IB Biology C2.1: Chemical signalling worked solutions

C. It is a cytokine, a signal protein that controls growth and immune responses and acts on nearby cells. A hormone is carried in the blood to distant cells, a neurotransmitter crosses a synaptic gap between a neuron and its target, and a calcium ion is not a protein.

B. Only cells with receptors whose binding site fits insulin can respond. A is wrong because the blood reaches all the cells, C because insulin does not enter the cell, and D because cAMP is not the second messenger for insulin.

B. Autoinducer builds up as the population grows, and past a threshold it switches on the light genes in every cell. A and C ignore the density effect, and D is wrong because the bacteria, not a host, make the light.

C. Testosterone is a lipid-soluble steroid, so it crosses the plasma membrane and binds an intracellular receptor. Insulin, epinephrine and acetylcholine are water-soluble and bind receptors in the plasma membrane.

D. Epinephrine binds the receptor, the receptor activates the G protein, the G protein activates adenylyl cyclase, and adenylyl cyclase makes cAMP. The other orders reverse at least one arrow.

B. The insulin receptor is a tyrosine kinase receptor, so binding makes the receptor phosphorylate tyrosines on itself. A describes a G protein receptor, C a ligand-gated channel and D a steroid receptor.

C. The receptor is itself an ion channel; it opens and sodium ions diffuse in, changing the membrane voltage. Acetylcholine does not enter the cell, and no G protein or transcription is involved.

A. A signal that switches on its own production amplifies itself, as autoinducer does in quorum sensing. B, C and D are ways a pathway is turned down, which is negative regulation.

Any five of: glucagon is a peptide, so it cannot cross the plasma membrane (1); it binds a specific receptor in the plasma membrane of the liver cell (1); binding activates a G protein (1); the G protein activates adenylyl cyclase, which makes cAMP, the second messenger (1); the cascade amplifies the signal because each active molecule activates many others (1); enzymes are activated that break glycogen down to glucose (1); the glucose is released into the blood (1).

One mark for a similarity: both are carried in the blood, bind a specific receptor, and act only on cells that have it (1). Paired differences, one mark per pair with both halves stated, maximum 5: testosterone is a lipid-soluble steroid that crosses the membrane / insulin is a water-soluble protein that cannot; testosterone binds an intracellular receptor in the cytoplasm or nucleus / insulin binds a transmembrane tyrosine kinase receptor; the testosterone-receptor complex binds DNA and promotes transcription / insulin binding causes autophosphorylation and a relay; insulin's relay moves vesicles with glucose transporters to the membrane / testosterone's response is new proteins from new mRNA; testosterone has no second messenger / insulin's relay passes the message on inside the cell.

Oestradiol, any three of: it is lipid-soluble and diffuses through the plasma membrane (1); it binds a receptor in the cytoplasm or nucleus (1); the activated receptor binds a specific DNA sequence (1); transcription of the target genes is promoted (1). Epinephrine, any three of: it binds a receptor in the plasma membrane and stays outside the cell (1); the receptor activates a G protein (1); the G protein activates adenylyl cyclase, which makes cAMP from ATP (1); cAMP, the second messenger, activates enzymes that change the cell's activity (1). Up to 3 marks for each hormone.

(a) Light per cell is low (0.2 to 0.9) up to 10^{7} cells per mL (1); it rises from 0.9 to 41, about 46-fold (41\div0.9=45.6), between 10^{7} and 10^{8}, then levels near 55 (1). (b) Cells release a diffusible autoinducer (1); the concentration rises with density and at low density is too low to act (1); above a threshold enough autoinducer binds the receptors and the light genes are switched on in the cells together (1).

(a) 31.0\div2.0=15.5 times (1). (b) With the blocker the rate (2.4) is close to the untreated 2.0 (1), so the G protein is needed between the receptor and the response (1). (c) The analogue restores the rate to 29.5 even though the G protein is blocked (1); so cAMP acts downstream of the G protein (1) and is enough to activate the enzymes that break down glycogen (1).

(a) (9.6-1.8)\div1.8\times100=433\% (1). (b) The kinase inhibitor lowers uptake to 2.1, close to the no-insulin value, so tyrosine kinase activity is needed (1); blocking vesicle fusion lowers it to 2.3, so vesicles have to fuse with the plasma membrane for uptake to rise (1). (c) Insulin binds the receptor on the outside of the cell (1); the receptor phosphorylates tyrosines and starts a relay (1); vesicles carrying glucose transporters move to the plasma membrane and fuse with it, so uptake rises (1).

