o How do SNPs arise? describe one example of an SNP cause of a genetic disease describe one example of an SNP that resulted in an advantage to the organism.
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o How do SNPs arise?
describe one example of an SNP cause of a genetic
disease
describe one example of an SNP that resulted in an
advantage to the organism.
Step by step
Solved in 2 steps
- Ca you please tell me which of these have a positive side chain and how to determine. picture of A.A. provided. Thank You!!!In an Hfr × F− conjugation, genes can be mapped roughlyby the time at which different alleles from the Hfr donorsfirst appear in F− exconjugants, and more precisely bycounting the exconjugants of each _________ classExplain how mutations occuro How do SNPs arise?describe one example of an SNP cause of a geneticdisease describe one example of an SNP that resulted in anadvantage to the organism.
- What is the transformation efficiency of your NEB Express I ^q cells? Show all WorkA student said, “The approach shown by the Chicago researchers is just conventional gene therapy with biomaterial carrier”. Is he or she correct? Why? based on “Targeted polyelectrolyte complex micelles treat vascular complications in vivo”, PNAS 2021, Vol. 118 No. 50 e2114842118;107:110210; https://doi.org/10.1073/pnas.2114842118Explain how site directed mutagenesis can be accomplished using M13 bacteriophage. Using this method often results in only 5% of plaques with mutant gene. Explain how the procedure has been modified to enrich for the number of plaques with the mutant gene.
- (1) Why the ratio of PE/GFP fluorescence is measured in the FACS experiment, instead of measuring only total PE fluorescence? (2) Explain the effect that each mutation causes in the function of MC4R, and how they can be linked to disease.For each of the E. coli strains that follow, indicate theeffect of the genotype on the expression of the trpEand trpC genes in the presence or absence of tryptophan. [In the wild type (R+ P+ o+ att+ trpE+ trpC+),trpC and trpE are fully repressed in the presence oftryptophan and are fully expressed in the absence oftryptophan.]R = repressor gene; Rnproduct cannot bind tryptophan; R− product cannot bind operatoro = operator for the trp operon; o− cannot bind repressoratt = attenuator; att− is a deletion of the attenuatorP = promoter; P− is a deletion of the trp operonpromotertrpE− and trpC− are null (loss-of-function) mutationsa. R+ P− o+ att+ trpE+ trpC+b. R− P+ o+ att+ trpE+ trpC+c. RnP+ o+ att+ trpE+ trpC+d. R− P+ o+ att− trpE+ trpC+e. R+ P+ o− att+ trpE+ trpC−/R− P+ o+ att+trpE− trpC+f. R+ P− o+ att+ trpE+ trpC−/R− P+ o+ att+trpE− trpC+g. R+ P+ o− att− trpE+ trpC−/R− P+ o− att+trpE− trpC+HOW THE RECOMBINANT PROTEIN COULD BE EXPRESSED IN E. COLI 1. EXPRESSION VECTOR. 2. FACTORS AFFECTING BACTERIAL EXPRESSION SYSTEM3. STRATEGIES TO IMPROVE THE PROTEIN EXPRESSION4. WAYS TO ENSURE THE PROTEIN IS ACTIVELY PRODUCED if have pic or figures that is better
- For the lac genotypes shown in the following table, predict whether the structural genes (Z) are constitutive, permanently repressed, or inducible in the presence of lactose. Genotype Constitutive Repressed Inducible I+O+Z+ * I-O+Z+ I-OCZ+ I-OCZ+/F=O+ I+OCZ+/F=O+ ISO+Z+ ISO+Z+/F=I+Suppose a genome-wide association study(GWAS) investigation found a particularsingle nucleotide polymorphism (SNP) in acertain gene to be associated withhypertension. How could you identify thecausal link of the specific SNP tohypertension?Im having trouble answering this question. What type of cells can be altered by GETs like CRISPR and what types of cells cannot and why is this so?