chromosome
      4. 16.3.3: RNA Splicing
      5. 16.3.4: The Initiation Complex and Translation Rate
      6. 16.3.5: Regulating Protein Activity and Longevity
    4. 16.4: Regulating Gene Expression in Cell Development
      1. 16.4.0: Gene Expression in Stem Cells
      2. 16.4.1: Cellular Differentiation
      3. 16.4.2: Mechanics of Cellular Differentation
      4. 16.4.3: Establishing Body Axes during Development
      5. 16.4.4: Gene Expression for Spatial Positioning
      6. 16.4.5: Cell Migration in Multicellular Organisms
      7. 16.4.6: Programmed Cell Death
    5. 16.5: Cancer and Gene Regulation
      1. 16.5.0: Altered Gene Expression in Cancer
      2. 16.5.1: Epigenetic Alterations in Cancer
      3. 16.5.2: Cancer and Transcriptional Control
      4. 16.5.3: Cancer and Post-Transcriptional Control
      5. 16.5.4: Cancer and Translational Control
  17. 17: Biotechnology and Genomics
    1. 17.1: Biotechnology
      1. 17.1.0: Biotechnology
      2. 17.1.1: Basic Techniques to Manipulate Genetic Material (DNA and RNA)
      3. 17.1.2: Molecular and Cellular Cloning
      4. 17.1.3: Reproductive Cloning
      5. 17.1.4: Genetic Engineering
      6. 17.1.5: Genetically Modified Organisms (GMOs)
      7. 17.1.6: Biotechnology in Medicine
      8. 17.1.7: Production of Vaccines, Antibiotics, and Hormones
    2. 17.2: Mapping Genomes
      1. 17.2.0: Genetic Maps
      2. 17.2.1: Physical Maps and Integration with Genetic Maps
    3. 17.3: Whole-Genome Sequencing
      1. 17.3.0: Strategies Used in Sequencing Projects
      2. 17.3.1: Use of Whole-Genome Sequences of Model Organisms
      3. 17.3.2: Uses of Genome Sequences
    4. 17.4: Applying Genomics
      1. 17.4.0: Predicting Disease Risk at the Individual Level
      2. 17.4.1: Pharmacogenomics, Toxicogenomics, and Metagenomics
      3. 17.4.2: Genomics and Biofuels
    5. 17.5: Genomics and Proteomics
      1. 17.5.0: Genomics and Proteomics
      2. 17.5.1: Basic Techniques in Protein Analysis
      3. 17.5.2: Cancer Proteomics
  18. 18: Evolution and the Origin of Species
    1. 18.1: Understanding Evolution
      1. 18.1.0: What is Evolution?
      2. 18.1.1: Charles Darwin and Natural Selection
      3. 18.1.2: The Galapagos Finches and Natural Selection
      4. 18.1.3: Processes and Patterns of Evolution
      5. 18.1.4: Evidence of Evolution
      6. 18.1.5: Misconceptions of Evolution
    2. 18.2: Formation of New Species
      1. 18.2.0: The Biological Species Concept
      2. 18.2.1: Reproductive Isolation
      3. 18.2.2: Speciation
      4. 18.2.3: Allopatric Speciation
      5. 18.2.4: Sympatric Speciation
    3. 18.3: Hybrid Zones and Rates of Speciation
      1. 18.3.0: Hybrid Zones
      2. 18.3.1: Varying Rates of Speciation
    4. 18.4: Evolution of Genomes
      1. 18.4.0: Genomic Similiarities between Distant Species
      2. 18.4.1: Genome Evolution
      3. 18.4.2: Whole-Genome Duplication
      4. 18.4.3: Gene Duplications and Divergence
      5. 18.4.4: Noncoding DNA
      6. 18.4.5: Variations in Size and Number of Genes
    5. 18.5: Evidence of Evolution
      1. 18.5.0: The Fossil Record as Evidence for Evolution
      2. 18.5.1: Fossil Formation
      3. 18.5.2: Gaps in the Fossil Record
      4. 18.5.3: Carbon Dating and Estimating Fossil Age
      5. 18.5.4: The Fossil Record and the Evolution of the Modern Horse
      6. 18.5.5: Homologous Structures
      7. 18.5.6: Convergent Evolution
      8. 18.5.7: Vestigial Structures
      9. 18.5.8: Biogeography and the Distribution of Species
  19. 19: The Evolution of Populations
    1. 19.1: Population Evolution
      1. 19.1.0: Defining Population Evolution
      2. 19.1.1: Population Genetics
      3. 19.1.2: Hardy-Weinberg Principle of Equilibrium
    2. 19.2: Population Genetics
      1. 19.2.0: Genetic Variation
      2. 19.2.1: Genetic Drift
      3. 19.2.2: Gene Flow and Mutation
      4. 19.2.3: Nonrandom Mating and Environmental Variance
    3. 19.3: Adaptive Evolution
      1. 19.3.0: Natural Selection and Adaptive Evolution
      2. 19.3.1: Stabilizing, Directional, and Diversifying Selection
      3. 19.3.2: Frequency-Dependent Selection
      4. 19.3.3: Sexual Selection
      5. 19.3.4: No Perfect Organism
  20. 20: Phylogenies and the History of Life
    1. 20.1: Organizing Life on Earth
      1. 20.1.0: Phylogenetic Trees
      2. 20.1.1: Limitations of Phylogenetic Trees
      3. 20.1.2: The Levels of Classification
    2. 20.2: Determining Evolutionary Relationships
      1. 20.2.0: Distinguishing between Similar Traits
      2. 20.2.1: Building Phylogenetic Trees
    3. 20.3: Perspectives on the Phylogenetic Tree
      1. 20.3.0: Limitations to the Classic Model of Phylogenetic Trees
      2. 20.3.1: Horizontal Gene Transfer
      3. 20.3.2: Endosymbiotic Theory and the Evolution of Eukaryotes
      4. 20.3.3: Web, Network, and Ring of Life Models
  21. 21: Viruses
    1. 21.1: Viral Evolution, Morphology, and Classification
      1. 21.1.0: Discovery and Detection of Viruses
      2. 21.1.1: Evolution of Viruses
      3. 21.1.2: Viral Morphology
      4. 21.1.3: Virus Classification
    2. 21.2: Virus Infections and Hosts
      1. 21.2.0: Steps of Virus Infections
      2. 21.2.1: The Lytic and Lysogenic Cycles of Bacteriophages
      3. 21.2.2: Animal Viruses
      4. 21.2.3: Plant Viruses
    3. 21.3: Prevention and Treatment of Viral Infections
      1. 21.3.0: Vaccines and Immunity
      2. 21.3.1: Vaccines and Anti-Viral Drugs for Treatment
    4. 21.4: Prions and Viroids
      1. 21.4.0: Prions and Viroids
  22. 22: Prokaryotes: Bacteria and Archaea
    1. 22.1: Prokaryotic Diversity
      1. 22.1.0: Classification of Prokaryotes
      2. 22.1.1: The Origins of Archaea and Bacteria
      3. 22.1.2: Extremophiles and Biofilms
    2. 22.2: Structure of Prokaryotes
      1. 22.2.0: Basic Structures of Prokaryotic Cells
      2. 22.2.1: Prokaryotic Reproduction
    3. 22.3: Prokaryotic Metabolism
      1. 22.3.0: Energy and Nutrient Requirements for Prokaryotes
      2. 22.3.1: The Role of Prokaryotes in Ecosystems
    4. 22.4: Bacterial Diseases in Humans
      1. 22.4.0: History of Bacterial Diseases
      2. 22.4.1: Biofilms and Disease
      3. 22.4.2: Antibiotics: Are We Facing a Crisis?
      4. 22.4.3: Bacterial Foodborne Diseases
    5. 22.5: Beneficial Prokaryotes
      1. 22.5.0: Symbiosis between Bacteria and Eukaryotes
      2. 22.5.1: Early Biotechnology: Cheese, Bread, Wine, Beer, and Yogurt
      3. 22.5.2: Prokaryotes and Environmental Bioremediation
  23. 23: Protists
    1. 23.1: Eukaryotic Origins
      1. 23.1.0: Early Eukaryotes
      2. 23.1.1: Characteristics of Eukaryotic DNA
      3. 23.1.2: Endosymbiosis and the Evolution of Eukaryotes
      4. 23.1.3: The Evolution of Mitochondria
      5. 23.1.4: The Evolution of Plastids
    2. 23.2: Characteristics of Protists
      1. 23.2.0: Cell Structure, Metabolism, and Motility
      2. 23.2.1: Protist Life Cycles and Habitats
    3. 23.3: Groups of Protists
      1. 23.3.0: Excavata
      2. 23.3.1: Chromalveolata: Alveolates
      3. 23.3.2: Chromalveolata: Stramenopiles
      4. 23.3.3: Rhizaria
      5. 23.3.4: Archaeplastida
      6. 23.3.5: Amoebozoa and Opisthokonta
    4. 23.4: Ecology of Protists
      1. 23.4.0: Protists as Primary Producers, Food Sources, and Symbionts
      2. 23.4.1: Protists as Human Pathogens
      3. 23.4.2: Protists as Plant Pathogens
  24. 24: Fungi
    1. 24.1: Characteristics of Fungi
      1. 24.1.0: Characteristics of Fungi
      2. 24.1.1: Fungi Cell Structure and Function
      3. 24.1.2: Fungi Reproduction
