C2006/F2402 ’12

Key to Review Questions for Exam #3

1. (Pax6 binds to similar DNA sequences in both genes) (Pax6 works with a different combination of TFs in lens & pancreas) Explanation: Pax6, a TF, would recognize a similar DNA sequence in both genes, which is conferred by the amino acids in Pax6’s DNA binding domain. However, PAX6 works with a different set of TFs in the different cell types. For example, activation of crystallin in the lens requires PAX6 and TFs “A” & “B” and activation of somatostatin in the pancreas requires PAX6 and TFs “C” & “D”. B-1. Pax6 could bind the DNA at (any of these). B-2. Pax6, Sox2, and L-Maf are (trans-factors) (proteins) (TFs) (nuclear). B-3. The binding sites for Pax6, Sox2 & L-Maf in the lens are (DNA) (nuclear) (a cis-element) Diagram for Problem 6-B:

TFs:
(or trans-factors)

Enhancer
(or cis-element)

+1

(or transcription initiation site) Explanation: You had to draw a diagram and label the following to get full credit: 1. Enhancer or cis element 2. TFs or trans-factors – labeling Pax6, Sox2 & L-Maf wasn’t enough 3. +1 or transcription initiation site C. The histone acetlytransferase (i) switches the chromatin configuration (loose euchromatin to loosest euchromatin) AND (ii) (increases transcription). Explanation: The enhancer, when Pax6, Sox2 & L-Maf bind, switches from loose to loosest euchromatin, increasing transcription. Regions of the DNA that are sometimes transcribed are always euchromatin, never heterochromatin. D. The region would (represent a hypersensitive site) & (be more digested than the crystallin coding region). Explanation: The enhancer while bound by Pax6, Sox2 & L-Maf has a paucity of nucleosomes and so is relatively exposed to DNase. Treatment of this enhancer with DNase, results in a hyper sensitive site. In contrast, the transcribed region of the crystallin gene (looser) has less nucleosomes than when this gene isn’t actively transcribed (loose) but has more nuclesomes than the enhancer (loosest). E. For somatic nuclear transfer to succeed (all of the above) must occur. Explanation: In order for somatic nuclear transfer to work, the heart cell’s DNA needs to reverse the differentiation process, so that the DNA expresses the correct genes for totipotent and can progress through the ensuing stages of potency (pluripotency, multipotency, etc.) to form the entire organism. For this to happen all of the above choices must be reset or changed. Reseting of the potency is performed by the various components present in the egg cytoplasm.

