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Here are three quotes from an printed interview with Francis Collins (look him u

ID: 72786 • Letter: H

Question

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

a. Typically, telomeres cap the chromasomal ends and protects them from the action of exonucleases. With the aging process the telomere length decreases that associated with increased production of a toxic protein called progerin. Progerin is a mutated version of lamin A, which is encoded by LMNA gene that involve in maintenance of the nucleus structure and repository of genetic information. The shortening of telomeres in cell division during aging process in individuals with normal LMNA genes alters the RNA splicing. As we know that RNA is a transcribed form of DNA which does not carry all of the linear information embedded in the DNA. Since, there are intervening letters of unused genetic information called introns are located in between the splices of exons that contain the code for building proteins. These introns to be removed by splicing mechanism that typically appears to be altered by telomere shortening. Here, the alteration in LMNA RNA splicing results in the accumulation of progerin.

b. Premature aging people (suffering from Hutchinson-Gilford progeria syndrome) cells can be compared with artificially made senescent cells.

c. Collins stated by "Connecting this rare disease phenomenon and normal aging is bearing fruit in an important way,"

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