    2. 24.2: Ecology of Fungi
      1. 24.2.0: Fungi Habitat, Decomposition, and Recycling
      2. 24.2.1: Mutualistic Relationships with Fungi and Fungivores
    3. 24.3: Classifications of Fungi
      1. 24.3.0: Chytridiomycota: The Chytrids
      2. 24.3.1: Zygomycota: The Conjugated Fungi
      3. 24.3.2: Ascomycota: The Sac Fungi
      4. 24.3.3: Basidiomycota: The Club Fungi
      5. 24.3.4: Deuteromycota: The Imperfect Fungi
      6. 24.3.5: Glomeromycota
    4. 24.4: Fungal Parasites and Pathogens
      1. 24.4.0: Fungi as Plant, Animal, and Human Pathogens
    5. 24.5: Importance of Fungi in Human Life
      1. 24.5.0: Importance of Fungi in Human Life
  25. 25: Seedless Plants
    1. 25.1: Early Plant Life
      1. 25.1.0: Early Plant Life
      2. 25.1.1: Evolution of Land Plants
      3. 25.1.2: Plant Adaptations to Life on Land
      4. 25.1.3: Sporophytes and Gametophytes in Seedless Plants
      5. 25.1.4: Structural Adaptations for Land in Seedless Plants
      6. 25.1.5: The Major Divisions of Land Plants
    2. 25.2: Green Algae: Precursors of Land Plants
      1. 25.2.0: Streptophytes and Reproduction of Green Algae
      2. 25.2.1: Charales
    3. 25.3: Bryophytes
      1. 25.3.0: Bryophytes
      2. 25.3.1: Liverworts and Hornworts
      3. 25.3.2: Mosses
    4. 25.4: Seedless Vascular Plants
      1. 25.4.0: Seedless Vascular Plants
      2. 25.4.1: Vascular Tissue: Xylem and Phloem
      3. 25.4.2: The Evolution of Roots in Seedless Plants
      4. 25.4.3: Ferns and Other Seedless Vascular Plants
      5. 25.4.4: The Importance of Seedless Vascular Plants
  26. 26: Seed Plants
    1. 26.1: Evolution of Seed Plants
      1. 26.1.0: The Evolution of Seed Plants and Adaptations for Land
      2. 26.1.1: Evolution of Gymnosperms
      3. 26.1.2: Evolution of Angiosperms
    2. 26.2: Gymnosperms
      1. 26.2.0: Characteristics of Gymnosperms
      2. 26.2.1: Life Cycle of a Conifer
      3. 26.2.2: Diversity of Gymnosperms
    3. 26.3: Angiosperms
      1. 26.3.0: Angiosperm Flowers
      2. 26.3.1: Angsiosperm Fruit
      3. 26.3.2: The Life Cycle of an Angiosperm
      4. 26.3.3: Diversity of Angiosperms
    4. 26.4: The Role of Seed Plants
      1. 26.4.0: Herbivory and Pollination
      2. 26.4.1: The Importance of Seed Plants in Human Life
      3. 26.4.2: Biodiversity of Plants
  27. 27: Introduction to Animal Diversity
    1. 27.1: Features of the Animal Kingdom
      1. 27.1.0: Characteristics of the Animal Kingdom
      2. 27.1.1: Complex Tissue Structure
      3. 27.1.2: Animal Reproduction and Development
    2. 27.2: Features Used to Classify Animals
      1. 27.2.0: Animal Characterization Based on Body Symmetry
      2. 27.2.1: Animal Characterization Based on Features of Embryological Development
    3. 27.3: Animal Phylogeny
      1. 27.3.0: Constructing an Animal Phylogenetic Tree
      2. 27.3.1: Molecular Analyses and Modern Phylogenetic Trees
    4. 27.4: The Evolutionary History of the Animal Kingdom
      1. 27.4.0: Pre-Cambrian Animal Life
      2. 27.4.1: The Cambrian Explosion of Animal Life
      3. 27.4.2: Post-Cambrian Evolution and Mass Extinctions
  28. 28: Invertebrates
    1. 28.1: Phylum Porifera
      1. 28.1.0: Phylum Porifera
      2. 28.1.1: Morphology of Sponges
      3. 28.1.2: Physiological Processes in Sponges
    2. 28.2: Phylum Cnidaria
      1. 28.2.0: Phylum Cnidaria
      2. 28.2.1: Class Anthozoa
      3. 28.2.2: Class Scyphozoa
      4. 28.2.3: Class Cubozoa and Class Hydrozoa
    3. 28.3: Superphylum Lophotrochozoa
      1. 28.3.0: Superphylum Lophotrochozoa
      2. 28.3.1: Phylum Platyhelminthes
      3. 28.3.2: Phylum Rotifera
      4. 28.3.3: Phylum Nemertea
      5. 28.3.4: Phylum Mollusca
      6. 28.3.5: Classification of Phylum Mollusca
      7. 28.3.6: Phylum Annelida
    4. 28.4: Superphylum Ecdysozoa
      1. 28.4.0: Superphylum Ecdysozoa
      2. 28.4.1: Phylum Nematoda
      3. 28.4.2: Phylum Arthropoda
      4. 28.4.3: Subphyla of Arthropoda
    5. 28.5: Superphylum Deuterostomia
      1. 28.5.0: Phylum Echinodermata
      2. 28.5.1: Classes of Echinoderms
      3. 28.5.2: Phylum Chordata
  29. 29: Vertebrates
    1. 29.1: Chordates
      1. 29.1.0: Characteristics of Chordata
      2. 29.1.1: Chordates and the Evolution of Vertebrates
      3. 29.1.2: The Evolution of Craniata and Vertebrata
      4. 29.1.3: Characteristics of Vertebrates
    2. 29.2: Fishes
      1. 29.2.0: Agnathans: Jawless Fishes
      2. 29.2.1: Gnathostomes: Jawed Fishes
    3. 29.3: Amphibians
      1. 29.3.0: Characteristics and Evolution of Amphibians
      2. 29.3.1: Modern Amphibians
    4. 29.4: Reptiles
      1. 29.4.0: Characteristics of Amniotes
      2. 29.4.1: Evolution of Amniotes
      3. 29.4.2: Characteristics of Reptiles
      4. 29.4.3: Evolution of Reptiles
      5. 29.4.4: Modern Reptiles
    5. 29.5: Birds
      1. 29.5.0: Characteristics of Birds
      2. 29.5.1: Evolution of Birds
    6. 29.6: Mammals
      1. 29.6.0: Characteristics of Mammals
      2. 29.6.1: Evolution of Mammals
      3. 29.6.2: Living Mammals
    7. 29.7: The Evolution of Primates
      1. 29.7.0: Characteristics and Evolution of Primates
      2. 29.7.1: Early Human Evolution
      3. 29.7.2: Early Hominins
      4. 29.7.3: Genus Homo
  30. 30: Plant Form and Physiology
    1. 30.1: The Plant Body
      1. 30.1.0: Plant Tissues and Organ Systems
    2. 30.2: Stems
      1. 30.2.0: Functions of Stems
      2. 30.2.1: Stem Anatomy
      3. 30.2.2: Primary and Secondary Growth in Stems
      4. 30.2.3: Stem Modifications
    3. 30.3: Roots
      1. 30.3.0: Types of Root Systems and Zones of Growth
      2. 30.3.1: Root Modifications
    4. 30.4: Leaves
      1. 30.4.0: Leaf Structure and Arrangment
      2. 30.4.1: Types of Leaf Forms
      3. 30.4.2: Leaf Structure, Function, and Adaptation
    5. 30.5: Plant Development
      1. 30.5.0: Meristems
      2. 30.5.1: Genetic Control of Flowers
    6. 30.6: Transport of Water and Solutes in Plants
      1. 30.6.0: Water and Solute Potential
      2. 30.6.1: Pressure, Gravity, and Matric Potential
      3. 30.6.2: Movement of Water and Minerals in the Xylem
      4. 30.6.3: Transportation of Photosynthates in the Phloem
    7. 30.7: Plant Sensory Systems and Responses
      1. 30.7.0: Plant Responses to Light
      2. 30.7.1: The Phytochrome System and Red Light Response
      3. 30.7.2: Blue Light Response
      4. 30.7.3: Plant Responses to Gravity
      5. 30.7.4: Auxins, Cytokinins, and Gibberellins
      6. 30.7.5: Abscisic Acid, Ethylene, and Nontraditional Hormones
      7. 30.7.6: Plant Responses to Wind and Touch
    8. 30.8: Plant Defense Mechanisms
      1. 30.8.0: Plant Defenses Against Herbivores
      2. 30.8.1: Plant Defenses Against Pathogens
  31. 31: Soil and Plant Nutrition
    1. 31.1: Nutritional Requirements of Plants
      1. 31.1.0: Plant Nutrition
      2. 31.1.1: The Chemical Composition of Plants
      3. 31.1.2: Essential Nutrients for Plants
    2. 31.2: The Soil
      1. 31.2.0: Soil Composition
      2. 31.2.1: Soil Formation
      3. 31.2.2: Physical Properties of Soil
    3. 31.3: Nutritional Adaptations of Plants
      1. 31.3.0: Nitrogen Fixation: Root and Bacteria Interactions
      2. 31.3.1: Mycorrhizae: The Symbiotic Relationship between Fungi and Roots
      3. 31.3.2: Nutrients from Other Sources
  32. 32: Plant Reproduction
    1. 32.1: Plant Reproductive Development and Structure
      1. 32.1.0: Plant Reproductive Development and Structure
      2. 32.1.1: Sexual Reproduction in Gymnosperms
      3. 32.1.2: Sexual Reproduction in Angiosperms
    2. 32.2: Pollination and Fertilization
