When a double-strand DNA break occurs in a eukaryotic cell, it may be repaired by either nonhomologous end joining or homologous recombination. How do these different repair mechanisms lead to potentially different outcomes?

Describe the 'end-replication problem' in eukaryotes. How is it resolved?

A fellow student considers the issues in Problem 22 and argues that there is a more straightforward, nongenetic experiment that could differentiate between the two types of mutations. The experiment requires no fancy genetics and would allow you to easily assay the products of the other SOS genes. Propose such an experiment.

Many of the gene products involved in DNA synthesis were initially defined by studying mutant E. coli strains that could not synthesize DNA.The dnaQ gene encodes the ε subunit of DNA polymerase. What effect is expected from a mutation in this gene?

Many of the gene products involved in DNA synthesis were initially defined by studying mutant E. coli strains that could not synthesize DNA.The dnaE gene encodes the α subunit of DNA polymerase III. What effect is expected from a mutation in this gene? How could the mutant strain be maintained?

Ataxia telangiectasia (OMIM 208900) is a human inherited disorder characterized by poor coordination (ataxia), red marks on the face (telangiectasia), increased sensitivity to X-rays and other radiation, and an increased susceptibility to cancer. Recent studies have shown that this disorder occurs as a result of mutation of the ATM gene. Propose a mechanism for how a mutation in the ATM gene leads to the characteristics associated with the disorder. Be sure to relate the symptoms of this disorder to functions of the ATM protein. Further, explain why DNA repair mechanisms cannot correct this problem.

A geneticist searching for mutations uses the restriction endonucleases SmaI and PvuII to search for mutations that eliminate restriction sites. SmaI will not cleave DNA with CpG methylation. It cleaves DNA at the restriction digestion sequence↓5′−CCC GGG−3′3′−GGG CCC−3′↑PvuII is not sensitive to CpG methylation. It cleaves DNA at the restriction sequence↓5′−CAG CTG−3′3′−GTC GAC−5′↑Explain why CpG dinucleotides are hotspots of mutation.