Question

Discuss the following problem. With age, somatic cells are thought to accumulate genomic “scars” as a result of the inaccurate repair of double-strand breaks by nonhomologous 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 protein- coding 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% protein-coding and 0.5% regulatory-is crucial information.)

Solution

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Nonhomologous end joining is a quick, but no so efficient solution for repairing double-strand breaks. As it is suggested, every single somatic cell has about 2000 mutations because of the failure of this repairing system (until the human being reaches the age of 70), and according to this, we can conjecture how many protein-coding genes will be affected.

We know that 98% of the human genome consists of noncoding genes and that only 2% of the genome is coding (1.5% are protein-coding, while 0.5% are regulatory). So, if one somatic cell has 2000 mutations that are randomly distributed through the cell genome we can estimate that only 30 protein-coding genes will be affected, or we can say less than 1% of all protein-coding genes.

Also, because of the fact that this type of repairing leaves "scars" it is obvious that accumulation of this mutation may finally lead to translocations and telomere fusion, which are considered as the marks of tumor cells. But, luckily there is one more repairing system, homologous recombination, which works side by side with previously mentioned, restoring the original DNA sequence in that way. Therefore, we can say that these mutations at this rate will not greatly affect normal cell function.

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