      1. 32.2.0: Pollination and Fertilization
      2. 32.2.1: Pollination by Insects
      3. 32.2.2: Pollination by Bats, Birds, Wind, and Water
      4. 32.2.3: Double Fertilization in Plants
      5. 32.2.4: Development of the Seed
      6. 32.2.5: Development of Fruit and Fruit Types
      7. 32.2.6: Fruit and Seed Dispersal
    3. 32.3: Asexual Reproduction
      1. 32.3.0: Asexual Reproduction in Plants
      2. 32.3.1: Natural and Artificial Methods of Asexual Reproduction in Plants
      3. 32.3.2: Plant Life Spans
  33. 33: The Animal Body: Basic Form and Function
    1. 33.1: Animal Form and Function
      1. 33.1.0: Characteristics of the Animal Body
      2. 33.1.1: Body Plans
      3. 33.1.2: Limits on Animal Size and Shape
      4. 33.1.3: Limiting Effects of Diffusion on Size and Development
      5. 33.1.4: Animal Bioenergetics
      6. 33.1.5: Animal Body Planes and Cavities
    2. 33.2: Animal Primary Tissues
      1. 33.2.0: Epithelial Tissues
      2. 33.2.1: Connective Tissues: Loose, Fibrous, and Cartilage
      3. 33.2.2: Connective Tissues: Bone, Adipose, and Blood
      4. 33.2.3: Muscle Tissues and Nervous Tissues
    3. 33.3: Homeostasis
      1. 33.3.0: Homeostatic Process
      2. 33.3.1: Control of Homeostasis
      3. 33.3.2: Homeostasis: Thermoregulation
      4. 33.3.3: Heat Conservation and Dissipation
  34. 34: Animal Nutrition and the Digestive System
    1. 34.1: Digestive Systems
      1. 34.1.0: Digestive Systems
      2. 34.1.1: Herbivores, Omnivores, and Carnivores
      3. 34.1.2: Invertebrate Digestive Systems
      4. 34.1.3: Vertebrate Digestive Systems
      5. 34.1.4: Digestive System: Mouth and Stomach
      6. 34.1.5: Digestive System: Small and Large Intestines
    2. 34.2: Nutrition and Energy Production
      1. 34.2.0: Food Requirements and Essential Nutrients
      2. 34.2.1: Food Energy and ATP
    3. 34.3: Digestive System Processes
      1. 34.3.0: Ingestion
      2. 34.3.1: Digestion and Absorption
      3. 34.3.2: Elimination
    4. 34.4: Digestive System Regulation
      1. 34.4.0: Neural Responses to Food
      2. 34.4.1: Hormonal Responses to Food
  35. 35: The Nervous System
    1. 35.1: Neurons and Glial Cells
      1. 35.1.0: Neurons and Glial Cells
      2. 35.1.1: Neurons
      3. 35.1.2: Glia
    2. 35.2: How Neurons Communicate
      1. 35.2.0: Nerve Impulse Transmission within a Neuron: Resting Potential
      2. 35.2.1: Nerve Impulse Transmission within a Neuron: Action Potential
      3. 35.2.2: Synaptic Transmission
      4. 35.2.3: Signal Summation
      5. 35.2.4: Synaptic Plasticity
    3. 35.3: The Nervous System
      1. 35.3.0: The Nervous System
    4. 35.4: The Central Nervous System
      1. 35.4.0: Brain: Cerebral Cortex and Brain Lobes
      2. 35.4.1: Brain: Midbrain and Brain Stem
      3. 35.4.2: Spinal Cord
    5. 35.5: The Peripheral Nervous System
      1. 35.5.0: Autonomic Nervous System
      2. 35.5.1: Sensory-Somatic Nervous System
    6. 35.6: Nervous System Disorders
      1. 35.6.0: Neurodegenerative Disorders
      2. 35.6.1: Neurodevelopmental Disorders: Autism and ADHD
      3. 35.6.2: Neurodevelopmental Disorders: Mental Illnesses
      4. 35.6.3: Other Neurological Disorders
  36. 36: Sensory Systems
    1. 36.1: Sensory Processes
      1. 36.1.0: Reception
      2. 36.1.1: Transduction and Perception
    2. 36.2: Somatosensation
      1. 36.2.0: Somatosensory Receptors
      2. 36.2.1: Integration of Signals from Mechanoreceptors
      3. 36.2.2: Thermoreception
    3. 36.3: Taste and Smell
      1. 36.3.0: Tastes and Odors
      2. 36.3.1: Reception and Transduction
    4. 36.4: Hearing and Vestibular Sensation
      1. 36.4.0: Sound
      2. 36.4.1: Reception of Sound
      3. 36.4.2: Transduction of Sound
      4. 36.4.3: The Vestibular System
      5. 36.4.4: Balance and Determining Equilibrium
    5. 36.5: Vision
      1. 36.5.0: Light
      2. 36.5.1: Anatomy of the Eye
      3. 36.5.2: Transduction of Light
      4. 36.5.3: Visual Processing
  37. 37: The Endocrine System
    1. 37.1: Types of Hormones
      1. 37.1.0: Hormone Functions
      2. 37.1.1: Lipid-Derived, Amino Acid-Derived, and Peptide Hormones
    2. 37.2: How Hormones Work
      1. 37.2.0: How Hormones Work
      2. 37.2.1: Intracellular Hormone Receptors
      3. 37.2.2: Plasma Membrane Hormone Receptors
    3. 37.3: Regulation of Body Processes
      1. 37.3.0: Hormonal Regulation of the Excretory System
      2. 37.3.1: Hormonal Regulation of the Reproductive System
      3. 37.3.2: Hormonal Regulation of Metabolism
      4. 37.3.3: Hormonal Control of Blood Calcium Levels
      5. 37.3.4: Hormonal Regulation of Growth
      6. 37.3.5: Hormonal Regulation of Stress
    4. 37.4: Regulation of Hormone Production
      1. 37.4.0: Humoral, Hormonal, and Neural Stimuli
    5. 37.5: Endocrine Glands
      1. 37.5.0: Hypothalamic-Pituitary Axis
      2. 37.5.1: Thyroid Gland
      3. 37.5.2: Parathyroid Glands
      4. 37.5.3: Adrenal Glands
      5. 37.5.4: Pancreas
      6. 37.5.5: Pineal Gland and Gonads
      7. 37.5.6: Organs with Secondary Endocrine Functions
  38. 38: The Musculoskeletal System
    1. 38.1: Types of Skeletal Systems
      1. 38.1.0: Functions of the Musculoskeletal System
      2. 38.1.1: Types of Skeletal Systems
      3. 38.1.2: Human Axial Skeleton
      4. 38.1.3: Human Appendicular Skeleton
    2. 38.2: Bone
      1. 38.2.0: Bone
      2. 38.2.1: Cell Types in Bones
      3. 38.2.2: Bone Development
      4. 38.2.3: Growth of Bone
      5. 38.2.4: Bone Remodeling and Repair
    3. 38.3: Joints and Skeletal Movement
      1. 38.3.0: Classification of Joints on the Basis of Structure and Function
      2. 38.3.1: Movement at Synovial Joints
      3. 38.3.2: Types of Synovial Joints
      4. 38.3.3: Bone and Joint Disorders
    4. 38.4: Muscle Contraction and Locomotion
      1. 38.4.0: Structure and Function of the Muscular System
      2. 38.4.1: Skeletal Muscle Fibers
      3. 38.4.2: Sliding Filament Model of Contraction
      4. 38.4.3: ATP and Muscle Contraction
      5. 38.4.4: Regulatory Proteins
      6. 38.4.5: Excitation–Contraction Coupling
      7. 38.4.6: Control of Muscle Tension
  39. 39: The Respiratory System
    1. 39.1: Systems of Gas Exchange
      1. 39.1.0: The Respiratory System and Direct Diffusion
      2. 39.1.1: Skin, Gills, and Tracheal Systems
      3. 39.1.2: Amphibian and Bird Respiratory Systems
      4. 39.1.3: Mammalian Systems and Protective Mechanisms
    2. 39.2: Gas Exchange across Respiratory Surfaces
      1. 39.2.0: Gas Pressure and Respiration
      2. 39.2.1: Basic Principles of Gas Exchange
      3. 39.2.2: Lung Volumes and Capacities
      4. 39.2.3: Gas Exchange across the Alveoli
    3. 39.3: Breathing
      1. 39.3.0: The Mechanics of Human Breathing
      2. 39.3.1: Types of Breathing
      3. 39.3.2: The Work of Breathing
      4. 39.3.3: Dead Space: V/Q Mismatch
    4. 39.4: Transport of Gases in Human Bodily Fluids
      1. 39.4.0: Transport of Oxygen in the Blood
      2. 39.4.1: Transport of Carbon Dioxide in the Blood
  40. 40: The Circulatory System
    1. 40.1: Overview of the Circulatory System
      1. 40.1.0: The Role of the Circulatory System
      2. 40.1.1: Open and Closed Circulatory Systems
      3. 40.1.2: Types of Circulatory Systems in Animals
    2. 40.2: Components of the Blood
      1. 40.2.0: The Role of Blood in the Body
      2. 40.2.1: Red Blood Cells
      3. 40.2.2: White Blood Cells
      4. 40.2.3: Platelets and Coagulation Factors
      5. 40.2.4: Plasma and Serum
    3. 40.3: Mammalian Heart and Blood Vessels