A person with GSD type (1) is most likely to develop hypoglycemia. the primary problem is with the (effector(s)) & there has been a change in the (controlled process(es)). Glucose release is controlled by adjusting the rate of Glucose-phosphate hydrolysis. B-2. not too little release between feedings (due to low glucagon or persistent insulin). the levels of blood sugar were probably (elevated) Explanation: The baby was exposed to high (maternal) blood sugar in utero. The major effector(s) causing the problem are (muscle) (liver). So they can develop hypoglycemia. Both occur in the liver. A-2.). a person has to be able to take sugar up from the blood. convert the lactate to glucose phosphate in liver. such as lactate. or from gluconeogenesis -. there is too much insulin for a normal level of sugar intake and/or blood sugar. All of these should be able to compensate for high blood sugar. when the infant is in the absorptive state. In GSD 1. not hydrolysis. not later in the post-absorptive. 3. and release the glucose. Explanation: The problem here is glucose release (the controlled process) by the liver (the effector). It takes a short while for the infant to readjust the levels of insulin production to match the levels of blood sugar. People with GSD6 can generate (& release) some glucose from gluconeogenesis in liver. A-1. When the child is born. They can’t break down liver glycogen. but the physiologically important process is glucose release. B-1. People with GSD1 can not release glucose from the liver at all – both glycogen breakdown and gluconeogenesis produce glucose phosphate. A normal person can compensate for low blood sugar by (glycogen breakdown) & (gluconeogenesis). and made high levels of insulin in response. and the glucose is trapped in side the cell if the phosphate cannot be removed. you had to explain the situation in people with each of the three types of GSD. but they can breakdown muscle glycogen to lactate. Therefore these people are very likely to develop hypoglycemia. Explanation: To compensate for high blood sugar. the person must be able to store the glucose by synthesizing glycogen (or fat). beyond immediate energy needs. and phosphatase removes the phosphate from the glucose. Explanation: The problem occurs right after feeding. Explanation: Liver is the primary effector for releasing glucose to correct for low blood sugar. . C.manufacture of glucose from smaller molecules. but they don’t release glucose – they release lactate. but it’s not as severe a problem as with type 1. remove the phosphate. or converts to glucose for release or storage (as glycogen). B. and the excess insulin causes too much glucose uptake and therefore hypoglycemia. a person with GSD type (5) is least likely.C2006/F2402 ’12 Key to Review Questions for Exam #3 2. & E. The glucose can come from glycogenolysis (depolymerization of glycogen). All these people can do that. Hypoglycemia shortly after feeding probably results primarily from abnormally (high glucose uptake). Explanation: To get full credit. The GSD types have problems with breaking down glycogen. Muscles also breakdown glycogen. The hypoglycemic infant is probably producing (too much insulin) . Therefore the hypoglycemia must be caused by too much uptake (due to the high insulin) right after feeding. if there is extra. D. not with making or storing it. A. Note that phosphorylase breaks down glycogen (a glucose polymer) to glucose phosphate. The regulated variable (glucose) and the desired value (the set point) remain unchanged. In the pregnant mother. which the liver either breaks down further for energy generation.

A. If it is big enough. and their problem is with muscle. There is a graded response in the receptor cells that is proportional to the stimulus – this is called the receptor potential. the bigger the receptor potential. When worms are first exposed to heat. pot. but the immediate response will be a receptor potential. cont. the sensory neurons (have a depolarizing receptor potential) & (fire action potentials). relative to the outside. and there is still a response to heat. A-4. What Cl. (Note this is a one cell system – the receptor cells themselves fire APs. and open the channels. The compounds in hot peppers probably (bind to TRPQ channel proteins) Explanation: C-1. because epithelial cells do not normally respond to capsaicin or heat. not an AP. B-4. and the detached patches do respond to capsaicin.) C-1. The receptor potential caused by capsaicin and the rec. 4. In this case the sensory neurons (have a depolarizing receptor potential). and if the total is over threshold. If capsaicin is present. Ca++. pot. one that is not made in normal epithelial cells. there is no possibility for generation of a second messenger. due to either heat or capsaicin.C2006/F2402 ’12 Key to Review Questions for Exam #3 Explanation of 3 D & E. Capsaicin changes (the distance to threshold) Explanation: There is no EPSP in receptor cells. (If there is enough heat. or depolarized.are higher on the outside of the cell. the cell is already partially depolarized and the amount of heat needed to depolarize to threshold is decreased. Na+. All three ions. and the cell will become less negative. A-3. Both capsaicin and heat open channels and depolarize the cells. So the obvious explanation is that the receptor is ionotropic – that is. the TRPQ channels do not transport Cl. In addition. There is no reason to invoke a separate receptor. the more APs. the receptor is part of the channel. so the ion won’t move even if the electrical gradient is favorable. In this case. The only new protein made in the recombinant epithelial cells. It is likely that the heat receptor proteins of the worm are (ionotropic). There is no separate receptor. the cell fires an AP. C-2. the rec. it reaches threshold and the cells fire action potentials. (Note: In the actual experiments. B-3..to (go out of the cell) (go in to the cell) (stay put – no significant movement across the membrane). If you increase the concentration of capsaicin you will increase (the number of spikes or APs) & (the absolute magnitude of the receptor potential). In this case. as heat does.) . pot. The bigger the rec. Given that the receptor is ionotropic. you expect the cells to become (hyperpolarized) (depolarized) (either way). an AP will be generated. Ca++ to (go out of the cell) (go in to the cell) (stay put – no significant movement across the membrane). the inside of the cell is negative.. caused by heat are summed. Explanation: In response to heat. Cl. So clearly the positive ions (cations) will move in if channels are opened for them. but they have normal liver function. In the detached patches. and should not have any part of the signaling system except the added TRPQ channels. is the TRPQ channel. In this case. and that the G protein or a membrane bound component can open the added channels without a soluble second messenger. it makes sense that capsaicin should bind to the receptor/channel itself. Since the muscle is not directly involved in release of glucose. They may generate less lactate (from muscle) for the liver to use for gluconeogenesis. This is sufficient to give a response to both heat and capsaicin. A-2. B-2. Na+ to (go out of the cell) (go in to the cell) (stay put – no significant movement across the membrane).will do if channels open depends on the electrical gradient (and the specificity of the channels). the response was measured. People with GSD5 have no problems with release of glucose from the liver. When the cells are exposed to heat. and corresponding G proteins. the TRPQ channels will open. (The only other possibility is that normal epithelial cells already have unused receptors for heat. The more channels are opened. It does not say in the problem whether or not there was a response to capsaicin in the detached patches. is depolarizing (see A). they are presynaptic only.) B-1.) C-2. you expect A-1. they are least likely to develop hypoglycemia. not an EPSP or IPSP. and Cl.

