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Flashcards · AP® Biology · Unit 4

Unit 4: Cell Communication and Cell Cycle flashcards

40 cards on topics 4.1 to 4.6. Pick a topic or study the whole unit.

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4.1 Cell Communication

What is needed for cell communication?
A signalling cell, a signal, a target cell with a receptor and a response. Receptors decide which cells are targets.
How do cells communicate by direct contact?
Through junctions: gap junctions (animals) and plasmodesmata (plants) join cytoplasm so ions and small molecules pass through. Or through surface molecules: an antigen-presenting cell shows antigen fragments to a helper T cell.
What are local regulators?
Signals released into the fluid around a cell that act on cells nearby: neurotransmitters at synapses, morphogens in embryos, quorum-sensing signals in bacteria and defence signals in plants.
How do hormones reach their targets?
They travel in the blood to the whole body (insulin, human growth hormone, thyroid hormones, testosterone, estrogen). They are not carried only to target organs; only cells with matching receptors respond.
What is quorum sensing?
Bacteria release a signal whose concentration rises with cell density; above a threshold, genes switch on together. Useful for jobs such as glowing or forming biofilms that work only when many cells act together.
How does a morphogen gradient work?
Concentration is high near the source and low far away, and different concentrations switch on different genes. A morphogen halving every 20 µm from 100 units is 25 units at 40 µm.
Does a signal cause the same response in every target cell?
No. The same signal can cause different responses in different target cells.

4.2 Introduction to Signal Transduction

What are the three stages of signal transduction?
Reception (ligand binds a specific receptor and changes its shape), transduction (relay molecules pass and amplify the signal) and response (a change in cell activity).
Where are receptors for different ligands found?
Water-soluble ligands bind receptors on the cell surface. Small nonpolar ligands (steroids, thyroid hormones) cross the membrane and bind receptors in the cytoplasm or nucleus, often changing gene expression.
How does a G protein-coupled receptor pathway work?
The ligand binds a GPCR (seven membrane passes), which activates a G protein (GDP → GTP). This activates adenylyl cyclase: ATP → cAMP (second messenger), which activates protein kinase, which acts on targets.
What do kinases and phosphatases do?
Kinases add phosphate (from ATP) to proteins; phosphatases remove it. A chain of kinases is a phosphorylation cascade. Phosphorylation does not always switch proteins on.
How is a signal amplified, and how do you calculate it?
Steps such as adenylyl cyclase and protein kinase each activate many molecules. Overall amplification = product of the factors at each step; divide where several molecules activate one. Three ×10 steps give 1000.
Why is a ligand-gated channel response faster than a GPCR pathway?
Binding opens the channel directly, so ions flow and the cell responds in milliseconds, with no chain of relay molecules.
What is the first messenger and what is the second messenger?
The ligand (such as a hormone) is the first messenger; cAMP is a second messenger made inside the cell. Do not confuse the GPCR (receptor) with the G protein.

4.3 Signal Transduction Pathways

How do fast and slow responses to a signal differ?
Fast responses switch existing enzymes, channels or transporters on or off (seconds to minutes). Slower responses activate a transcription factor, changing gene expression and the proteins made (minutes to days).
What happens if a receptor's ligand-binding site is blocked or mutated?
The ligand cannot bind, nothing downstream is switched on and there is no response, even with plenty of signal. Extra ligand does not overcome it.
What does a component stuck "on" do to a pathway?
A gain-of-function mutation or toxin in the receptor, relay protein or kinase gives a response with no signal, unless a later step is blocked.
Where does an inhibitor partway down a pathway block the response?
From that step on: the response is blocked even if earlier steps are on. A stuck-on relay protein upstream of an inhibited kinase gives no response.
How can signal pathways cause apoptosis?
Some pathways trigger ordered, programmed cell death, for example removing tissue between developing digits. It is not cells bursting from damage.
How can signal pathways change phenotype?
New proteins made after a signal can change the phenotype: fruit ripening with ethylene, bacteria glowing by quorum sensing, HOX genes setting the body plan.

