Why are diseases due to microsatellite amplification, even though they have a monogenic pattern of inheritance, considered within non-classical inheritance? Explain the term dynamic mutation
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- Is it possible for a severe mutation-causing hereditary condition to pass down from generation to generation without creating symptoms? Explain.Our understanding of maternal effect genes has been greatly aided by their identification in experimental organisms such as Drosophila melanogaster and Caenorhabditis elegans. In experimental organisms with a short generation time, geneticists have successfully searched for mutant alleles that prevent the normal process of embryonic development. In many cases, the offspring die at early embryonic or larval stages. These are called maternal effect lethal alleles. How would a researcher identify a mutation that produced a recessive maternal effect lethal allele?Why are the concepts of variable expressivity, incomplete penetrance, and delayed age of onset so important in relation to genetic diseases?
- A rare dominant mutation expressed at birth was studiedin humans. Records showed that six cases were discoveredin 40,000 live births. Family histories revealed that in twocases, the mutation was already present in one of the parents.Calculate the spontaneous mutation rate for this mutation.What are some underlying assumptions that may affect ourconclusions?Why would a mutation in a somatic cell of a multicellular organism not necessarily result in a detectable phenotype?Leber Congenital Amaurosis (LCA) causes progressive vision loss due to defects in the gene that encodes RPE65 isomerase. Affected individuals are homozygous recessive for mutant alleles of the RPE65 gene. You are trying to determine the molecular nature of the mutations in three individuals with LCA. For ease of analysis, you may assume that each individual is homozygous for the same mutant allele (though the three individuals have different mutations than each other). You use the polymerase chain reaction to amplify DNA from each patient and you determine the sequence of the DNA and compare it to unaffected individuals. You identify the following differences. Note that the non-template strand of DNA is given and the changes are highlighted using red boldface. You can assume that the sequences are in the first reading frame (eg. the first three nucleotides of each sequence is a codon). The coding region of the gene is 1602 bp and the position of the sequences shown below is…
- Explain the difference between a gain-of-functionmutation and a dominant-negative mutation. Why areboth these types of mutation usually dominant?APOE gene has been found to be a major contributor to sporadic Alzheimer's disease (AD), by acting as an age-of-onset modifier for the common relatively late-onset forms of the disease. Among four alleles causing early onset of AD, the epsilon4 allele (APOE4) disrupts this function. If you generate transgenic monkeys in which the normal allele of APOE gene is knocked out, what phenotype will you expect for those knockout monkeys? A. The APE mRNA expression will be completely suppressed. B. They slow down the development of AD. C. They develop AD early. D. They don't show any AD symptom.Lesch-Nyhan syndrome is due to a mutation in a gene that encodesa protein called hypoxanthine-guanine phosphoribosyltransferase(HPRT). HPRT is an enzyme that functions in purine metabolism.People afflicted with this syndrome have severe neurodegenerationand loss of motor control. The pedigree below contains severalindividuals with Lesch-Nyhan syndrome, shown with blacksymbols. Based on this pedigree, does this syndrome appearto be inherited by an autosomal recessive, autosomal dominant,X-linked recessive, or X-linked dominant pattern? Explainyour reasoning.
- In McCune-Albright syndrome, fibrous connective tissue replaces bone, tan patches (café-au-lait spots) dot the skin, and hormone abnormalities cause early puberty and malfunction of the thyroid, pituitary, and adrenal glands. The phenotype is highly variable, and all patients are somatic mosaics for the mutation, which is in the gene GNAS1. Why is the condition seen only in mosaics?How would you explain gene expression? How is it that a particular genotype is actually expressed as a phenotype? I am looking for details here, including an explanation of the molecular mechanisms involved.(a) How does the duplication of individual genes occur? (b) individual that inherit a genetic condition known as xeroderma pigmentosum exhibit an extreme sensitivity to sunlight exposure and often develop skin cancer by the age of 10. What repair pathway is most likely disrupted as a result of such mutation? Explain why?