This set of Cytogenetics Multiple Choice Questions & Answers (MCQs) focuses on “Silencing and Genomic Imprinting”.
1. Genomic imprinting in autosomes is seen in _________________ percent of the genes.
Explanation: In autosomes most of the alleles can be expressed from both the parents. But a very shoet part i.e. <1% shows genomic imprinting.
2. Differential expression of the genetic material depending on its parentage of inheritance gives____________
Explanation: Genomic imprinting states that the alleles of some genes vary in their or expression depending on the fact that they are inherited from the mother or the father.
3. In Igf2 of human ______________ allele is expressed, and Igfr of mice __________ allele is expressed.
a) Maternal, maternal
b) Paternal, paternal
c) Maternal, paternal
d) Paternal, maternal
Explanation: The insulin like growth factor Igf for human shows that there only the paternal allele is expressed, but in its receptor, in case of mice the maternal allele is expressed. Thus both the alles must be present for proper function of the signal.
4. Which of the following doesn’t agree with XIST?
a) It codes for an mRNA that coats the inactive X chromosome into a bar body
b) It is the only gene that is active in inactive X chromosome
c) The embryo cells shows that maternal allele XIST is active over paternal
d) Inactivation is seen in somatic cells
Explanation: XIST allele in case of the embryo doesn’t show any imprinting. Imprinting is seen in case of the extra-embryonic cells.
5. The imprinting of genes has an epigenetic mode of regulation.
Explanation: Imprinting is ascertained by the methylation of certain C residues in CpG islands in the promoter region of a gene. Thus, it is not genetic but epigenetic regulation.
6. Choose the wrong statement in the regulation of imprinting.
a) Methylation of the C residues are seen in the CpG islands
b) The methylation prevents binding of the RNA polymerase
c) Genes are methylated at random
d) Deletion of gene with methylated CpG islands will have no effect
Explanation: In the case of imprinting which of the allele’s CpG island is methylated depends on the parent from which it is inherited. This shows that the methylation is not random but related to imprinting.
7. In mice if you delete the Igf2 gene from a female, the progeny will_____________
a) Be smaller
c) No major change
d) Be larger
Explanation: In mice the Igf2 genes from the female parent is methylated and inactivated by imprinting and only the male one is expressed. Thus, absence of the respective gene in mother shows no significant effect. However, if it were male hen the progeny would be smaller.
8. In mice H19 and Igf2 genes are controlled by the same enhancer. Which of the following is true?
a) The enhancer enhances both the gene on promoter binding
b) In one chromosome both the genes are expressed and in other they are not
c) Igf2 shows paternal imprinting, H19 shows maternal imprinting
d) Both the genes show paternal imprinting
Explanation: It is much of a surprise although both the genes can be enhanced by the same enhancer element located downstream of H19 both are not enhanced at once. In maternal gene the H19 is expressed and in paternal gene the Igf2 is expressed.
9. In mice the expression of Igf2 and H199 is only controlled by methylation.
Explanation: In addition to methylation the control is achieved by the presence of an insulator CTCB that helps by preventing the enhancer interaction of Igf2 in the maternal chromosome.
10. Choose the wrong statement from the following.
a) Maternal Igf2 is methylated to prevent expression
b) Paternal H19 is methylated to avoid expression
c) The enhancer can lead to expression of H19 in maternal gene
d) The enhancer can’t lead to expression of Igf2 in paternal gene
Explanation: It is true that the maternal Igf2 is not expressed in mice but the mechanism is via blockage of the enhancer by an insulator called CTCB binding to the CCCTC sequence in between the two adjacent genes. Rest of the options is correct.
11. During _________________ both the H19 alleles are ___________________
a) Oogenesis, inactivated
b) Oogenesis, activated
c) Oogenesis, hyper-activated
d) Spermatogenesis, activated
Explanation: The genomic imprinting has to be reset in every generation. This is achieved via the means that the genes that are maternally inherited are activated during oogenesis and paternally inherited genes are inactivated during the same and reverse for spermatogenesis. H19 is maternally inherited.
12. What will happen if an individual receives two copies of a gene from the same parent?
b) One gene will be automatically inactivated
c) Both the genes will show their product
d) Nothing much will be seen
Explanation: This condition gives rise to UPD or uni parental disomy. Here as the imprinting relation will be hampered, the individual may lack any active copy of the gene leading to developmental defects.
13. Which of the following is incorrect for Pader will syndrome?
a) This is due to failure of inheritance of several non-imprint genes
b) It is seen for chromosome 15
c) It causes loss of active genes in 15q11-q13
d) It occurs when the region containing specific genes in the maternal chromosome are missing
Explanation: In case of Pader Willi syndrome the genes 15q11-q13 contained in the paternal chromosome are missing which leads to the defects. It is not due to the maternal factors missing.
14. When the specific non-imprint gene from the chromosome 15 of the mother s missing it leads to _________________
a) Pader Willi syndrome
b) Angelman syndrome
c) Down’s syndrome
d) Klinefelter syndrome
Explanation: In Angelman syndrome the gene in the maternal chromosome 15 region 15q11-q13 is missing which leads to the absence of any functional copy of the gene at all as paternal copy is methylated and inactivated.
15. In Angelman syndrome we don’t see___________
b) Speech impairment
c) Overeating urge
d) Unprovoked laughter
Explanation: The urge to overeat is a symptom of the Pader Willi syndrome and it is not seen in case of Angelman syndrome. While the remaining options are seen in Angelman syndrome due to lack of a functional copy of maternally imprinted gene.
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