4.4 Feedback

What is negative feedback?
A loop in which the response reduces the original change, keeping a variable near its set point. Examples: end-product inhibition of the first enzyme in a pathway, blood glucose, body temperature. "Negative" does not mean harmful.
What is positive feedback?
A loop in which the response amplifies the original change: childbirth (oxytocin), lactation, fruit ripening (ethylene → more ethylene), blood clotting. It does not keep a variable stable; always say what ends it.
How is blood glucose regulated?
High glucose: pancreas β cells release insulin, cells take up glucose and the liver makes glycogen. Low glucose: α cells release glucagon and the liver breaks down glycogen. Glucagon is a hormone; glycogen is a storage carbohydrate.
How do type 1 and type 2 diabetes differ?
Type 1: β cells destroyed, so insulin is very low and glucose is high. Type 2: target cells resist insulin, so glucose is high while insulin is normal or high.
What are the parts of a feedback loop?
Stimulus, sensor, control centre, effector and response. It is feedback because the response acts on the stimulus; a break in any link stops the correction.
What stops the positive feedback loop in childbirth?
The birth removes the pressure on the cervix, so oxytocin release stops increasing.

4.5 Cell Cycle

What are the stages of the cell cycle?
Interphase (G1, S, G2), then mitosis, then cytokinesis. G1: growth and copying organelles. S: DNA replication. G2: protein synthesis, ATP production, centrosome duplication. Interphase is not a resting stage.
What is G0?
A non-dividing state outside the cycle. Many G0 cells can re-enter with the right cues.
What happens in each phase of mitosis?
Prophase: chromosomes condense, spindle forms, envelope breaks down. Metaphase: chromosomes line up at the equator. Anaphase: sister chromatids pulled to opposite poles. Telophase: envelopes re-form, spindle breaks down.
How does cytokinesis differ in animal and plant cells?
Animal cells divide by a cleavage furrow; plant cells build a cell plate from Golgi vesicles. Plant cells do not form a cleavage furrow.
How do chromosome and chromatid numbers change through the cycle?
For 2n chromosomes: G1 2n chromosomes, 2n chromatids. G2 to metaphase: 2n chromosomes, 4n chromatids (DNA doubled). Anaphase whole cell: 4n chromosomes. Each daughter: 2n. S phase doubles DNA, not chromosome number.
How do you calculate a mitotic index?
(cells in mitosis ÷ total cells, including interphase) × 100. 30 of 240: 12.5%. Time in a stage = (cells in stage ÷ total) × cycle length, assuming cells are not dividing in step.
Why are the daughter cells of mitosis genetically identical?
S phase makes exact copies of every chromosome, and anaphase sends one sister chromatid of each chromosome to each pole. Mitosis is used for growth, repair and asexual reproduction.

4.6 Regulation of Cell Cycle

How do cyclins and CDKs control the cell cycle?
CDKs are kinases present in about constant amounts but active only when bound to a cyclin. Cyclins are made steadily then destroyed quickly. Active cyclin-CDK phosphorylates targets that drive the next stage; destroying cyclin switches CDK off.
What do the G1, G2 and M checkpoints check?
G1: cell size, nutrients, signals, DNA damage. G2: DNA fully replicated and undamaged. M (spindle): every chromosome attached to both poles, otherwise anaphase is delayed.
What happens if a cell fails a checkpoint?
It pauses and repairs, enters G0 or undergoes apoptosis. A failed checkpoint does not always kill the cell.
What happens if a mitotic cyclin is not broken down?
CDK stays active and the cell cannot leave mitosis. If cyclin is not made, CDK stays inactive and the cell stops at that checkpoint.
How do mutations lead to cancer?
Mutations make "drive" proteins overactive or "stop" proteins fail, so cells divide with damaged DNA and avoid apoptosis. Usually several mutations are needed, not one.
Is apoptosis always harmful?
No. Programmed cell death removes damaged or unneeded cells and shapes organs in development. Too much apoptosis, though, loses healthy cells.
Are cyclins enzymes?
No. CDKs are the kinases; cyclins are regulatory proteins whose concentration rises and falls. CDK activity, not CDK amount, rises and falls.

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