H Biology Final Exam

Signal Transduction

• Peptide hormones are polar and can’t enter the cell, needs receptors on the exterior of target cells (insulin).

• Steroid hormones are nonpolar and can enter the cell, has intracellular receptors (test/estrogen).

3 stages of Signal Transduction:

1. Reception

   • Signal molecule binds to the G-protein Receptor.

   • Receptor is specific to the signal molecule (lock & key osrs).

2. Signal Transduction

   • GPR activation by binding of signal molecule activates a G protein called the shuttle protein.

   • Activation of shuttle protein activates an enzyme, typically adenylyl cyclase, turning ATP into cAMP.

3. Response

   • cAMP, the second messenger molecule, amplifies the signal and activates protein kinase (typically Protein Kinase A) to spread and drive cellular response.

   • PKA phosphorylates target proteins in the cell, amplifying the signal.

Adaptive (AKA Acquired) Immune Response (B & T cells)

Cell-Mediated Immune Response

1. Macrophage engulfs a pathogen and presents its antigens on the surface using MHC II proteins.

2. A T cell receptor on a naive helper T cell binds to the antigen-MHC complex.

3. This causes the macrophage to release Interleukin-1 (IL-1).

4. IL-1 activates the helper T cell, which then releases Interleukin-2 (IL-2).

5. IL-2 stimulates the helper T cell to rapidly divide → an army of cloned helper T cells.

6. IL-2 also activates cytotoxic T cells, which:

   • Recognize infected body cells (presenting antigens via MHC I).

   • Kill them using perforins and enzymes that trigger apoptosis.

Humoral Immune Response

1. IL-2 from helper T cells also activates B cells that have encountered the same antigen.

2. B cells undergo clonal selection and divide rapidly.

3. Some B cells become memory B cells:

   • These "remember" the antigen and respond quickly upon re-infection.

4. Most B cells become plasma cells:

   • Plasma cells produce and secrete up to 2,000 antibodies per second.

5. Antibodies are Y-shaped proteins that:

   • Bind specifically to antigens.

   • Mark pathogens for destruction by phagocytes or complement proteins.

Neuron Communication

1. Electrical Signal (Action Potential)

   1. neuron @ Resting Membrane Potential is around a -70mV charge, maintained by the Sodium-Potassium pump (3Na+ in, 2K+ out)

   2. Na+ flows into the neuron because of the stimulus, and cell reaches threshold potential at -55V.

   3. Stimulus opens Voltage-Gated Sodium Channels, and so a lot of Na+ flows into the neuron (depolarization).

   4. @ +30mV, Voltage-Gated Sodium Channels close, and Voltage-Gated Potassium Channels open, so K+ diffuses out of the neuron.

      • K+ also leaks through K+ leak channels and the Sodium-Potassium pump.

   5. Resting Membrane Potential returns to a negative state (repolarization).

   6. Refractory period occurs, and stimulated Voltage-Gated Sodium Channels cannot be opened again for a few ms because they are temporarily inactive.

      • Charge in an axon cannot flow backwards.

      • K+ still flows out because of the Voltage-Gated Potassium Channels still being open, charge is more negative than -70mV (hyperpolarization).

2. Synaptic Transmission (Chemical Synapse)

   1. The action potential reaches the axon terminal, which is at +30mV.

   2. Voltage-Gated Ca2+ channels open, and Calcium rushes into the synapse.

   3. Calcium triggers a mechanism causing neurotransmitter vesicles to fuse with membranes and drop the neurotransmitters (ACh) into the synaptic cleft.

   4. Neurotransmitters release into the synapse, and open a “chemically gated” ligand Na+ channel to start the Action Potential again in the post-synaptic cell.

• Some places in Neuron’s don’t have gaps, they are connected by Connexons or Gap Junctions.

  • Ions can pass through neurons.

  • Action Potential is directly transferred through neurons.

• Drugs at the synapse can either mimic neurotransmitters (agonist) to activate Action Potentials or block neurotransmitters (antagonist)

Hardy Weinberg

1. No genetic drift — must have stable allele frequency

   • Must have a large population size.

   • Bottleneck Effect can cause genetic drift, population decrease because of natural disasters and change in gene frequency.

   • Founder Effect, small population of species breaks off and founds their own population, so new gene frequency might not match that of the old one.

2. No gene flow

   • No individuals can leave or enter the population being observed.

3. No mutations

   • Variation occurs, which adds to the gene pool.

4. Random Mating

   • Mating is not influenced by specific traits such as behavior or appearance.

   • If individuals prefer certain traits in reproduction, genotype and allele frequencies will change.

5. No natural selection

   • Certain alleles improve ability for survival, and so these organisms are able to survive longer and possibly leave more offspring, affecting the allele frequency of the population.

• Allele Frequency

  • p + q = 1 (dominant, recessive)

• Genotype Frequency

  • p² + 2pq + q² = 1 (homo. dominant, heterozygous, homo. recessive)

HWE provides a mathematical model to study populations and prove that microevolution exists.

HWE’s Null Hypothesis — predicts that allele frequencies won’t change over time, and there are underlying issues in a population if allele frequencies change.

Evidence for Evolution (Build a Phylogeny)

• Common Ancestry

  • Two species have more recent common ancestry if their DNA or appearance is similar.

  • Pay attention to AA sequences and molecular data.

  • Even being able to compare the data means that there is some genetic similarity and common ancestry between species, no matter how different they appear to be.

  • If two species diverge earlier, then that means that there is more time for genetic mutations, adaptations, and natural selection to occur in a population.

Ecology Principles

• Carrying Capacity

  • Definition: The maximum population size an environment can support without degrading the environment.

  • Example: If population data shows a plateau or crash, it's likely the population has hit its carrying capacity.

• Limiting Factors

  • Definition: Environmental factors (e.g., food, space, water, predation) that restrict population growth.

  • Types:

    • Density-dependent: effects increase as population density increases (e.g., disease, competition).

    • Density-independent: affect populations regardless of size (e.g., natural disasters).

• Predator-Prey Relationships

  • Definition: Predator and prey populations often follow cyclical patterns.

  • Application: If prey population increases, predator population may rise afterward, followed by a drop in prey.

• Succession

  • Primary Succession: Begins on bare rock (no soil).

  • Secondary Succession: Happens after a disturbance in an area that already has soil.

  • Predicts which species will colonize and dominate over time.

• Niche and Competition

  • Niche: An organism’s role in the ecosystem (what it eats, where it lives, etc.).

  • Competitive Exclusion Principle: No two species can occupy the same niche indefinitely.

  • Inference: If two species compete, one may be outcompeted or forced into a different niche.

• Energy Flow and Trophic Levels

  • Only ~10% of energy is transferred from one trophic level to the next.

  • Top predators have less energy available → smaller populations.

• Biotic vs Abiotic Factors

  • Biotic: Living components (predators, competition, disease).

  • Abiotic: Nonliving (temperature, light, pH, rainfall).

  • Prediction: Changes in abiotic conditions often explain shifts in species populations or behavior.

• Biodiversity and Ecosystem Stability

  • More biodiversity → more stable and resilient ecosystems.

  • A loss in biodiversity can make ecosystems more vulnerable to changes or collapse.