With age, somatic cells are thought to accumulate genomic \"scars\" as a result

Question

With age, somatic cells are thought to accumulate genomic "scars" as a result of the inaccurate repair of double-strand breaks by end-joining (NHEJ). Estimates based on the frequency of breaks in primary human fibroblasts suggest that by age 70 each human somatic cell may carry some 2000 NHEJ-induced mutations due to inaccurate repair. If these mutations were distributed randomly around the genome, how many genes would you expect to be affected? Would you expect cell function to be compromised? Why or why not? (Assume that 2% of the genome-1.5% coding and 0.5% regulatory-is crucial information.)

Explanation / Answer

In mutation in the NHEJ leads to the two broken ends are rejoined without deletions or rearrangements in the genome. Totally 1000 genes may be affected in the entire genome. Because of the Telomere dysfunction through inhibition of TRF2 resulted in the end-to-end fusions through the non-homologous end-joining (NHEJ) between the C-strand of one telomere to the G-strand of another. This also includes degradation of the 3’ overhang and subsequent telomere end joining by DNA ligase. Normal cells are also attempt to prevent the inability of chromosomes which can arise from telomere fusions by signalling cell cycle arrest.

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