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- Describe the mechanism by which cAMP receptorprotein (CRP), the regulatory protein for catabolite repression, functions. Use the lactose operon as an example.A researcher discovered Suramin as a potent and selective inhibitor of Mycobacterium tuberculosis RecA protein and the SOS response. What would be the outcome if the action of RecA was inhibited during the SOS response? O LexA would not autolyse, and therefore the transcription of DNA repair genes would not occur; the bacteria would likely not survive. O LexA would autolyse, and therefore the transcription of repair genes would not occur; that would be lethal to the bacteria. LexA would autolyse, and therefore the transcription of DNA repair genes would occur; and the bacteria will be susceptible to antibiotics. LexA would not autolyse, and therefore the transcription of repair genes would occur; essentially that would be lethal to the bacteria.Phorbol esters have been observed to induce the transcription of AP-1–influenced genes. Explain how this processcould occur. What are the consequences of AP-1 transcription? What role does intermittent exposure to phorbol estershave on an individual’s health?
- What would be the effect of a drug that altered the structure of allolactose so that it was unable to bind to the regulator protein?When CAMP binds to the Catabolite Activator Protein (CAP), it causes a conformational change on the protein, which results in binding to the CAP- binding site on the DNA and molecule is known as a(n) of the lac operon. This conformational change induced by the binding of another transcription activation; allosteric effect transcription repression; binding effect translation; distortion effect mutation; interactive effect attenuation; compression effect O O O ODescribe how the components of the trp operon system are affected by a mutation in trpC? Why is it that once enviornmental tryptophan is inserted into the cell, only the trp repressor is activated (turned on)?
- The ras protein is a mutated G protein that lacks GTPase activity. How does the absence of this activity affect the adenylyl cyclase pathway?Now read this abstract from a 2013 journal article What is the authors' explanation of how Gal80p works? Note UASG from the question above is the same as UASGAL The DNA-binding transcriptional activator Gal4 and its regulators Gal80 and Gal3 constitute a galactose-responsive switch for the GAL genes of Saccharomyces cerevisiae. Gal4 binds to GAL gene UASGAL. (upstream activation sequence in GAL gene pro- moter) sites as a dimer via its N-terminal domain and activates transcription via a C-terminal transcription activation domain (AD). In the absence of galactose, a Gal80 dimer binds to a dimer of Gal4, masking the Gal4AD. Galactose triggers Gal3-Gal80 interaction to rapidly initiate Gal4-mediated transcription activation. Just how Gal3 alters Gal80 to relieve Gals0 inhibition of Gal4 has been unknown, but previous analyses of Gal80 mutants suggested a possible competition between Gal3-Gal80 and Gal80 self-association interactions. Here we assayed Gal80-Gal80 interactions and tested for…What effect does binding of the IRF protein to the IRE in the mRNA encoding ferritin have on the production of ferritin? Briefly explain why this effect is observed.
- A mutation occurred on the lacI (repressor) gene resulting in a constant production of beta-galactosidase and permease, even in the absence of lactose. Provide an explanation for the effect of this mutation on the repressor protein moleculeArginine is one of the amino acids that serves as a building block for protein synthesis. Arginine biosynthesis depends on the expression of the arg operon, which encodes ArgC (a reductase) and ArgB (acetylglutamate kinase). Which of the following statements regarding mutation of the arginine biosynthesis repressor ArgR is true? O A 1-bp insertion in the argR gene would result in a mutant able to grow in the absence of arginine, O A 1-bp deletion in the argB gene would result in a mutant unable to transcriptionally regulate the arg operon encoding argB. O A 1bp insertion in the argC gene would result in a mutant able to grow in the absence of arginine. O A 1-bp deletion in the argR gene would result in a mutant that represses the arg operon when grown in the presence of arginine. None of the above.If you wanted to engineer the initiator caspase from the Fas/FasL extrinsic apoptosis pathway to function in the intrinsic pathway (e.g. in response to DNA damage), which of the following would be the most likely approach to succeed? O Replace the extrinsic pathway's initiator caspase Death Effector Domain with a CARD domain O Replace the Fas Death Domain with a cytochrome C binding domain O Generate a version of the Fas receptor that localizes to the mitochondrial intermembrane space 80 O Replace the intrinsic pathway's initiator caspase CARD domain with a Death Effector Domain F3 0 $ 4 DOD DOO R F4 S % 5 T No new data to save. Last checked at 3:01pm Submit Qu B4 ♫ 8 tv A F5 < 6 MacBook Air F6 Y & 7 F7 * 8 X F8 ( 9