Even in the presence of a Ras-GAP, a single amino acid change in as renders it incapable of hydrolyzing GTP. This mutation is known as Ras+ and is a cancer-causing mutation. What effect do you think this mutation will have on signaling downstream of Ras+? Why? a)A mutation would turn on the signaling pathway all of the time. b)Even if a route is mutated, it can still be turned on or off. c)Due to a mutation, the signaling pathway would always be off.

A temperature-sensitive mutant allele of Ras causes the Ras protein to be fixed in the GDP-bound state at the nonpermissive temperature. What phenotype would you expect a cell homozygous for this mutation to have at the nonpermissive temperature? A.)  It would stop dividing. B.) It would divide continuously. C.) It would divide normally.

You have isolated different mutants (reg1 and reg2) causing constitutive expression of the emu operon (which has genes emu1 and emu2). One mutant contains a defect in a DNA-binding site, and the other has a loss-of-function defect in the gene encoding a protein that binds to the site. Is the DNA-binding protein a positive or negative regulator of gene expression?

Tryptophan (Trp) attenuation is an extra mechanism of regulation of trp operon when trp level is too high. Attenuation causes premature transcription termination. b)    Predict what will happen if trp repressor lose its allosteric effect.

According to the research article: “Telomerase Modulates Wnt Signalling by Association with Target Gene Chromatin,” how did the authors determine that TERT, Brg1, and beta catenin were all part of the same protein complex on TCF sites in vivo? Describe the assay used to determine this.

Eukaryotic signal transduction pathways often involve multiple proteins transmitting a signal from the cell surface to the nucleus. What advantage is gained through the use of multiple steps? Many signal transduction pathways are used in different cell types for entirely different purposes, leading to the transcription of different genes. How might different cell types be able to use a single signal transduction pathway to bring about such different results?

why does the activation of M-cdk also result in the activation of Cdc25? What is the mechanism behind it?

Wilms tumor 1, or nephroblastoma, is caused by mutations in the WT1 gene, which encodes a transcription factor. You have identified a novel variant in WT1: Arg422Pro.   You have control cells and cells that have been engineered to carry the homozygous WT1 p.Arg422Pro mutation. You want to assess effects of this mutation on a variety of endpoints. For each endpoint listed below, choose the one technique is best suited to answer the question.   Choose from: array CGH, qRT-PCR, qPCR, RNA-seq, FISH, in situ hybridization, western blot, immunostaining, WT1 ChIP-seq, WT1 ChIP-PCR, ATAC-seq, 3C     Endpoint Technique? WT1 protein amount (quantitative) Western blot WT1 protein binding to all enhancers, genome-wide Chip-seq WT1 mRNA amount (quantitative)   WT1 protein subcellular localization   Quantitative assessment of all mRNAs in these cells (genome-wide) RNAseq Chromatin interactions between a specific WT1 chromatin binding site (identified above)…

Consider the example that actin mRNA localization is important for fibroblast migration. What would you predict to be the consequence of deleting the zip code sequence element of the actin mRNA?

LysR regulators like llvY repress transcription from their own promoters. This is called a negative feedback loop. Why might negative feedback be a good way to control expression of a transcriptional repressor? This type of negative feedback loop ensures that ilvC transcription will always be repressed when llvY levels are low, and ilvC will be transcribed highly when llvY levels are high. This type of negative feedback regulation ensures that ilvY is never transcribed. Since llvY is a transcriptional repressor, it will slow down cell growth by blocking transcription. So, llvY represses it's own transcription so that no llvY can ever be made, and the cell can grow. This type of negative feedback loop ensures that there is always a moderate amount of llvY. When IlvY levels fall too low, transcription from the promoter will increase since IlvY won't be able to repress it's own promoter. This negative feedback also ensures that IlVY levels don't rise too high - when llvY levels are high,…