So a cell that has been determined to be mesoderm has already by definition been specified to be mesoderm. If gonad is removed 6 weeks into development. At the time of transplantation in this case. 8B: Unlike most of the organs in our body. A. i. C2006/F2402 ’12 Key to Review Questions for Exam #3 . 8C: This question asks what would be different from Terry in the case study if we removed the gonad before the gonad differentiated into testes. is associated with tighter chromatin and decreased TF accessibility to DNA. AMH would not be produced and the Mullerian ducts would remain. The testes secretes two molecules that are important for sex determination of the other sex organs. C. Somatic nuclear transfer (SNT) is a method where the nucleus of a differentiated cell is placed inside an egg cell which has had its nuclear DNA removed. If the gonads were removed before they differentiated into testes. Only at the final stage do they differentiate – express the proteins that confer the cell with the structure and function of that specific cell type. regardless of whether or not testosterone is produced. 6. as a result of H3 K9 acetylation. Methylation of H3 K9 (tightens chromatin) (decreases TF accessibility to DNA). Acetylation of H3 K9 (loosens chromatin) (increases TF accessibility to DNA). the AMH secreted by the testes would destroy the Mullerian ducts.e. If you don’t have the receptor for testosterone (the androgen receptor) testosterone will not be detected. At the time of transplantation tin this case. testosterone and anti-Mullerian hormone (AMH). A. 8. determined and differentiated to become skin cells. the mouse skin cells were (specified) (differentiated) (determined). the (Mullerian duct remains) Explanations: 8A: The sex chromosomes only determines the fate of the somatic tissues of the gonads and then once this is determined the somatic tissue of the gonad determines the fate of the germ cells. In the case study. is associated with looser chromatin and increased TF accessibility. All of the organs that are normally affected by testosterone would respond in the same way. where the testes were present until birth. no response. the cells were (specified). 7. Which of these reproductive organs are bipotential? (external genitalia) (gonads). A. In somatic nuclear transfer (mitochondrial DNA and nuclear DNA are derived from different cells) Explanation: iPS cells are created by infecting differentiated cells with the DNA that encodes four transcription factors. The only tissue that responds to AMH is the Mullerian duct. B. B.C2006/F2402 ’12 Key to Review Questions for Exam #3 5. B. The sex chromosomes directly determine the fate of (gonads). Increased transcription. A. In induced pluripotent (iPS) cells (mitochondria DNA and most of the nuclear DNA are derived from the same cell) B. Explanation: As cells progress down the cell fate cascade they are specified (will change fate if transplanted) and determined (won’t change fate if transplanted) multiple times. the external genitalia and the gonads can become two different tissues. the ducts and the external genitalia. determination and at the end stage differentiation. The Mullerian ducts and the Wollfian ducts can each only form specific organs. Explanation: Decreased transcription. caused by H3 K9 methylation. In B the cells are specified to become skin (under normal circumstances they would develop into skin cells) but are not determined or differentiated since they will change their fate when transplanted. The cells always progress in the following order: specification. In A the cells are expressing the proteins that confer a skin phenotype and they do not change their cell fate after transplantation so they are specified. In SNT the mitochondrial DNA is derived from the egg and the nuclear DNA is derived from the nucleus of the somatic donor cell. As a result the nuclear DNA and the mitochondrial DNA come from the same cell but the nucleus now also contains the DNA of the four transcription factors that was infected.