      1. 40.3.0: Structures of the Heart
      2. 40.3.1: Arteries, Veins, and Capillaries
      3. 40.3.2: The Cardiac Cycle
    4. 40.4: Blood Flow and Blood Pressure Regulation
      1. 40.4.0: Blood Flow Through the Body
      2. 40.4.1: Blood Pressure
  41. 41: Osmotic Regulation and the Excretory System
    1. 41.1: Osmoregulation and Osmotic Balance
      1. 41.1.0: Introduction to Osmoregulation
      2. 41.1.1: Transport of Electrolytes across Cell Membranes
      3. 41.1.2: Concept of Osmolality and Milliequivalent
      4. 41.1.3: Osmoregulators and Osmoconformers
    2. 41.2: Nitrogenous Wastes
      1. 41.2.0: Nitrogenous Waste in Terrestrial Animals: The Urea Cycle
      2. 41.2.1: Nitrogenous Waste in Birds and Reptiles: Uric Acid
    3. 41.3: Excretion Systems
      1. 41.3.0: Contractile Vacuoles in Microorganisms
      2. 41.3.1: Flame Cells of Planaria and Nephridia of Worms
      3. 41.3.2: Malpighian Tubules of Insects
    4. 41.4: Human Osmoregulatory and Excretory Systems
      1. 41.4.0: Kidney Structure
      2. 41.4.1: Nephron: The Functional Unit of the Kidney
      3. 41.4.2: Kidney Function and Physiology
    5. 41.5: Hormonal Control of Osmoregulatory Functions
      1. 41.5.0: Epinephrine and Norepinephrine
      2. 41.5.1: Other Hormonal Controls for Osmoregulation
  42. 42: The Immune System
    1. 42.1: Innate Immune Response
      1. 42.1.0: Innate Immune Response
      2. 42.1.1: Physical and Chemical Barriers
      3. 42.1.2: Pathogen Recognition
      4. 42.1.3: Natural Killer Cells
      5. 42.1.4: The Complement System
    2. 42.2: Adaptive Immune Response
      1. 42.2.0: Antigen-presenting Cells: B and T cells
      2. 42.2.1: Humoral Immune Response
      3. 42.2.2: Cell-Mediated Immunity
      4. 42.2.3: Cytotoxic T Lymphocytes and Mucosal Surfaces
      5. 42.2.4: Immunological Memory
      6. 42.2.5: Regulating Immune Tolerance
    3. 42.3: Antibodies
      1. 42.3.0: Antibody Structure
      2. 42.3.1: Antibody Functions
    4. 42.4: Disruptions in the Immune System
      1. 42.4.0: Immunodeficiency
      2. 42.4.1: Hypersensitivities
  43. 43: Animal Reproduction and Development
    1. 43.1: Reproduction Methods
      1. 43.1.0: Methods of Reproducing
      2. 43.1.1: Types of Sexual and Asexual Reproduction
      3. 43.1.2: Sex Determination
    2. 43.2: Fertilization
      1. 43.2.0: External and Internal Fertilization
      2. 43.2.1: The Evolution of Reproduction
    3. 43.3: Human Reproductive Anatomy and Gametogenesis
      1. 43.3.0: Male Reproductive Anatomy
      2. 43.3.1: Female Reproductive Anatomy
      3. 43.3.2: Gametogenesis (Spermatogenesis and Oogenesis)
    4. 43.4: Hormonal Control of Human Reproduction
      1. 43.4.0: Male Hormones
      2. 43.4.1: Female Hormones
    5. 43.5: Fertilization and Early Embryonic Development
      1. 43.5.0: Fertilization
      2. 43.5.1: Cleavage, the Blastula Stage, and Gastrulation
    6. 43.6: Organogenesis and Vertebrate Formation
      1. 43.6.0: Organogenesis
      2. 43.6.1: Vertebrate Axis Formation
    7. 43.7: Human Pregnancy and Birth
      1. 43.7.0: Human Gestation
      2. 43.7.1: Labor and Birth
      3. 43.7.2: Contraception and Birth Control
      4. 43.7.3: Infertility
  44. 44: Ecology and the Biosphere
    1. 44.1: The Scope of Ecology
      1. 44.1.0: Introduction to Ecology
      2. 44.1.1: Organismal Ecology and Population Ecology
      3. 44.1.2: Community Ecology and Ecosystem Ecology
    2. 44.2: Biogeography
      1. 44.2.0: Biogeography
      2. 44.2.1: Energy Sources
      3. 44.2.2: Temperature and Water
      4. 44.2.3: Inorganic Nutrients and Other Factors
      5. 44.2.4: Abiotic Factors Influencing Plant Growth
    3. 44.3: Terrestrial Biomes
      1. 44.3.0: What constitutes a biome?
      2. 44.3.1: Tropical Wet Forest and Savannas
      3. 44.3.2: Subtropical Deserts and Chaparral
      4. 44.3.3: Temperate Grasslands
      5. 44.3.4: Temperate Forests
      6. 44.3.5: Boreal Forests and Arctic Tundra
    4. 44.4: Aquatic Biomes
      1. 44.4.0: Abiotic Factors Influencing Aquatic Biomes
      2. 44.4.1: Marine Biomes
      3. 44.4.2: Estuaries: Where the Ocean Meets Fresh Water
      4. 44.4.3: Freshwater Biomes
    5. 44.5: Climate and the Effects of Global Climate Change
      1. 44.5.0: Climate and Weather
      2. 44.5.1: Causes of Global Climate Change
      3. 44.5.2: Evidence of Global Climate Change
      4. 44.5.3: Past and Present Effects of Climate Change
  45. 45: Population and Community Ecology
    1. 45.1: Population Demography
      1. 45.1.0: Population Demography
      2. 45.1.1: Population Size and Density
      3. 45.1.2: Species Distribution
      4. 45.1.3: The Study of Population Dynamics
    2. 45.2: Environmental Limits to Population Growth
      1. 45.2.0: Exponential Population Growth
      2. 45.2.1: Logistic Population Growth
      3. 45.2.2: Density-Dependent and Density-Independent Population Regulation
    3. 45.3: Life History Patterns
      1. 45.3.0: Life History Patterns and Energy Budgets
      2. 45.3.1: Theories of Life History
    4. 45.4: Human Population Growth
      1. 45.4.0: Human Population Growth
      2. 45.4.1: Overcoming Density-Dependent Regulation
      3. 45.4.2: Age Structure, Population Growth, and Economic Development
    5. 45.5: Community Ecology
      1. 45.5.0: The Role of Species within Communities
      2. 45.5.1: Predation, Herbivory, and the Competitive Exclusion Principle
      3. 45.5.2: Symbiosis
      4. 45.5.3: Ecological Succession
    6. 45.6: Innate Animal Behavior
      1. 45.6.0: Introduction to Animal Behavior
      2. 45.6.1: Movement and Migration
      3. 45.6.2: Animal Communication and Living in Groups
      4. 45.6.3: Altruism and Populations
      5. 45.6.4: Mating Systems and Sexual Selection
    7. 45.7: Learned Animal Behavior
      1. 45.7.0: Simple Learned Behaviors
      2. 45.7.1: Conditioned Behavior
      3. 45.7.2: Cognitive Learning and Sociobiology
  46. 46: Ecosystems
    1. 46.1: Ecology of Ecosystems
      1. 46.1.0: Ecosystem Dynamics
      2. 46.1.1: Food Chains and Food Webs
      3. 46.1.2: Studying Ecosystem Dynamics
      4. 46.1.3: Modeling Ecosystem Dynamics
    2. 46.2: Energy Flow through Ecosystems
      1. 46.2.0: Strategies for Acquiring Energy
      2. 46.2.1: Productivity within Trophic Levels
      3. 46.2.2: Transfer of Energy between Trophic Levels
      4. 46.2.3: Ecological Pyramids
      5. 46.2.4: Biological Magnification
    3. 46.3: Biogeochemical Cycles
      1. 46.3.0: Biogeochemical Cycles
      2. 46.3.1: The Water (Hydrologic) Cycle
      3. 46.3.2: The Carbon Cycle
      4. 46.3.3: The Nitrogen Cycle
      5. 46.3.4: The Phosphorus Cycle
      6. 46.3.5: The Sulfur Cycle
  47. 47: Conservation Biology and Biodiversity
    1. 47.1: The Biodiversity Crisis
      1. 47.1.0: Loss of Biodiversity
      2. 47.1.1: Types of Biodiversity
      3. 47.1.2: Biodiversity Change through Geological Time
      4. 47.1.3: The Pleistocene Extinction
      5. 47.1.4: Present-Time Extinctions
    2. 47.2: The Importance of Biodiversity to Human Life
      1. 47.2.0: Human Health and Biodiversity
      2. 47.2.1: Agricultural Diversity
      3. 47.2.2: Managing Fisheries
    3. 47.3: Threats to Biodiversity
      1. 47.3.0: Habitat Loss and Sustainability
      2. 47.3.1: Overharvesting
      3. 47.3.2: Exotic Species
      4. 47.3.3: Climate Change and Biodiversity
    4. 47.4: Preserving Biodiversity
      1. 47.4.0: Measuring Biodiversity
      2. 47.4.1: Changing Human Behavior in Response to Biodiversity Loss
      3. 47.4.2: Ecological Restoration