(a) R1 (1). Any two of: the response begins after 2 ms, much faster than R2 (1); it needs sodium ions outside the cell (1); the G protein blocker has no effect (1); cAMP does not change (1). (b) R2 works through a chain of steps, G protein, then adenylyl cyclase, then cAMP, then enzyme activation (1); each step takes time, while binding at R1 opens a channel directly (1).

Any five of: oestradiol is lipid-soluble and enters the cell (1); it binds a nuclear/intracellular receptor in GnRH-secreting hypothalamic cells (1); the activated receptor binds DNA and promotes transcription (1); progesterone enters endometrial cells and binds its receptor (1); the receptor changes gene expression in the endometrium (1); this regulates development and function of the endometrium, for implantation and the maintenance of pregnancy (1).

Channels open and Ca^{2+} enters the cytoplasm (1); the rise in concentration above a low resting level is the signal, and calcium binds proteins to trigger a response such as vesicles fusing with the membrane (1); calcium is removed again by pumps, which ends the signal (1).

Hydrophobic amino acids sit in the region in contact with the phospholipid tails and hold the protein in the bilayer (1); hydrophilic amino acids lie on the parts in contact with the water inside and outside the cell (1); the binding site on the outer face has a shape and charges that fit the ligand (1); so only that ligand binds and the receptor changes shape (1).

(a) Toxin is 88 for the wild type at high density but 2 at low density (1); the mutant stays low at both densities, 2 and 4 (1). (b) The wild type releases autoinducer, which accumulates as density rises (1); above a threshold it binds receptors and switches on the toxin gene (1); the mutant cannot make autoinducer, so the gene stays off (1). (c) Adding autoinducer restores toxin even at low density: 80 (1), so it is the concentration of autoinducer, and not density itself, that triggers the response (1). (d) A drug that blocks the receptor stops cells reading the signal (1), so the toxin is not made even when autoinducer is high (1).

(a) 15\times1\times40=600 cAMP per second (2: one for the multiplication, one for the value). (b) The G protein stays active (1); adenylyl cyclase keeps making cAMP, so the response is prolonged / not switched off (1). (c) Negative feedback (1); the enzyme lowers the level of cAMP, so the pathway is turned down (1); with the enzyme blocked, cAMP would keep rising or stay high (1).

(a) Negative feedback (1); acting on the release of H by the gland (1). (b) (100-62)\div100\times100=38\% (1). (c) With I blocked, nothing lowers the release of H (1), so the level stays high or rises instead of settling at 28 (1). (d) A second system doubles every minute: 3, 6, 12, 24; the next value is 48 (1); it must level off eventually because a substrate or receptor becomes limiting (1).

(a) L: the bead stops it entering and it does nothing, so its receptor is inside the cell (1); it changes transcription of gene X, consistent with an activated receptor binding DNA (1). M: still works on a bead that cannot enter, so its receptor is in the plasma membrane (1); the rise in cAMP suggests a G protein receptor (1). (b) L is lipid-soluble, small enough to cross the bilayer, like a steroid hormone (1). (c) The change in gene X takes 45 minutes because transcription and translation are needed, while M acts within seconds through second messengers (1).

(a) The activated receptor recognises a specific DNA base sequence (1); only genes with that sequence are switched on in that cell (1). (b) RNA polymerase transcribes the gene into mRNA (1); the mRNA leaves the nucleus and is translated at ribosomes, where tRNA anticodons pair with mRNA codons (1); amino acids join to make the new protein that carries out the response (1). (c) The response needs transcription and translation, which take longer than activating enzymes that are already present (1).

(a) Negative feedback (1); the rise in glucose causes insulin release, which lowers glucose, and the fall reduces insulin release (1). (b) Facilitated diffusion (1); glucose moves down its concentration gradient through the transporter without ATP (1). (c) Insulin binds the receptor and a relay follows (1); vesicles with transporters fuse with the plasma membrane, increasing the number of transporters there (1).

(a) It breaks down acetylcholine, so the channel closes and the resting potential returns (1). (b) Acetylcholine is not removed, so it keeps binding the receptors (1); the sodium channels stay open or reopen, so sodium keeps entering (1); the postsynaptic membrane stays depolarised and the response is prolonged (1). (c) The active site has a shape and charges that fit acetylcholine (1), so only that substrate binds and is broken down (1).