Suppose, you want to detect the CAG repeat expansion within a particular gene (30 repeats in normal changes to 250 repeats in disease) in a certain disease. How will you diagnose this disease condition?
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Q: To detect the CAG repeat expansion with a particular gene where 30 repeats in Normal changes to 250…
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- Suppose, you want to detect the CAG repeat expansion within a particular gene (30 repeats in normal changes to 250 repeats in disease) in a certain disease. How will you diagnose this disease condition?
- Can you identify Y chromosome microdeletion (which involves the deletion of AZF locus) using conventional karyotyping? If not, then why?
- How will you diagnose a chromosomal translocation event? (Discuss any one of the processes)
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- To detect the CAG repeat expansion with a particular gene where 30 repeats in Normal changes to 250 repeats in a certain disease, how can we diagnose the condition. How To identify Y chromosome microdeletion ( which involves the deletion of AZF locus) using conventional karyotyping? If not then why. How will you diagnose a chromosomal translocation event?. For the following types of chromosomal rearrangements,would it theoretically ever be possible to obtain aperfect reversion of the rearrangement? If so, wouldsuch revertants be found only rarely, or would theybe relatively common?a. A deletion of a region including five genesb. A tandem duplication of a region including five genesc. A pericentric inversiond. A Robertsonian translocatione. A mutation caused by a transposable elementjumping into a protein-coding exon of a geneAt the end of the short arm of human chromosome 16 (16p), several genes associated with disease are present, including thalassemia and polycystic kidney disease. When that region of chromosome 16 was sequenced, gene-coding regions were found to be very close to the telomere-associated sequences. Could there be a possible link between the location of these genes and the presence of the telomere-associated sequences? What further information concerning the disease genes would be useful in your analysis?
- You have identified a SNP marker that in one largefamily shows no recombination with the locus causinga rare hereditary autosomal dominant disease.Furthermore, you discover that all afflicted individuals in the family have a G base at this SNP on theirmutant chromosomes, while all wild-type chromosomes have a T base at this SNP. You would like tothink that you have discovered the disease locus andthe causative mutation but realize you need to consider other possibilities.a. What is another possible interpretation of the results?b. How would you go about obtaining additional genetic information that could support or eliminateyour hypothesis that the base-pair difference is responsible for the disease?You learned in Problem 21 in Chapter 7 that theneurodegenerative disease ALS can be caused by expansion of a hexanucleotide repeat region (5′-GGGGCC-3′)outside of the open reading frame (but within the firstintron) of the gene called C9ORF72. While a normalC9ORF72 allele has 2–23 copies of the hexanucleotiderepeat unit, dominant disease-causing alleles have hundreds or even thousands of copies. Researchers observed that the first intron of theC9ORF72 disease allele is transcribed not only fromthe normal template strand of DNA, but also from thenontemplate strand. Even more unusual, both types ofrepeat-region transcripts are translated in all six readingframes in an AUG-independent manner—a processcalled repeat-associated non-ATG translation, or RANtranslation. These discoveries led to the hypothesisthat the proteins made from the repeats mightcontribute to ALS.a. What polypeptides are made from the repeat-regiontranscripts?b. According to the RAN translation hypothesis, whyare…Familial retinoblastoma, a rare autosomal dominant defect, arose in a large family that had no prior history of the disease. Consider the following pedigree (the darkly colored symbols represent affected individuals): a. Circle the individual(s) in which the mutation most likely occurred. b. Is the person who is the source of the mutation affected by retinoblastoma? Justify your answer. c. Assuming that the mutant allele is fully penetrant, what is the chance that an affected individual will have an affected child?
- As shown in Figure 13-14, what is the fundamental distinction between a pair-rule gene and a segment-polaritygene?You have identified a gene that is located on human chromosome 20 and wish to identify its location within the mouse genome. On which chromosome would you be most likely to find the mouse counterpart of this gene?If the bandicoot genome is 3.62 x 109 base pairs, and the "highly repetitive DNA" fraction is composed entirely of copies of sequence 5'TGCGTGTGTGC3' and its complement, how many copies of this sequence are present in the bandicoot genome?
- In each of the illustrations below, a segment of a chromosome has two copies of a transposable element. In panel a, they are oriented in the same direction, whereas in panel b they are in opposite directions. A double strand break occurs in element A and is repaired by homologous recombination using element B as a repair template. For each case, what will the chromosome look like after homologous recombination occurs? Choose one of the five options below, 1-5.The occurrence of multiple transposons within the genome oforganisms has been suggested as a possible cause of chromosomalrearrangements such as deletions, translocations, and inversions.How could the occurrence of transposons promote these types ofstructural rearrangements?Consider the following two wild type chromosomes: AB•CDEFGH I•JKLMN What kind of rearrangement is observed in the mutated chromosomes below? AB•CLMN I•JKDEFGH A. non-reciprocal translocation B. tandem duplication C. reciprocal translocation D. displaced duplication E. deletion