The differentiated cell whose nucleus was used as a donor for SCNT was less potent.9. B. What could you expect regarding the fetal development of this individual? (male levels of testosterone) (testes are present) B. Sertoli cells of the testes should secrete AMH. 10. becoming more potent? (creation of zygote using SCNT) & (iPS cell creation). and female genitalia will develop by default. Explanation for 10: iPS cells and zygotes created by SCNT are pluripotent and totipotent respectively. Which of the following progresses in the opposite direction. If there is no reductase. Explanation for 9: Both Cdx2 and Oct4 are turned on at the 8 cell stage. but they all involve increases in differentiation and decreases in potency. male external genitalia will not develop. which should cause degeneration of the Mullerian ducts. Which of the following changes increases potency and occur in the natural process of human development? (none of these). Bivalent methylation is the state of master regulatory genes before they are turned on – when they are not expressed. Leydig cells should secrete testosterone which sustains the Wolffian duct. Which of these proteins during normal development do not have their histones bivalently methylated at H3K4 and H3K27 simultaneously? (Cdx2) & (Oct4). so they do not have a period when they are poised to go on. What could you determine regarding this individuals chromosomes and the expression of genes on those chromosomes? (XY individual) (Sry expressed) (testosterone receptor expressed) C. but not yet expressed. All the other changes listed occur during human development. They can be turned on or off by removing one of the methyl groups. that is very early. If the person had both Mullerian ducts and Wolffian ducts. As a child which of the following should be present? (clitoris) (testes) (labia major) (Wolffian duct derivatives). However. Explanation for 12: A. there will be no DHT because conversion of testosterone to DHT will be blocked. and develops into male genitalia (penis and scrotum) only if DHT is present. 11. If tissues derived from Wolffian ducts are present. the fetus must have developed testes that produced male levels of testosterone (in the fetus) to sustain the Wolffian ducts. otherwise it develops into female structures (clitoris and labia major). as were the cells transformed by the 4 genes used to make iPS cells. The SRY gene must be expressed (to trigger testes formation and testosterone production) and the testosterone receptor must be expressed (for the Wolffian ducts to respond to the testosterone). If this individual had both Mullerian and Wolffian ducts what could you conclude? (Leydig cells are okay) (Sertoli cells aren’t functioning properly). but ready to go either way. Natural human development does not include SCNT or creation of iPS cells – these require laboratory manipulations. B. If there is testosterone. C. You would expect this person to be XY. A. you assume the person had high testosterone (from working Leydig cells) but not AMH (so Sertoli cells aren’t working properly). The SRY gene on the Y should turn on production of proteins needed to develop testes. . Explanation for 11: The initial stages of differentiation should be normal for a male. The perineum is bipotential. 12. granulosa and thecal cells wouldn’t form. A.

Master your semester with Scribd & The New York Times

Special offer for students: Only $4.99/month.

Master your semester with Scribd & The New York Times

Cancel anytime.