With age, somatic cells are thought to accumulategenomic “scars” as a result of the inaccurate repair of dou-ble-strand breaks by nonhomologous end joining (NHEJ).Estimates based on the frequency of breaks in primaryhuman fibroblasts suggest that by age 70, each humansomatic cell may carry some 2000 NHEJ-induced muta-tions due to inaccurate repair. If these mutations weredistributed randomly around the genome, how many pro-tein-coding genes would you expect to be affected? Wouldyou expect cell function to be compromised? Why or whynot? (Assume that 2% of the genome—1.5% protein-cod-ing and 0.5% regulatory—is crucial information.)
With age, somatic cells are thought to accumulategenomic “scars” as a result of the inaccurate repair of dou-ble-strand breaks by nonhomologous end joining (NHEJ).Estimates based on the frequency of breaks in primaryhuman fibroblasts suggest that by age 70, each humansomatic cell may carry some 2000 NHEJ-induced muta-tions due to inaccurate repair. If these mutations weredistributed randomly around the genome, how many pro-tein-coding genes would you expect to be affected? Wouldyou expect cell function to be compromised? Why or whynot? (Assume that 2% of the genome—1.5% protein-cod-ing and 0.5% regulatory—is crucial information.)
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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With age, somatic cells are thought to accumulate
genomic “scars” as a result of the inaccurate repair of dou-
ble-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 muta-
tions due to inaccurate repair. If these mutations were
distributed randomly around the genome, how many pro-
tein-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-cod-
ing and 0.5% regulatory—is crucial information.)
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