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Ch. 15 - Gene Mutation, DNA Repair, and Transposition

Klug 12th Edition

Ch. 15 - Gene Mutation, DNA Repair, and Transposition

Problem 22

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Chapter 15, Problem 22

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

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Key Concepts

Here are the essential concepts you must grasp in order to answer the question correctly.

End-Replication Problem

The end-replication problem refers to the difficulty eukaryotic cells face in fully replicating the ends of linear chromosomes during DNA replication. DNA polymerases can only synthesize DNA in one direction and require a primer, which means that the very end of the chromosome cannot be completely copied, leading to progressive shortening of the DNA with each cell division.

Recommended video:

Semiconservative Replication

Telomeres

Telomeres are repetitive nucleotide sequences located at the ends of eukaryotic chromosomes that protect them from degradation and prevent the loss of essential genetic information during replication. They act as a buffer zone, ensuring that the coding regions of the DNA are not affected by the end-replication problem, thus maintaining genomic stability.

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Telomeres and Telomerase

Telomerase

Telomerase is an enzyme that adds repetitive nucleotide sequences to the telomeres, counteracting the end-replication problem. It is particularly active in stem cells and germ cells, allowing these cells to maintain their telomere length and continue dividing without losing vital genetic information, thus playing a crucial role in cellular aging and cancer biology.

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Telomeres and Telomerase

Previous problem

Related Practice

Textbook Question

Speculate on how improved living conditions and medical care in the developed nations might affect human mutation rates, both neutral and deleterious.

Textbook Question

In maize, a Ds or Ac transposon can alter the function of genes at or near the site of transposon insertion. It is possible for these elements to transpose away from their original insertion site, causing a reversion of the mutant phenotype. In some cases, however, even more severe phenotypes appear, due to events at or near the mutant allele. What might be happening to the transposon or the nearby gene to create more severe mutations?

Textbook Question

It is estimated that about 0.2 percent of human mutations are due to TE insertions, and a much higher degree of mutational damage is known to occur in some other organisms. In what way might a TE insertion contribute positively to evolution?

Textbook Question

The SOS repair genes in E. coli (discussed in Chapter 15) are negatively regulated by the lexA gene product, called the LexA repressor. When a cell's DNA sustains extensive damage, the LexA repressor is inactivated by the recA gene product (RecA), and transcription of the SOS genes is increased dramatically. One of the SOS genes is the uvrA gene. You are a student studying the function of the uvrA gene product in DNA repair. You isolate a mutant strain that shows constitutive expression of the UvrA protein. Naming this mutant strain uvrAᶜ, you construct the diagram shown above in the right-hand column showing the lexA and uvrA operons: Outline a series of genetic experiments that would use partial diploid strains to determine which of the two possible mutations you have isolated.

Textbook Question

The human genome contains approximately 10⁶ copies of an Alu sequence, one of the best-studied classes of short interspersed elements (SINEs), per haploid genome. Individual Alu units share a 282-nucleotide consensus sequence followed by a 3'-adenine-rich tail region [Schmid (1998)]. Given that there are approximately 3 x 10⁹ base pairs per human haploid genome, about how many base pairs are spaced between each Alu sequence?

Textbook Question

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?