12.2: Patterns of Inheritance

12.2.1: Genes as the Unit of Heredity

Genes exist in pairs within an organism, with one of each pair inherited from each parent.

Learning Objective

Describe the structure of a gene and how offspring inherit genes from each parent

Key Points

  • A gene is a stretch of DNA that helps to control the development and function of all organs and working systems in the body.
  • Genes are passed from parent to offspring; the combination of these genes affects all aspects of the human body, from eye and hair color to how well the liver can process toxins.
  • A human will inherit 23 chromosomes from its mother and 23 from its father; together, these form 23 pairs of chromosomes that direct the inherited characteristics of the individual.
  • If the two copies of a gene inherited from each parent are the same, that individual is said to be homozygous for the gene; if the two copies inherited from each parent are different, that individual is said to be heterozygous for the gene.

Key Terms

genetics

the branch of biology that deals with the transmission and variation of inherited characteristics, in particular chromosomes and DNA

chromosome

a structure in the cell nucleus that contains DNA, histone protein, and other structural proteins

gene

a unit of heredity; the functional units of chromosomes that determine specific characteristics by coding for specific proteins

Pairs of Unit Factors, or Genes

Mendel proposed that paired unit factors of heredity were transmitted faithfully from generation to generation by the dissociation and reassociation of paired factors during gametogenesis and fertilization, respectively. After he crossed peas with contrasting traits and found that the recessive trait resurfaced in the F2 generation, Mendel deduced that hereditary factors must be inherited as discrete units. This finding contradicted the belief at that time that parental traits were blended in the offspring.

A gene is made up of short sections of DNA that are contained on a chromosome within the nucleus of a cell. Genes control the development and function of all organs and all working systems in the body. A gene has a certain influence on how the cell works; the same gene in many different cells determines a certain physical or biochemical feature of the whole body (e.g., eye color or reproductive functions). All human cells hold approximately 21,000 different genes.

Genetics is the science of the way traits are passed from parent to offspring. For all forms of life, continuity of the species depends upon the genetic code being passed from parent to offspring. Evolution by natural selection is dependent on traits being heritable. Genetics is very important in human physiology because all attributes of the human body are affected by a person's genetic code. It can be as simple as eye color, height, or hair color. Or it can be as complex as how well your liver processes toxins, whether you will be prone to heart disease or breast cancer, and whether you will be color blind.

Genetic inheritance begins at the time of conception. You inherited 23 chromosomes from your mother and 23 from your father . Together they form 22 pairs of autosomal chromosomes and a pair of sex chromosomes (either XX if you are female, or XY if you are male). Homologous chromosomes have the same genes in the same positions, but may have different alleles (varieties) of those genes. There can be many alleles of a gene within a population, but an individual within that population only has two copies and can be homozygous (both copies the same) or heterozygous (the two copies are different) for any given gene.

