Name the mutation at the protein level which is the basis for mutant A-1 Would a nonsense mutation in protein A be an enhancer or suppressor mutation of mutant B-1 Name the mutation at the phenotype level when a new function is acquired: ____morphic
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Name the mutation at the protein level which is the basis for mutant A-1
Would a nonsense mutation in protein A be an enhancer or suppressor mutation of mutant B-1
Name the mutation at the
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- Name the mutation at the protein level which is the basis for mutant B-1 Would a nonsense mutation in protein A be an enhancer or suppressor mutation of mutant B-1 Name the mutation at the phenotype level when a new function is acquired: ____morphic Name one mutation which is a suppressor of bri1-5Identify the two general functions of the proteins encoded bytumor-suppressor genes.Mutations that inactivate p53 have a recessive phenotype, whereas mutations affecting Ras are dominant. Explain the difference.
- Would the following alterations to Src be oncogenic? Explain. (a) The deletion or inactivation of the SH3 domain. (b) The mutation of Tyr 416 to Phe.MSH2 is a gene commonly associated with HNPCC (Hereditary nonpolyposis colorectal cancer). This gene encodes a protein that is involved in mismatch repair. Why are individuals who are heterozygous for the deletion mutation of MSH2 gene (MSH2+/MSH2-) from birth are very likely to develop colon cancer very early in their lives?The human phenotype is regulated by epigenetic control of gene expression. Discuss the three main types of epigenetic regulation, illustrating your answer with examples of diseases arising from impairment of each of these processes. 600 words.
- Changes in epigenetic modifications alter the accessibility and transcription of DNA. Describe how environmental stimuli, such as ultraviolet light exposure, could modify gene expression.Indicate whether the protein binds directly or indirectly (assuming it does) to DNA and whether to the enhancer or promote 1.) TATA box binding protein (TBP), Repressor, and Basal factorsWhich of the following does NOT pertain to the myoblast-determining gene 1?*a. It is a master gene.b. It is a silencing gene.c. It produces a transactivating protein.d. It activates its own gene. Gene silencing involves which type of histone modification?* a. acetylation of histone 4 b. dimethylation of histone 3 c. trimethylation of histone 4 d. trimethylation of histone 3 Given the required environment, the totipotency of the nucleus can allow which of the following?* a. a committed cell to undergo dedifferentiation b. a committed cell to undergo terminal differentiation c. a terminally differentiated cell to produce a complete organism d. a terminally differentiated cell to produce specific types of tissues An induced pluripotent cell is described by which of the following?* a. It is a committed cell that undergoes redifferentiation. b. It is a committed cell that undergoes dedifferentiation. c. It is a terminally…
- What are the details of the epigenetic processes involved in gene regulation of Histone Modification and DNA methylation? Summarizing these concepts please: All possible enzymes involved ; Reader/writer/eraser designation for the enzyme; Effect on gene expression or consequences; function of the modification''The chemical carcinogen dimethylbenz[a]anthra-cene (DMBA) must be an extraordinarily specific mutagensince 90% of the skin tumors it causes have an A-to-T alter-ation at exactly the same site in the mutant Ras gene.'' Is this statement true? Explain why or why not.A man in his early 30s suddenly developed weakness in hishands and neck, followed weeks later by burning musclepain—all symptoms of late-onset muscular dystrophy. Hisinternist ordered genetic tests to determine whether he had oneof the most common adult-onset muscular dystrophies—myotonicdystrophy type 1 (DM1) or myotonic dystrophy type 2 (DM2). Thetests detect mutations in the DMPK and CNBP genes, the onlygenes known to be associated with DM1 and DM2. While awaitingthe results of the gene tests, the internist explained that thedisease-causing mutations in these genes do not result in changesto the coding sequence. Rather, myotonic dystrophies resultfrom increased, or expanded, numbers of tri- and tetranucleotiderepeats in the 3 untranslated region of the DMPK or CNBP genes.The doctor went on to explain that the presence of RNAs withexpanded numbers of repeats leads to aberrant alternative splicingof other mRNAs, causing widespread disruption of cellular pathways.This discussion…