what is the significance of mutations in the emergence of new genetic properties (alleles) that may result (or not) in new phenotypic characteristics? (Recall that not all SNPs affect phenotype.)
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- A haplotype is a set of DNA variations, or polymorphisms, that tend to be inherited together. A haplotype can refer to a combination of alleles or to a set of single nucleotide polymorphisms (SNPs) found on the same chromosome. Each SNP represents a difference in a single nucleotide. For example, an SNP may replace the cytosine (C) with thymine (T) in a certain stretch of DNA. SNPs occur normally throughout a person’s DNA. They occur almost once in every 1,000 nucleotides on average, which means there are roughly 4 to 5 million SNPs in a person's genome. These variations may be unique or occur in many individuals; Most commonly, these variations are found in the DNA between genes. They can act as biological markers, helping scientists locate genes that are associated with disease. When SNPs occur within a gene or in a regulatory region near a gene, they may play a more direct role in disease by affecting the gene’s function. Nucleotide Position…A woman diagnosed with early-onset Alzheimer's due to a mutation of the APP genehas children with a man that has no family history of familial Alzheimer's. Give the probability of each possible genotype with corresponding phenotype. (The woman has two possible allele combinations. You must show both possibilities)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.
- Huntington's disease is a very rare, debilitating disease that affects approximately 1 in 10,000 people. The disease is caused by a particular type of genetic mutation (large number of CAG repeats) in a gene called huntingtin (HTT). Designate the disease-causing allele HTTP and the non-disease- causing allele HTTN. We know that individuals with genotype HTTN will not develop Huntington's Disease, but people with either HTTD/HTTP or HTTN/HTTD will develop the disease. Which allele is dominant--HTTN or HTTP? Explain your reasoning thoroughly, using the correct definition of dominance.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?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.
- Huntington disease (HD) can arise from a rare, short, in-frame addition of CAG nucleotide triplets within the huntingtin (HTT) gene coding region, which creates a disease-causing allele with the symptoms only appearing later in life. Using this information, describe an experiment that could be undertaken to determine whether a currently healthy young individual is a carrier of the HD-causing mutation. Describe the method you would use and how you would interpret the results of this experiment.You are working in the lab with two known carcinogens found in cigarette smoke: Benzo(a)pyren (BaP) and nitrosamine ketone (NNK). BaP is an aromatic hydrocarbon and the mechanism of carcinogenesis is through oxidation reactions with DNA. NNK is a nitrosoamine. Describe how these two kinds of carcinogens lead to mutations. (Be detailed. Remember you are graded on effort/completeness.)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…
- A complex biochemical pathway is shown below, along with the alleles that either promote or inhibit each step of the pathway leading to a phenotype. Gene A has alleles A and a, B has alleles B and b, and so forth. Genes B and C are duplicate dominant epistatic lethal as heterozygotes (i.e. Bb Cc are lethal). Genes D and E are duplicate dominant epistatic (i.e. dd eg = desired phenotype). If I were to cross AA Bb cc Dd Ee with aa BB Cc Dd e, (i) (ii) What proportion of all offspring don't show the phenotype? What proportion of offspring survive? Gene A Gene B B Gene D a Gene C Gene ESuppose that you could undergo genetic testing at age 18 for susceptibility to a genetic disease that would not appear until middle age and has no available treatment. a. What would be some of the possible reasons for having such a genetic test and some of the possible reasons for not having the test? b. Would you personally want to be tested? Explain your reasoning.Suppose that you are studying the role of Protein B, which you believe plays a role in regulating PCD/Apoptosis in mice. You create two lines of mutant mice. One (bb) is homozygous for a loss-of-function allele of gene B. The other (Bb) is heterozygous, with one wild-type allele and one loss-of function allele. Initially you pay particular attention to two phenotypes of the resulting mice:(i) The morphology of their paws (see picture)(ii) The size of their brains & shape of their skulls. The bb mice have unusually large brains and unusual protrusions from their skulls. Suggest one other aspect of mouse morphology or physiology that you might expect to be altered in the absence of Protein B. Briefly explain your reasoning. Also, based on the apparent effect of Protein B on the likelihood of PCD/Apoptosis, would you classify Protein B as the product of a proto-oncogene or of a tumor suppressor gene?