Gene pairs enable genetic combinations

Gene pairs enable genetic combinations

A child will inherit half of its genes (one of each of its 23 pairs) from its mother and the other half from its father.

12.2.2: Phenotypes and Genotypes

The observable traits expressed by an organism are referred to as its phenotype and its underlying genetic makeup is called its genotype.

Learning Objective

Distinguish between the phenotype and the genotype of an organism

Key Points

  • Mendel used pea plants with seven distinct traits or phenotypes to determine the pattern of inheritance and the underlying genotypes.
  • Mendel found that crossing two purebred pea plants which expressed different traits resulted in an F1 generation where all the pea plants expressed the same trait or phenotype.
  • When Mendel allowed the F1 plants to self-fertilize, the F2 generation showed two different phenotypes, indicating that the F1 plants had different genotypes.

Key Terms

genotype

the combination of alleles, situated on corresponding chromosomes, that determines a specific trait of an individual, such as "Aa" or "aa"

phenotype

the appearance of an organism based on a multifactorial combination of genetic traits and environmental factors, especially used in pedigrees

Phenotypes and Genotypes

The observable traits expressed by an organism are referred to as its phenotype. An organism's underlying genetic makeup, consisting of both physically visible and non-expressed alleles, is called its genotype. Johann Gregor Mendel's (1822–1884) hybridization experiments demonstrate the difference between phenotype and genotype.

Mendel crossed or mated two true-breeding (self-pollinating) garden peas, Pisum saivum, by manually transferring pollen from the anther of a mature pea plant of one variety to the stigma of a separate mature pea plant of the second variety. Plants used in first-generation crosses were called P0, or parental generation one, plants. Mendel collected the seeds belonging to the P0 plants that resulted from each cross and grew them the following season. These offspring were called the F1, or the first filial (filial = offspring, daughter or son), generation. Once Mendel examined the characteristics in the F1 generation of plants, he allowed them to self-fertilize naturally. He then collected and grew the seeds from the F1 plants to produce the F2, or second filial, generation .

Mendelian crosses

Mendelian crosses

In one of his experiments on inheritance patterns, Mendel crossed plants that were true-breeding for violet flower color with plants true-breeding for white flower color (the P generation). The resulting hybrids in the F1 generation all had violet flowers. In the F2 generation, approximately three-quarters of the plants had violet flowers, and one-quarter had white flowers.

When true-breeding plants in which one parent had white flowers and one had violet flowers were cross-fertilized, all of the F1 hybrid offspring had violet flowers . That is, the hybrid offspring were phenotypically identical to the true-breeding parent with violet flowers. However, we know that the allele donated by the parent with white flowers was not simply lost because it reappeared in some of the F2 offspring. Therefore, the F1 plants must have been genotypically different from the parent with violet flowers.

In his 1865 publication, Mendel reported the results of his crosses involving seven different phenotypes, each with two contrasting traits. A trait is defined as a variation in the physical appearance of a heritable characteristic. The characteristics included plant height, seed texture, seed color, flower color, pea pod size, pea pod color, and flower position. To fully examine each characteristic, Mendel generated large numbers of F1 and F2 plants, reporting results from 19,959 F2 plants alone. His findings were consistent. First, Mendel confirmed that he had plants that bred true for white or violet flower color. Regardless of how many generations Mendel examined, all self-crossed offspring of parents with white flowers had white flowers, and all self-crossed offspring of parents with violet flowers had violet flowers. In addition, Mendel confirmed that, other than flower color, the pea plants were physically identical.

12.2.3: The Punnett Square Approach for a Monohybrid Cross

A Punnett square applies the rules of probability to predict the possible outcomes of a monohybrid cross and their expected frequencies.

Learning Objective

Describe the Punnett square approach to a monohybrid cross

Key Points

  • Fertilization between two true-breeding parents that differ in only one characteristic is called a monohybrid cross.
  • For a monohybrid cross of two true-breeding parents, each parent contributes one type of allele resulting in all of the offspring with the same genotype.
  • A test cross is a way to determine whether an organism that expressed a dominant trait was a heterozygote or a homozygote.

Key Terms

heterozygous

of an organism which has two different alleles of a given gene

homozygous

of an organism in which both copies of a given gene have the same allele

monohybrid

a hybrid between two species that only have a difference of one gene

Punnett square

a graphical representation used to determine the probability of an offspring expressing a particular genotype

Punnett Square Approach to a Monohybrid Cross

When fertilization occurs between two true-breeding parents that differ in only one characteristic, the process is called a monohybrid cross, and the resulting offspring are monohybrids. Mendel performed seven monohybrid crosses involving contrasting traits for each characteristic. On the basis of his results in F1 and F2 generations, Mendel postulated that each parent in the monohybrid cross contributed one of two paired unit factors to each offspring and that every possible combination of unit factors was equally likely.

To demonstrate a monohybrid cross, consider the case of true-breeding pea plants with yellow versus green pea seeds. The dominant seed color is yellow; therefore, the parental genotypes were YY (homozygous dominant) for the plants with yellow seeds and yy (homozygous recessive) for the plants with green seeds, respectively. A Punnett square, devised by the British geneticist Reginald Punnett, can be drawn that applies the rules of probability to predict the possible outcomes of a genetic cross or mating and their expected frequencies.To prepare a Punnett square, all possible combinations of the parental alleles are listed along the top (for one parent) and side (for the other parent) of a grid, representing their meiotic segregation into haploid gametes . Then the combinations of egg and sperm are made in the boxes in the table to show which alleles are combining. Each box then represents the diploid genotype of a zygote, or fertilized egg, that could result from this mating. Because each possibility is equally likely, genotypic ratios can be determined from a Punnett square. If the pattern of inheritance (dominant or recessive) is known, the phenotypic ratios can be inferred as well. For a monohybrid cross of two true-breeding parents, each parent contributes one type of allele. In this case, only one genotype is possible. All offspring are Yy and have yellow seeds.

Punnett square analysis of a monohytbrid cross

Punnett square analysis of a monohytbrid cross

In the P generation, pea plants that are true-breeding for the dominant yellow phenotype are crossed with plants with the recessive green phenotype. This cross produces F1 heterozygotes with a yellow phenotype. Punnett square analysis can be used to predict the genotypes of the F2 generation.

A self-cross of one of the Yy heterozygous offspring can be represented in a 2 × 2 Punnett square because each parent can donate one of two different alleles. Therefore, the offspring can potentially have one of four allele combinations: YY, Yy, yY, or yy. Notice that there are two ways to obtain the Yy genotype: a Y from the egg and a y from the sperm, or a y from the egg and a Y from the sperm. Both of these possibilities must be counted. Recall that Mendel's pea-plant characteristics behaved in the same way in reciprocal crosses. Therefore, the two possible heterozygous combinations produce offspring that are genotypically and phenotypically identical despite their dominant and recessive alleles deriving from different parents. They are grouped together. Because fertilization is a random event, we expect each combination to be equally likely and for the offspring to exhibit a ratio of YY:Yy:yy genotypes of 1:2:1. Furthermore, because the YY and Yy offspring have yellow seeds and are phenotypically identical, applying the sum rule of probability, we expect the offspring to exhibit a phenotypic ratio of 3 yellow:1 green. Indeed, working with large sample sizes, Mendel observed approximately this ratio in every F2 generation resulting from crosses for individual traits.

Beyond predicting the offspring of a cross between known homozygous or heterozygous parents, Mendel also developed a way to determine whether an organism that expressed a dominant trait was a heterozygote or a homozygote. Called the test cross , this technique is still used by plant and animal breeders. In a test cross, the dominant-expressing organism is crossed with an organism that is homozygous recessive for the same characteristic. If the dominant-expressing organism is a homozygote, then all F1 offspring will be heterozygotes expressing the dominant trait. Alternatively, if the dominant expressing organism is a heterozygote, the F1 offspring will exhibit a 1:1 ratio of heterozygotes and recessive homozygotes. The test cross further validates Mendel's postulate that pairs of unit factors segregate equally.

