Biochemistry
9th Edition
ISBN: 9781319114671
Author: Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.
Publisher: W. H. Freeman
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The transcription of a gene called YFG (your favorite
gene) is activated when three transcription factors (TFA,
TFB, TFC) interact to recruit the co-activator CRX. TFA,
TFB, TFC, and CRX and their respective binding sites
constitute an enhanceosome located 10 kb from the transcription start site. Draw a diagram showing how you
think the enhanceosome functions to recruit RNA polymerase to the promoter of YFG.
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- Gal4 is a transcription factor that activates transcription of galactose metabolism genes in yeast. These genes are ‘turned on’ when yeast cells need to metabolize galactose. To identify promoter sequences necessary for regulation of transcription of GAL1, reporter gene fusions were made and introduced into yeast cells. Deletions of GAL1 promoter were cloned upstream of LacZ gene. β-Galactosidase activity was measured in presence of galactose. Shown below is a representation of the results obtained. In the diagrams below (not to scale!): • Construct 1 contains ~ 130bp of the promoter, which is predicted to have all the predicted/putative proximal promoter elements (indicated by the solid boxes) needed to regulate transcription of GAL1.• The stippled box is the core promoter.• The arrow represents the transcriptional start site for the reporter gene Lac Z• Number of + signs represents level of transcription• Star represents a mutation in DNA sequence at that location (few nucleotides…arrow_forwardMany viruses that infect eukaryotic cells express genes that alterthe regulation of host gene expression to promote viral replication.For example, herpes simplex virus-1 (HSV-1) expresses aprotein called ICP0, which is necessary for successful viral infectionand replication within the host. Lutz et al. (2017. Viruses9: 210) showed that ICP0 can act as a ubiquitin ligase and targetthe redundant transcriptional repressors ZEB1 and ZEB2,which leads to upregulation of the miR-183 cluster (a set of threemiRNAs transcribed from the same locus). How may ICP0 expression in a host cell lead to upregulationof the miR-183 cluster?arrow_forward24arrow_forward
- Many viruses that infect eukaryotic cells express genes that alterthe regulation of host gene expression to promote viral replication.For example, herpes simplex virus-1 (HSV-1) expresses aprotein called ICP0, which is necessary for successful viral infectionand replication within the host. Lutz et al. (2017. Viruses9: 210) showed that ICP0 can act as a ubiquitin ligase and targetthe redundant transcriptional repressors ZEB1 and ZEB2,which leads to upregulation of the miR-183 cluster (a set of threemiRNAs transcribed from the same locus). Speculate on how miR-183 cluster upregulation may benefitthe virus.arrow_forwardGiven the Table below concerning the lac operon, match the letter with what would be occurring for each scenario. Repressor is bound to the operator, cAMP complex is bound and transcription is prevented. Allolactose is bound to the repressor, cAMP complex is bound, and transcription is prevalent. Allolactose is bound to the repressor, cAMP complex is not assembled, and transcription is slow Repressor is bound to the operator, cAMP complex is not assembled, and transcription is prevented.arrow_forwardHow does the 4 feature of transcription factors namely the structural motifs of DNA binding protein, activation domains, multiple transcription factors and enhancers help in the design of a building block tool. U can use the SrY gene as ur building block tool. Pls explain in details using those features of the transcription factors. In 400 wordsarrow_forward
- Negative supercoiling of DNA favors the transcription of genes because it facilitates unwinding. However, not all promoter sites are stimulated by negative supercoiling. The promoter site for topoisomerase II itself is a noteworthy exception. Negative supercoiling decreases the rate of transcription of this gene. Propose a possible mechanism for this effect and suggest a reason why it may occur.arrow_forwardFor some time, it was not clear whether lac repressor inhibits lac operon transcription by inhibiting the binding of RNA polymerase to its promoter or by allowing transcription initiation but blocking elongation past the site of bound repressor. How might you distinguish between these possibilities?arrow_forwardAlternative splicing happens in both pro- and eukaryotes. True O False The yeast Gal80 protein inhibits transcription, but by binding to a transcriptional activator protein instead of to an operator. True O Falsearrow_forward
- Why must chromatin be remodeled at a eukaryotic promoter? Histone proteins must be added to the promoter so they can recruit RNA polymerase II Histone proteins are blocking promoter sequences recognized by general transcription factors (GTFs) Space needs to be made for the ribosome to bind to a nascent (i.e. newly transcribed) mRNA Because enhancer regions need to be exposed for general transcription factor binding To allow the spliceosome to remove exons from the mRNA during transcriptionarrow_forwardBriefly name and explain five mechanisms by which transcription factors activate transcription, with specific reference to targets in the basal transcription complexarrow_forwardIIVY is a LysR regulator, and it helps control transcription of a neighboring gene, ilvC. IlvY can either bend the DNA and block RNAP's access to ilvC's -35 promoter site, or it can allow access to the ilvC -35 site, thereby promoting ilvC transcription. What determines whether llvY is repressing or activating transcription from the ilvC promoter? The presence of the co-inducer acetolactate - acetolactate binds to llvY and changes llvY's shape such that it doesn't block the -35 of the ilvC promoter. IlvY represses ilvC transcription when the IlvC protein is bound to llvY, and it activates ilvC transcription when the lvC protein is not present to bind to llvY. The presence of the co-inducer valine - when valine is present, it binds llvY and causes llvY to repress transcription from the ilvC promoter. The presence of the co-inducer acetolactate - acetolactate induces negative supercoiling at the ilvC promoter, which represses ilvC transcription.arrow_forward
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