An additional gene, called W, is found that affects the synthesis of enzymes 1 and 2. Mutant d has a recessive mutation in gene W. genotype enzyme activity without fictamine with fictamine strain W Y Z 1 2 wild-type + + + mutant a + + mutant b + + mutant c + mutant d + ++ ++ Once again, justify each answer in one sentence. i) Is gene W most likely a positive or a negative regulator? ii) Is the activity of W activated or inactivated by the presence of fictamine? + + + + + + + ++ ¦ : ++ ++ -- ++ ++ ! ! ! ! : : ++
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- Mutations in the HPRT1 gene in humans result in atleast two clinical syndromes. Consult OMIM (www.omim.org) by querying HPRT1; you will only needto look briefly at the top three hits (files #300322,300323, and 308000).a. What is the full name of the HPRT1 enzyme?b. On which chromosome is the HPRT1 gene located?c. Mutations in HPRT1 are associated with two different syndromes. What are these syndromes? Foreach, answer the following questions: (i) What arethe symptoms associated with the syndrome? (ii) Isthe mutant allele that causes the syndrome dominant, recessive, codominant, or incompletely dominant with respect to the normal allele, or do specialconditions apply? (iii) Is the syndrome associatedwith a loss-of-function or a gain-of-function disease allele? (iv) Does the syndrome display allelicheterogeneity? (v) Does the syndrome display locus heterogeneity? (Note: You do not need to understand everything in the OMIM entries to answerthese questions.)Figure 1-15 shows the family tree, or pedigree, for LouiseBenge (Individual VI-1) who suffers from the diseaseACDC because she has two mutant copies of the CD73gene. She has four siblings (VI-2, VI-3, VI-4, and VI-5)who have this disease for the same reason. Do all of the10 children of Louise and her siblings have the samenumber of mutant copies of the CD73 gene, or mightthis number be different for some of the 10 children?Fill up the blank __________s are blood diseases caused by mutationsthat eliminate or reduce the production of globinpolypeptides from one of the clusters but not the other.These mutations can include deletions of specific genesor the LCR in either cluster.
- Give only typing answer with explanation and conclusion A healthy asymptomatic 27 year old female, Susan, presents to your clinic with known family history of Spastic Paraplegia 4 caused by pathogenic SPAST mutation identified in her mother. She wants to know the risk that she will develop symptoms eventually based on this information. the penetrance of SPAST mutation is approximately 85% for women and 96% for men.A/a O A"/a afa Q afa Q Unsupplemented Supplemented b A"/a offspring Unsupplemented mother Supplemented mother This question relates to the aqouti mice research discussed in the lecture. What did the researchers observe in the experimental group (AVYA x aa) that was fed diets high in methyl donors? They gained weight rapidly. Increased expression of aqouti gene. Reduced risk of chronic disease Higher percentage of yellow offspring.There are six types of agglutinogen named C,D, E and c,d,e.the first three are dominant and last three are recessive.discuss
- Angelica just learned that her paternal uncle, Aaron, passed away from hypertrophic cardiomyopathy (autosomal dominant). Angelica’s father was killed in a duty as a young man, and therefore, his status is unknown. Her two sisters, Eliza and Peggy, have been tested for the known causative mutation in the family and do not have it. What is the chance that Angelica has the familial mutation for HCM? Group of answer choices 1/33 1/10 1/21Like Hurler syndrome, Fabry disease involves an abnormal accumulationof substances within lysosomes. However, the lysosomesof individuals with Fabry disease show an abnormal accumulationof lipids. The defective enzyme is α-galactosidase A, which is alysosomal enzyme that functions in lipid metabolism. The enzymaticdefect causes cell damage, especially to the kidneys, heart,and eyes. The gene that encodes α-galactosidase A is found on theX chromosome. Let’s suppose a phenotypically unaffected coupleproduces two sons with Fabry disease and one phenotypicallyunaffected daughter. What is the probability that the daughter willhave an affected son?Cx is a member of the family of connexin genes that encode the proteins of gap junction intercellular channels. Cx proteins in one cell form hemi-channels in the plasma membrane. Hemi-channels in adjacent cells dock to form complete intercellular channels through which ions and small molecules diffuse from cell to cell. Distinct Cx mutations were identified in three different families, F1, F2 and F3, affected by the same disease. To study their functional properties, normal (wild type, wt) and mutant (m) Cx proteins were expressed in cultured cells. Translation of the proteins was checked (Fig. 3). A extracellular EC 1 SM TM 1 membrane 2 3 4 F10 intracellular N F2 EC 2 F3 oricand c B 42 kDa C 42 kDa 35 kDa Control wt m-F1 m-F2 PM C PM C PM C PM C Western blot anti-Cx Control wt PM C m-F1 PM C PM C = Metabolically labelled m-F2 PM C m-F3 PM C m-F3 PM C WSEY Fig. 3 mont (A). Membrane topology of Cx protein indicating positions of mutations. Cx is an integral membrane protein with 4…
- Some people have a genetic predisposition for developing priondiseases. Examples are described in Table 25.6. In the case ofGerstmann-Straüssler-Scheinker disease, the age of onset istypically 30–50 years, and the duration of the disease (whichleads to death) is about 5 years. Suggest a possible explanationwhy someone can live for a relatively long time withoutsymptoms and then succumb to the disease in a relativelyshort time.Hurler syndrome is due to a mutation in a gene that encodes aprotein called α-l-iduronidase. This protein functions withinlysosomes as an enzyme that breaks down mucopolysaccharides(a type of polysaccharide that has many acidic groups attached).When this enzyme is defective, excessive amounts of the mucopolysaccharides dermatan sulfate and heparin sulfate accumulatewithin the lysosomes, especially in liver cells and connectivetissue cells. This accumulation leads to symptoms such as anenlarged liver and spleen, bone abnormalities, corneal clouding,heart problems, and severe neurological problems. The pedigreebelow contains three members affected with Hurler syndrome,indicated with black symbols. Based on this pedigree, does thissyndrome appear to follow autosomal recessive, autosomaldominant, X-linked recessive, or X-linked dominant inheritance?Explain your reasoning.Melanoma, 45 Colon cancer, 40 Sarcoma, 45 Breast Lung cancer, 53 cancer, 32 Stomach cancer, 50 Brain cancer, 18 Osteosarcoma, 3 Leukemia, 19 Rhabdomyosarcoma, 14 Answer the following subparts :- A. What do you notice in this pedigree as compared to Rb or BRCA1/2? B. Why do you think that so many cancer types are associated with inherited defects in p53? Please need detailed answer I want to learn please please I will upvote god promise|