Question

1) During meiosis, an oocyte divides twice and generate 4 haploid cells. Cohesin proteins hold homologous chromosomes AND chromatids together. Experimental evidence shows these are loaded onto the chromosomes in S phase. Cohesin at the centromeres are released by securins during anaphase. SOme cohesin components such as SMC1 are down-regulated in older oocytes. If this is the case, at what stage(s) would you expect to see mis-segregating DNA?

a. Meiosos I

b. both meiosis I and II

c. none of these stages, i.e. noDNA mis-segregation

d. meiosis II

2. You are comparing the properties of normal cells vs cancer cells in cell culture experiments. Which of the following properties you expect to find in normal cells but NOT in cancer cells based on the information you have learned?

a. They can be grown in a culture dish.

b. Their growth is promoted by addition of growth factors.

c. They continue to divide even if there is DNA change.

d. They can be epithelial origin.

e. Their growth is inhibited after a complete monolayer of cells is formed in a dish.

3. What major events occur during anaphase?

a. Sister chromatids separate and are pulled to opposite polers.

b. Chromosomes attach to spindle fibers.

c. Chromosomes are located at opposite ends of the cell and nuclear envelopes begin to re-form.

d. Chromosomes replicate.

e. Chromosomes condense and the nuclear envelope disappears.

4. Which of the following statements about GPCR signing is NOT TRUE?

a. The second messengers generated through the GPCR signaling pathways can directly activate some channels.

b.The binding of a signaling molecule to a GPCR can lead to activate of many heterotrimeric G-protein complex.

c. The Galpha subunit, when activated, will hydrolyze GTP into GDP.

d. The same GPCR can have multiple effects via different downstream signaling pathways.

5. which of the following is not an event happened during prophase?

a. True nuclear lamina is disassembled by the depolymerization of the main filaments.

b. fragmentation of Golgi complex and Er.

c. Chromosomal material condenses to form compact mitotic chromosomes.

d. Chromosomal microtubules attach to kinetochores.

e. All the above

6.A signal molecule can only stimulate one type of specific membrane receptor across various types of cells, such as epithelial cells and muscle cells, and affects the same cellular activities.

a. True

b. False

7. One of the key properties of GPCR signaling cascade is its ability if signal simplification. Which of the following steps contributes to this property.

a. arrestin binding to GPCR

b. generation of second messengers by effector enzymes downstream of either Ga or GBy

c. receptors activation

d. hydrolysis of GTP

e. receptor-mediated endocytosis

8.Which of these combinations most likely lead to tumor growth?

a. Loss of a tumor suppressor genes

b. Both proto-oncogenes mutate to form an oncogene

c. One proto-oncogene allele mutates to form an oncogene and a function of a tumor suppressor gene is lost.

d. One proto-oncogene allele mutates to form an oncogene

Answer 1

Ans: 1) Chromosome segregation takes place during anaphase I and anaphase II of meiosis I and meiosis II so if the downregulation of SMC1 is taking place than the DNA mis-segregation takes place during both meiosis I and meiosis II i.e.option B.

2) Normal cells when placed on a tissue culture dish, they proliferate until the surface of the dish is covered by a single layer of cells just touching each other. So the only property wwe xpect to find in normal cells and not in cancer cells is their growth is inhibited after a complete monolayer of cells is formed in a dish. Option E

3) Anaphase is the stage of mitosis after the process of metaphase, when replicated chromosomes are split and the newly-copied chromosomes (daughter chromatids) are moved to opposite poles of the cell. So the correct option is Sister chromatids separate and are pulled to opposite polers. Option A

4) When a ligand binds to the GPCR it causes a conformational change in the GPCR, which allows it to act as a guanine nucleotide exchange factor (GEF). The GPCR can then activate an associated G protein by exchanging the GDP bound to the G protein for a GTP. The G protein's α subunit, together with the bound GTP, can then dissociate from the β and γ subunits to further affect intracellular signaling proteins or target functional proteins directly depending on the α subunit type.

Signaling by activated Gα-GTP is terminated by GTP hydrolysis, a reaction catalyzed by the Gα subunit itself that yields the inactive form, Gα-GDP.

G Protein Coupled Receptors (GPCRs) perceive many extracellular signals and transduce them to heterotrimeric G proteins, which further transduce these signals intracellular to appropriate downstream effectors and thereby play an important role in various signaling pathways.

So the binding of signalling molecule to a GPCR leads to the activation of the heterotrimeric G protein linked iwth the receptor. So the only statement that is not true about GPCR is The binding of a signaling molecule to a GPCR can lead to activate of many heterotrimeric G-protein complex.i.e. option B.

5) In G2 ohase the fragmentation of golgi complex and endoplasmic reticulum takes place which means that option B is the only event that does not takes place during prophase.

6) Signaling molecules are the molecules that are responsible for transmitting information between cells in your body. Signalling molecules will bind to the receptor only when the confromation of that receptor is unique for that particular receptor it's just like a lock and key arrangement where one key unlocks only a single lock similarly the signalling molecule will bind to the receptor having the conformation suitable for the binding of that signal molecule. So its true that A signal molecule can only stimulate one type of specific membrane receptor across various types of cells.

7) I think it's signal amplification which means the larger impact of a single signal molecule and this is because GPCR signalling have multiple effects via different downstream signaling pathways and this is because of the production of various secondary messengers which are able to activate various kinase proteins various ion channles and so on. So the correct option is option B.

8) In the cell the tumor suppressor genes alleles are in dominant form and proto-oncogenes alleles are in recessive form so a single mutation in the proto-oncogene will leads to the gain of function mutation converting protooncogene into oncogene and mutation is both the alleles of tumor suppressor gene will lead to loss of function mutation and cause the loss of functionality of tumor suppressor gene. So the best combination for tumor growth is One proto-oncogene allele mutates to form an oncogene and a function of a tumor suppressor gene is lost i.e. option C.