How would you test a hypothesis that a genetic condition, such as neurofibromatosis, is due to a transposon?
Added by Kiara R.
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Identify the Gene: The first step would be to identify the gene or genes associated with neurofibromatosis. This could be done through genetic sequencing and comparison of genomes from individuals with and without the condition. Show more…
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Adi S.
After completing her master's degree in Biotechnology, Barisha was hired as a Lab Technician for a Biotech research company. Her project is to assist her bosses in determining the likelihood of curing hemophilia at the fetal stage using CRISPR technology. Hemophilia is an X-linked recessive disorder. CRISPR is a gene-editing technique. Barisha's first task was to trace the appearance of hemophilia in other animals in order to see how the affected gene regions (hemophilia A and hemophilia B) vary. She found the affected genes in most primates, from chimpanzees down to small New World monkeys. Curiously, they also show up in rodents. This suggests mice might be a suitable research model. 1. In five words, describe how Barisha found the hemophilia sequences in other animals? A. She read up on it. B. She BLASTED the human sequences. C. She was good at guessing. D. She used a CLUSTAL alignment. 2. If hemophilia is an X-linked recessive disorder, who is it more likely to affect? A. The condition will appear more frequently in females since they carry two X chromosomes. B. Males will be affected more frequently since they only have one X chromosome. C. Females will develop the disorder more frequently since males only have one X chromosome. D. Males will never be affected since they only have one X chromosome. 3. What is the likelihood for an affected father transmitting hemophilia to his son? A pedigree or probability could provide the answer as well as simple rationalization. A. 0% since it is an X-linked condition. B. 25% since it is a recessive condition. C. 50% since he donates one allele and the boy's mother donates the other allele. D. 100% since he will always donate the affected X-allele to his son. 4. If Barisha wants to see where the nucleotide sequences differ from one another in the accessions for the animals she found on NCBI compared to humans, what does she need to do? A. Make a cladogram using phylogenetic.fr. B. Examine each sequence individually and compare them against one another. C. Make an alignment using CLUSTAL Omega. D. Import FASTA files into Trex to generate a Newick code. 5. If Barisha's company eventually wants to genetically engineer a solution to the disorder, what would they use as a research model for their initial lab work? A. Barisha! Why do you think she was hired? B. Donated oocytes from women. C. Donated sperm from men. D. Lab mice.
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(10 points) Dr. John Q. Scientist is a researcher who investigates the functions of a transmembrane protein found only in human liver cells. This transmembrane protein was named HLOR-1 (human liver orphan receptor-L, i.e., a receptor-like molecule for which a biological ligand has not yet been identified). HLOR-1 was cloned by way of "reverse genetics" based on a genetic disorder (phenotype observed in adulthood) that associates a genetic marker allele at 100% frequency. Further, upon complete cDNA cloning, with a sequence analysis, and computer modeling work, it is believed that the predicted structure of HLOR-1 resembles that of a growth factor receptor; hence the name HLOR-1. With the HLOR-1 cDNA in hand, John wishes to determine if mutations in the HLOR-1 gene are causative to the human genetic disorder, with the help of his talented and dedicated research team: 1): (5 points) Graduate student Bob was assigned the task of expressing a variant HLOR-1 protein in a human liver cell line. Bob generated five independent sub-lines of the cells, each with a chromosome integration of the HLOR-1 variant cDNA driven by a proper promoter and over-expressing the corresponding protein. Four of Bob's sub-lines produced a phenotype consistent in cell physiology with the manifestations of the genetic disorder, but one of his sub-lines did not produce this phenotype despite the expression of the variant HLOR-1 protein. Would Bob and John be able to conclude that the HLOR-1 variant is the cause of the genetic disorder? Why or why not? 2). (5 points) Post-doctoral fellow Jane was assigned the task of generating transgenic mice that over-express the variant HLOR-1 protein in adult mouse liver. Given Bob's results, could Jane get away with generating just one sub-strain/line of the transgenic mice over-expressing the variant HLOR-1 in the liver and presenting the disease phenotype, yet still help John make a strong argument about the variant HLOR-1 expression being the cause of the disorder? Why or why not?
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