45. - 48. Here are three quotes from an printed interview with Francis Collins (

Question

45. - 48. Here are three quotes from an printed interview with Francis Collins (look him up),
i. " Collin’s lab team found that in cells growing in the lab, when they used a chemical to un-cap the chromosome ends, it altered gene splicing and led to progerin production and
cellular senescence.

ii. “It’s clear that progerin turns on as a cell is approaching senescence,” Collins said.
Collin’s lab team found that in cells growing in the lab, when they used a chemical to un-cap the chromosome ends, it altered gene splicing and led to progerin production and cellular
senescence.
iii. “While I can’t prove it, it seems likely that progerin itself is part of normal, programmed senescence,” Collins said. “If we understood that, maybe we would be able to come up with
a strategy to deal with the process of normal aging.”

a) We've heard that before, that gene splicing alters with age - what does that mean?

b) According to statement ii, they were comparing artificially made senescent cells to the cells of people with what condition?

c) When stating that progerin production is part of normal aging, what theory of aging is he implicitly endorsing? Explain.

Explanation / Answer

Following are the answers of the different parts:

a) As suggested by Prof. Collins, gene splicing alters with age. This may arise from age-related alterations in splicing factor expression, and further alters normal proteins to their mutated versions, resulting in cell senescence.

b) The condition to being referred by Prof. Collins, is Progeria. Progeria is a rare syndrome in children which is characterized by physical symptoms indicative of premature old age.

c) In this part, Prof. Collins is referring to telomerase theory of aging. Telomeres are short stretch of nucleotides which protect the normal DNA strands of a cell. Telomerase is an enzyme that can extend the structure of telomeres so that cells continue to maintain their ability to divide, and restrict aging. Normal mammalian somatic cells donot express telomerase and in the absence of telomerase activity telomere shortening results which in turn leads to premature aging. Current research from Prof. Collins's lab suggests that short or dysfunctional telomeres activate production of progerin, which further leads to age-related cell damage.

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