Example of a test cross

Example of a test cross

A test cross can be performed to determine whether an organism expressing a dominant trait is a homozygote or a heterozygote.

12.2.4: Alternatives to Dominance and Recessiveness

With the inclusion of incomplete dominance, codominance, multiple alleles, and mutant alleles, the inheritance of traits is complex process.

Learning Objective

Discuss incomplete dominance, codominance, and multiple alleles as alternatives to dominance and recessiveness

Key Points

  • Incomplete dominance is the expression of two contrasting alleles such that the individual displays an intermediate phenotype.
  • Codominance is a variation on incomplete dominance in which both alleles for the same characteristic are simultaneously expressed in the heterozygote.
  • Diploid organisms can only have two alleles for a given gene; however, multiple alleles may exist at the population level such that many combinations of two alleles are observed.
  • The complete dominance of a wild-type phenotype over all other mutants often occurs as an effect of "dosage" of a specific gene product: the wild-type allele supplies the correct amount of gene product whereas the mutant alleles cannot.
  • One mutant allele can also be dominant over all other phenotypes, including the wild type.

Key Terms

codominance

a condition in which both alleles of a gene pair in a heterozygote are fully expressed, with neither one being dominant or recessive to the other

incomplete dominance

a condition in which the phenotype of the heterozygous genotype is distinct from and often intermediate to the phenotypes of the homozygous genotypes

allele

one of a number of alternative forms of the same gene occupying a given position on a chromosome

Alternatives to Dominance and Recessiveness

Mendel's experiments with pea plants suggested that: (1) two "units" or alleles exist for every gene; (2) alleles maintain their integrity in each generation (no blending); and (3) in the presence of the dominant allele, the recessive allele is hidden and makes no contribution to the phenotype. Therefore, recessive alleles can be "carried" and not expressed by individuals. Such heterozygous individuals are sometimes referred to as "carriers." Further genetic studies in other plants and animals have shown that much more complexity exists, but that the fundamental principles of Mendelian genetics still hold true.

Mendel's results, that traits are inherited as dominant and recessive pairs, contradicted the view at that time that offspring exhibited a blend of their parents' traits. However, the heterozygote phenotype occasionally does appear to be intermediate between the two parents. For example, in the snapdragon , Antirrhinum majus, a cross between a homozygous parent with white flowers (CWCW) and a homozygous parent with red flowers (CRCR) will produce offspring with pink flowers (CRCW). This pattern of inheritance is described as incomplete dominance, denoting the expression of two contrasting alleles such that the individual displays an intermediate phenotype. The allele for red flowers is incompletely dominant over the allele for white flowers. However, the results of a heterozygote self-cross can still be predicted, just as with Mendelian dominant and recessive crosses. In this case, the genotypic ratio would be 1 CRCR:2 CRCW:1 CWCW, and the phenotypic ratio would be 1:2:1 for red:pink:white.

Example of incomplete dominance

Example of incomplete dominance

These pink flowers of a heterozygote snapdragon result from incomplete dominance.

A variation on incomplete dominance is codominance, in which both alleles for the same characteristic are simultaneously expressed in the heterozygote. An example of codominance is the MN blood groups of humans. The M and N alleles are expressed in the form of an M or N antigen present on the surface of red blood cells. Homozygotes (LMLM and LNLN) express either the M or the N allele, and heterozygotes (LMLN) express both alleles equally. In a self-cross between heterozygotes expressing a codominant trait, the three possible offspring genotypes are phenotypically distinct. However, the 1:2:1 genotypic ratio characteristic of a Mendelian monohybrid cross still applies.

Mendel implied that only two alleles, one dominant and one recessive, could exist for a given gene. We now know that this is an oversimplification. Although individual humans (and all diploid organisms) can only have two alleles for a given gene, multiple alleles may exist at the population level such that many combinations of two alleles are observed. Note that when many alleles exist for the same gene, the convention is to denote the most common phenotype or genotype among wild animals as the wild type (often abbreviated "+"); this is considered the standard or norm. All other phenotypes or genotypes are considered variants of this standard, meaning that they deviate from the wild type. The variant may be recessive or dominant to the wild-type allele. An example of multiple alleles is coat color in rabbits . Here, four alleles exist for the c gene. The wild-type version, C+C+, is expressed as brown fur. The chinchilla phenotype, cchcch, is expressed as black-tipped white fur. The Himalayan phenotype, chch, has black fur on the extremities and white fur elsewhere. Finally, the albino, or "colorless" phenotype, cc, is expressed as white fur. In cases of multiple alleles, dominance hierarchies can exist. In this case, the wild-type allele is dominant over all the others, chinchilla is incompletely dominant over Himalayan and albino, and Himalayan is dominant over albino. This hierarchy, or allelic series, was revealed by observing the phenotypes of each possible heterozygote offspring.

Example of multiple alleles for rabbit coat color

Example of multiple alleles for rabbit coat color

Four different alleles exist for the rabbit coat color (C) gene.

The complete dominance of a wild-type phenotype over all other mutants often occurs as an effect of "dosage" of a specific gene product, such that the wild-type allele supplies the correct amount of gene product whereas the mutant alleles cannot. For the allelic series in rabbits, the wild-type allele may supply a given dosage of fur pigment, whereas the mutants supply a lesser dosage or none at all. Alternatively, one mutant allele can be dominant over all other phenotypes, including the wild type. This may occur when the mutant allele somehow interferes with the genetic message so that even a heterozygote with one wild-type allele copy expresses the mutant phenotype. One way in which the mutant allele can interfere is by enhancing the function of the wild-type gene product or changing its distribution in the body. One example of this is the Antennapedia mutation in Drosophila . In this case, the mutant allele expands the distribution of the gene product; as a result, the Antennapedia heterozygote develops legs on its head where its antennae should be.

Example of a mutant allele interfering with the function of a wild-type gene

Example of a mutant allele interfering with the function of a wild-type gene

As seen in comparing the wild-type Drosophila (left) and the Antennapedia mutant (right), the Antennapedia mutant has legs on its head in place of antennae.

12.2.5: Sex-Linked Traits

A gene present on one of the sex chromosomes (X or Y in mammals) is a sex-linked trait because its expression depends on the sex of the individual. 

Learning Objective

Distinguish between sex-linked traits and other forms of inheritance

Key Points

  • In mammals, females have a homologous pair of X chromosomes, whereas males have an XY chromosome pair.
  • The Y chromosome contains a small region of similarity to the X chromosome so that they can pair during meiosis, but the Y is much shorter and contains fewer genes.
  • Males are said to be hemizygous because they have only one allele for any X-linked characteristic; males will exhibit the trait of any gene on the X-chromosome regardless of dominance and recessiveness.
  • Most sex-linked traits are actually X-linked, such as eye color in Drosophila or color blindness in humans.

Key Terms

sex chromosomes

A chromosome involved with determining the sex of an organism, typically one of two kinds.

carrier

A person or animal that transmits a disease to others without itself contracting the disease.

X-linked

Associated with the X chromosome.

hemizygous

Having some single copies of genes in an otherwise diploid cell or organism.

Sex Determination

In humans, as well as in many other animals and some plants, the sex of the individual is determined by sex chromosomes. However, there are other sex determination systems in nature. For example, temperature-dependent sex determination is relatively common, and there are many other types of environmental sex determination. Some species, such as some snails, practice sex change adults start out male, then become female. In tropical clown fish, the dominant individual in a group becomes female while the others are male.

The sex chromosomes are one pair of non-homologous chromosomes. Until now, we have only considered inheritance patterns among non-sex chromosomes, or autosomes. In addition to 22 homologous pairs of autosomes, human females have a homologous pair of X chromosomes, whereas human males have an XY chromosome pair. Although the Y chromosome contains a small region of similarity to the X chromosome so that they can pair during meiosis, the Y chromosome is much shorter and contains many fewer genes. When a gene being examined is present on the X chromosome, but not on the Y chromosome, it is said to be X-linked.

