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- What phenotypes do you think a homozygous tra1hsn animal with a loss of function Egl-1 mutation would have.The cystic fibrosis gene encodes a chloride channel protein necessary for normal cellular functions. Let us assume that if at least 5% normal channels are present, the affected individual has mild symptoms of cystic fibrosis. Having less than 5% normal channels produces severe symptoms. At least 50% of the channels must be expressed for the individual to be phenotypically normal. This gene has various mutant recessive alleles: Predict the percent of functional channels and severity of symptoms for the following genotypes: a. heterozygous for CF100 b. homozygous for CF100 c. heterozygous, with one copy of CF100 and one of CF3 d. heterozygous, with one copy of CF1 and one copy of CF3One of the two genes known to be mutated in cases of Hypokalemic periodic paralysis (which is inherited in an autosomal dominant pattern but known to affect males more often than females) is the calcium voltage-gated channel subunit alpha1 S (CACNA1S). What is known about the gene is recorded here: https://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000081248;r=1:201039512-201112451 Please navigate to the link above and use the information and link-outs from the page to answer the following question. GIVE YOUR ANSWER AS A NUMBER ONLY, NO UNITS: What is the size in amino acid residues of the CACNA1S transcript named CACNA1S-202? Answer: The size of the CACNA1S transcript named CACNA1S-202 is how many amino acid residues.
- One of the two genes known to be mutated in cases of Hypokalemic periodic paralysis (which is inherited in an autosomal dominant pattern but known to affect males more often than females) is the calcium voltage-gated channel subunit alpha1 S (CACNA1S). What is known about the gene is recorded here: https://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000081248;r=1:201039512-201112451 Please navigate to the link above and ensure that you click to reveal the transcript table. Then use the information in the table to answer the following question. PLEASE GIVE YOUR ANSWER AS A NUMBER ONLY, NO UNITS What is the size in base pairs of the CACNA1S transcript named CACNA1S-202? Answer: The size of the CACNA1S transcript named CACNA1S-202 isOne of the two genes known to be mutated in cases of Hypokalemic periodic paralysis (which is inherited in an autosomal dominant pattern but known to affect males more often than females) is the calcium voltage-gated channel subunit alpha1 S (CACNA1S). What is known about the gene is recorded here: https://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000081248;r=1:201039512-201112451 Please navigate to the link above and use the information and link-outs from the page to answer the following questions ANSWER ONLY IN UPPERCASE LETTERS, NO UNITS: Using the left-hand menu to view the sequence for CACNA1S, what are the last three nucleic acid bases of exon 1?One of the two genes known to be mutated in cases of Hypokalemic periodic paralysis (which is inherited in an autosomal dominant pattern but known to affect males more often than females) is the calcium voltage-gated channel subunit alpha1 S (CACNA1S). What is known about the gene is recorded here: https://www.ensembl.org/Homo_sapiens/Gene/Summary?db=core;g=ENSG00000081248;r=1:201039512-201112451 Please navigate to the link above and use the information and link-outs from the page to answer the following question. What is the NCBI accession number (including the version) of the RefSeq Match for the first transcript (CACNA1S-201)?
- Sickle-cell anemia is a recessive autosomal disorderthat is caused by an amino acid substitution in theβ-hemoglobin protein. The DNA mutation underlyingthis substitution is a SNP that alters a GAG codon forthe amino acid glutamate to a GTG that codes a valine.The frequency of sickle-cell anemia among AfricanAmericans is about 1/400. What is the frequency ofthis GTG codon in the β-hemoglobin gene amongAfrican Americans?How can one most effectively silence the myofilament gene unc-22 in C. elegans to produce the twitching phenotype? O A. Screen thousands of strains for a spontaneous unc-22 mutation O B. Soak worms in mutagenic solutions of EMS and screen the progeny OC. Inject antisense strands of unc-22 RNA into worm ovaries, which will be taken up by germ line cells and expressed in progeny O D. Inject a high dose of unc-22 MRNA into worm ovaries, which will be taken up by germ line cells and expressed in progeny O E. Culture worms with E. coli transformed with a plasmid that codes for a dsRNA unc-22 constructIn the nematode C. elegans, homozygosity for the e mutant allele causes an extreme "uncoordinated" phenotype, where the worm completely loses its ability to move. Examination of 100 individuals with genotype e/e reveals that 60 mutant worm can't move at all, 35 show a very reduced ability to move, and the remaining 5 seem to have a completely wild-type phenotype with respect to movement ability. These observations suggest that e has O incomplete penetrance and variable expressivity O low expressivity and variable penetrance Ohigh expressivity and variable penetrance O high penetrance and incomplete expressivity
- Considering Figure 2-13, if you had a homozygous double mutant m3/m3 m5/m5, would you expect it to be mutant in phenotype? (Note: This line would have two mutant sites in the same coding sequence.)In the nematode C. elegans, some worms have blisteredcuticles due to a recessive mutation in one of the bligenes. Someone studying a suppressor mutation thatsuppressed bli-3 mutations wanted to know if it wouldalso suppress mutations in bli-4. They had a strain thatwas homozygous for this recessive suppressor mutation,and its phenotype was wild type.a. How would they determine whether this recessivesuppressor mutation would suppress mutations in bli-4?In other words, what is the genotype of the wormsrequired to answer the question?b. What cross(es) would they do to make these worms?c. What results would they expect in the F2 if(1) it did act as a suppressor of bli-4?(2) it did not act as a suppressor of bli-4?The Wnt planar polarity signaling pathway nor-mally ensures that each wing cell in Drosophila has a sin-gle hair. Overexpression of the Frizzled gene from a heat-shock promoter (hs-Fz) causes multiple hairs to grow frommany cells (Figure Q15–5A). This phenotype is suppressedif hs-Fz is combined with a heterozygous deletion (DshΔ)of the Dishevelled gene (Figure Q15–5B). Do these resultsallow you to order the action of Frizzled and Dishevelledin the signaling pathway? If so, what is the order? Explainyour reasoning