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

Chapter 15, Problem 22

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

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Hello everyone and welcome to today's video. So telomeres contain these long repetitive sequences which protect the coding sequence from degradation during DNA replication. However, in every cell division the length of the telomeres decreases what happens to a cell once the telomere reaches the critical length. So let's break this down. We have these telomeres and the function of these telomeres is to protect their chromosomes because they're protecting they serve as a cap for these DNA cutting sequences. Now, with every cell division, the telomere length decreases. So what happens to a cell once the telomere reaches its critical length or once it gets too short? Well first of all the cell is not going to be able to divide anymore. And then as these D. N. A coding sequences get more and more affected eventually the sale will die because it's D. N. A. Is being degraded. Another term for this is sent essence. This is the process where the cell first is not able to divide and eventually it dies due to this loss of the telomeres. Because of this answer choice D. Is the correct answer to our question. I really hope this helped you and I hope to see you on the next one.
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.

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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?
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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?
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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.
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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?
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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?
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