Human male karyotype

Human male karyotype

A human males possesses XY chromosomes, as seen in the bottom left of this karyotype. The Y chromosome is much shorter than the X chromosome, unlike all of the other homologous chromosome pairs.

X-Linked Traits

Insects also follow an XY sex-determination pattern and like humans, Drosophila males have an XY chromosome pair and females are XX. Eye color in Drosophila was one of the first X-linked traits to be identified, and Thomas Hunt Morgan mapped this trait to the X chromosome in 1910. 

In fruit flies, the wild-type eye color is red (XW) and is dominant to white eye color (Xw). Because this eye-color gene is located on the X chromosome only, reciprocal crosses do not produce the same offspring ratios. Males are said to be hemizygous, because they have only one allele for any X-linked characteristic. Hemizygosity makes the descriptions of dominance and recessiveness irrelevant for XY males because each male only has one copy of the gene. Drosophila males lack a second allele copy on the Y chromosome; their genotype can only be XWY or XwY. In contrast, females have two allele copies of this gene and can be XWXW, XWXw, or XwXw.

Eye color in Drosophila is an example of a X-linked trait

Eye color in Drosophila is an example of a X-linked trait

In Drosophila, the gene for eye color is located on the X chromosome. Clockwise from top left are brown, cinnabar, sepia, vermilion, white, and red. Red eye color is wild-type and is dominant to white eye color.

X-Linked Crosses

In an X-linked cross, the genotypes of F1 and F2 offspring depend on whether the recessive trait was expressed by the male or the female in the P1 generation. With regard to Drosophila eye color, when the P1 male expresses the white-eye phenotype and the female is homozygous red-eyed, all members of the F1 generation exhibit red eyes. The F1 females are heterozygous (XWXw), and the males are all XWY, having received their X chromosome from the homozygous dominant P1 female and their Y chromosome from the P1 male. 

A subsequent cross between the XWXw female and the XWY male would produce only red-eyed females (with XWXW or XWXw genotypes) and both red- and white-eyed males (with XWY or XwY genotypes). Now, consider a cross between a homozygous white-eyed female and a male with red eyes. The F1 generation would exhibit only heterozygous red-eyed females (XWXw) and only white-eyed males (XwY). Half of the F2 females would be red-eyed (XWXw) and half would be white-eyed (XwXw). Similarly, half of the F2 males would be red-eyed (XWY) and half would be white-eyed (XwY).

Punnett square analysis of Drosophila eye color

Punnett square analysis of Drosophila eye color

Punnett square analysis is used to determine the ratio of offspring from a cross between a red-eyed male fruit fly (XWY) and a white-eyed female fruit fly (XwXw).

X-Linked Recessive Disorders in Humans

Sex-linkage studies provided the fundamentals for understanding X-linked recessive disorders in humans, which include red-green color blindness and Types A and B hemophilia. Because human males need to inherit only one recessive mutant X allele to be affected, X-linked disorders are disproportionately observed in males. Females must inherit recessive X-linked alleles from both of their parents in order to express the trait. 

Color perception in different types of color blindness

Color perception in different types of color blindness

In this chart you can see what people with different types of color blindness can see versus the normal color vision line at top.

Recessive Carriers

When they inherit one recessive X-linked mutant allele and one dominant X-linked wild-type allele, they are carriers of the trait and are typically unaffected. Carrier females can manifest mild forms of the trait due to the inactivation of the dominant allele located on one of the X chromosomes. However, female carriers can contribute the trait to their sons, resulting in the son exhibiting the trait, or they can contribute the recessive allele to their daughters, resulting in the daughters being carriers of the trait. Although some Y-linked recessive disorders exist, typically they are associated with infertility in males and are, therefore, not transmitted to subsequent generations.

Inheritance of a recessive X-linked disorder

Inheritance of a recessive X-linked disorder

The son of a woman who is a carrier of a recessive X-linked disorder will have a 50 percent chance of being affected. A daughter will not be affected, but she will have a 50 percent chance of being a carrier like her mother.

12.2.6: Lethal Inheritance Patterns

Inheriting two copies of mutated genes that are nonfunctional can have lethal consequences.

Learning Objective

Describe recessive and dominant lethal inheritance patterns

Key Points

  • An inheritance pattern in which an allele is only lethal in the homozygous form and in which the heterozygote may be normal or have some altered non-lethal phenotype is referred to as recessive lethal.
  • The dominant lethal inheritance pattern is one in which an allele is lethal both in the homozygote and the heterozygote; this allele can only be transmitted if the lethality phenotype occurs after reproductive age.
  • Dominant lethal alleles are very rare because the allele only lasts one generation and is, therefore, not usually transmitted.
  • In the case where dominant lethal alleles might not be expressed until adulthood, the allele may be unknowingly passed on, resulting in a delayed death in both generations.

Key Terms

dominant lethal

an inheritance pattern is one in which an allele is lethal both in the homozygote and the heterozygote; this allele can only be transmitted if the lethality phenotype occurs after reproductive age

recessive lethal

an inheritance pattern in which an allele is only lethal in the homozygous form and in which the heterozygote may be normal or have some altered non-lethal phenotype

mutation

any heritable change of the base-pair sequence of genetic material

Lethal Inheritance Patterns

A large proportion of genes in an individual's genome are essential for survival. Occasionally, a nonfunctional allele for an essential gene can arise by mutation and be transmitted in a population as long as individuals with this allele also have a wild-type, functional copy. The wild-type allele functions at a capacity sufficient to sustain life and is, therefore, considered to be dominant over the nonfunctional allele. However, consider two heterozygous parents that have a genotype of wild-type/nonfunctional mutant for a hypothetical essential gene. In one quarter of their offspring, we would expect to observe individuals that are homozygous recessive for the nonfunctional allele. Because the gene is essential, these individuals might fail to develop past fertilization, die in utero, or die later in life, depending on what life stage requires this gene. An inheritance pattern in which an allele is only lethal in the homozygous form and in which the heterozygote may be normal or have some altered non-lethal phenotype is referred to as recessive lethal.

For crosses between heterozygous individuals with a recessive lethal allele that causes death before birth when homozygous, only wild-type homozygotes and heterozygotes would be observed. The genotypic ratio would therefore be 2:1. In other instances, the recessive lethal allele might also exhibit a dominant (but not lethal) phenotype in the heterozygote. For instance, the recessive lethal Curly allele in Drosophila affects wing shape in the heterozygote form, but is lethal in the homozygote.

Dominant Lethal Alleles

A single copy of the wild-type allele is not always sufficient for normal functioning or even survival. The dominant lethal inheritance pattern is one in which an allele is lethal both in the homozygote and the heterozygote; this allele can only be transmitted if the lethality phenotype occurs after reproductive age. Individuals with mutations that result in dominant lethal alleles fail to survive even in the heterozygote form. Dominant lethal alleles are very rare because, as you might expect, the allele only lasts one generation and is not transmitted. However, just as the recessive lethal allele might not immediately manifest the phenotype of death, dominant lethal alleles also might not be expressed until adulthood. Once the individual reaches reproductive age, the allele may be unknowingly passed on, resulting in a delayed death in both generations. An example of this in humans is Huntington's disease in which the nervous system gradually wastes away . People who are heterozygous for the dominant Huntington allele (Hh) will inevitably develop the fatal disease. However, the onset of Huntington's disease may not occur until age 40, at which point the afflicted persons may have already passed the allele to 50 percent of their offspring.

Effects of Huntington's disease on neurons

Effects of Huntington's disease on neurons

The neuron in the center of this micrograph (yellow) has nuclear inclusions characteristic of Huntington's disease (orange area in the center of the neuron). Huntington's disease occurs when an abnormal dominant allele for the Huntington gene is present.

Attributions

  • Genes as the Unit of Heredity
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  • Phenotypes and Genotypes
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  • Alternatives to Dominance and Recessiveness
    • "Boundless." http://www.boundless.com/. Boundless Learning CC BY-SA 3.0.
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  • Sex-Linked Traits
    • "Boundless." http://www.boundless.com/. Boundless Learning CC BY-SA 3.0.
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