Chapter 14: Problem 6
Why are organisms that have a haploid life cycle valuable tools for mutagenesis studies?
Short Answer
Step by step solution
Key Concepts
These are the key concepts you need to understand to accurately answer the question.
Chapter 14: Problem 6
Why are organisms that have a haploid life cycle valuable tools for mutagenesis studies?
These are the key concepts you need to understand to accurately answer the question.
All the tools & learning materials you need for study success - in one app.
Get started for freeIn maize, a \(D s\) or \(A c\) transposon can cause mutations in genes at or near the site of transposon insertion. It is possible for these elements to transpose away from their original 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?
Two related forms of muscular dystrophy-Duchenne muscular dystrophy (DMD) and Becker muscular dystrophy (BMD)-are both recessive, X-linked, single-gene conditions caused by point mutations, deletions, and insertion in the dystrophin gene. Bach mutated form of dystrophin is one allele. Of the two diseases, DMD is much more severe. Given your knowledge of mutations, the genetic code, and translation, propose an explanation for why the two disorders differ greatly in severity.
Blectrophilic oxidants are known to create the modified base named 7,8 -dihydro- 8 -axoguanine (oxoG) in DNA. Whereas guanine base-pairs with cytosine, oxoG base-pairs with either cytosine or adenine. (a) What are the sources of reactive oxidants within cells that cause this type of base alteration? (b) Drawing on your knowledge of nucleotide chemistry, draw the structure of \(0 \times 0 \mathrm{G},\) and, below it, draw guanine. Opposite guanine, draw cytosine, including the hydrogen bonds that allow these two molecules to base- pair, Does the structure of oxoG, in contrast to guanine, provide any hint as to why it basepairs with adenine? (c) Assume that an unrepaired oxoG lesion is present in the helix of DNA opposite cytosine. Predict the type of mutation that will occur following several rounds of replication. (d) Which DNA repair mechanisms might work to counteract an oxoG lesion? Which of these is likely to be most effective?
Cystic fibrosis (CF) is a severe autosomal recessive disorder in humans that results from a chloride ion channel defect in epithelial cells, More than 500 mutations have been identified in the 24 exons of the responsible gene \((C F T R,\) or cystic fibrosis transmembrane regulator), including dozens of different missense mutations, frameshift mutations, and splice-site defects. Although all affected CF individuals demonstrate chronic obstructive lung disease, there is variation in whether or not they exhibit pancreatic enzyme insufficiency (PI). Speculate as to which types of mutations are likely to give rise to less severe symptoms of CF, including only minor PI. Some of the 300 sequence alterations that have been detected within the exon regions of the \(C F T R\) gene do not give rise to cystic fibrosis. Taking into account your knowledge of the genetic code, gene expression, protein function, and mutation, describe why this might be so.
Distinguish between proofreading and mismatch repair.
What do you think about this solution?
We value your feedback to improve our textbook solutions.