Please answer asap and answer it in short and content should not be palgarised QUESTION 1Which of tike following best describes how functions of regulatory transcription factor proteins modification occur in eukaryotic ceO A. The modification of the function of eukaryotic regulatory transcription factor proteins in eukaryotic celis occurs when they bind asmall effector molecule, such as a hormone, to form a hormone-receptor complex that binds DNA and activates or inactivatestranscription.O B. The modification of the function of eukaryotic regulatory transcription factor proteins in eukaryotic cells occurs when either twosimilar or non-similar regulatory transcription factor proteins interact with one another, forming a homodimeric protein or aheterodimeric protein that binds DNA to activate or inactivale transcription.C. The modification of the function of eukaryotic regulatory transcription factor proteins in eukaryotic cells occurs when regulatorytranscription factor proteins bind to DNA and are covalently modified through phosphorylation by kinases to activate or inactivatetranscription.D. Answers A, B and C are the correct answer choices for this question.E. None of the answers is the correct answer choice for this question

The regulatory transcription factors are the molecules that activate or inhibit the transcription of…

QUESTION 1 Which of the following best describes how functions of regulatory transcription factor proteins modification occur in eukaryotic cels? OA. The modification of the function of eukaryotic regulatory transcription factor proteins in eukaryotic cells occurs when they bind a small effector molecule, such as a hormone, to form a hormone-receptor complex that binds DNA and activates or inactivates transcription. O B. The modification of the function of eukaryotic regulatory transcription factor proteins in eukaryotic cells occurs when elther two similar or non-similar regulatory transcription factor proteins interact with one another, forming a homodimeric protein or a heterodimeric protein that binds DNA to activate or inactivate transcription. OC. The modification of the function of eukaryotic regulatory transcription factor proteins in eukaryotic cels occurs when regulatory transcription factor proteins bind to DNA and are covalently modified through phosphorylation by kinases to activate or inactivate transcription. D.Answers A, B and C are the correct answer choices for this question. E. None of the answers is the correct answer choice for this question

QUESTION 1 Which of the following best describes how functions of regulatory transcription factor proteins modification occur in eukaryotic cels? OA. The modification of the function of eukaryotic regulatory transcription factor proteins in eukaryotic cells occurs when they bind a small effector molecule, such as a hormone, to form a hormone-receptor complex that binds DNA and activates or inactivates transcription. O B. The modification of the function of eukaryotic regulatory transcription factor proteins in eukaryotic cells occurs when elther two similar or non-similar regulatory transcription factor proteins interact with one another, forming a homodimeric protein or a heterodimeric protein that binds DNA to activate or inactivate transcription. OC. The modification of the function of eukaryotic regulatory transcription factor proteins in eukaryotic cels occurs when regulatory transcription factor proteins bind to DNA and are covalently modified through phosphorylation by kinases to activate or inactivate transcription. D.Answers A, B and C are the correct answer choices for this question. E. None of the answers is the correct answer choice for this question

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter10: From Proteins To Phenotypes

Section: Chapter Questions

Problem 21QP: Transcriptional regulators are proteins that bind to promoters (the 5-flanking regions of genes) to...

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Transcriptional regulators are proteins that bind to promoters (the 5-flanking regions of genes) to regulate their transcription. Assume that a particular transcription regulator normally promotes transcription of gene X, a transport protein. If a mutation makes this regulator gene nonfunctional, would the resulting phenotype be similar to a mutation in gene X itself? Why or why not?
Bong Question #1: The diagram below depicts the regulatory regions for two (made-up) genes, which contain cis-regulatory sequences X, Y, and Z and bind to transcriptional regulatory proteins: zelo led diogot bolgate SMARTY – a transcriptional ACTIVATOR protein, which is present in all neuronal cells and binds to cis-regulatory sequence, X1oq & vino 19vewod.152 moldong sai mut tum BRAWNY-a transcriptional ACTIVATOR protein, which is present in all muscle cells and binds to cis-resgulatory sequence, Yolgulum di ko malo na SNARKY - a transcriptional REPRESSOR protein, which is present in peripheral neurons only and binds to cis-regulatory sequence Z 100 bio se i da se lotimo broup gniwollt od 19 bolgate ons zegg or we de base do no me to stir noitesup od went of sistemos seu anoitesup 15wens horle 10oldog woy ni gnius stoted 1910 ni tatayot ovizasovo got no rade od lliw anioq azia oo ingene Aroom or b X y Jeol VELY gan 100 Tonnodige ΤΑΤΑ, 229nibrow dong H .aodto diw atse meldong mov.no o…
Understanding why these receptors are present when they are not supposed to be is important in finding new treatments for Cushing's syndrome. When the sequences for the promoters for the receptor genes were analyzed there was no common sequences found. This led to the theory that the loss of methylation of cytosine in the promoters of these genes was leading to their inappropriate expression. How could the loss of cytosine methylation lead to overexpression of the receptor genes? O a. Increased histone acetyltransferase activity O b. Decreased histone deacetylase activity Oc Decreased histone acetyltransferase activity O d. Increased histone deacetylase activity
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?
The retinoblastoma tumor suppressor gene Rb (RB1) codes forthe retinoblastoma protein (pRB). pRB prevents the progression of the cell cycle through G1 if DNA has been damaged. Itdoes so in part because it binds a transcription-activatingdimer referred to as E2F-DP. The pRB-E2F/DP complex recruits a histone deacetylase to chromatin. Explain.
If I have discovered a mutation in the glucocorticoid reception that does not prevent thebinding of glucocorticoid hormone to the protein but prevents the ability of the receptor toactivate transcription, what are all of the possible defects that may explain why transcriptioncannot be activated?
Many currently marketed drugs exert their pharmacological effects by binding to ligand-activated transcription factors and modulating gene expression. One example, are various drugs that target the estrogen receptor to treat breast cancer, osteoporosis and post-menopausal symptoms. Below is a ChIP experiment examining the effects of no drug treatment (C), the natural hormone estrogen (E) and the drugs tamoxifen (T) and raloxifene (R) on recruitment of coactivators (SRC-1 and CBP), Histone Deacetylase Complexes (HDACs) and acetylation of histones associated with the C-myc gene. Which of the following statements are correct based on this data (select all that apply)?
Explain the role/importance of the localization of GTPase-activating protein (Ran-GAP) in BOTH nuclear export and import. What would occur if there was a loss of function mutation in Ran-GAP? What would occur if Ran-GAP was localized in the nucleus?
The transcription factor Pax6 is required continuallyduring the life of a mouse (or a human) for the development and maintenance of the retina. HomozygousPax6 knockout mice die soon after birth because Pax6protein is also required in essential organs, such as thepancreas.a. In order to study the role of Pax6 in eye development, a researcher wants to generate a mouse thatexpresses Pax6 everywhere except in its eyes.Describe how you could construct such a mouse.b. Suppose the scientist wants to create a mousesimilar to that in part (a), but in which the eye cellsfrom which Pax6 function has been removed nowexpress GFP. Marking the cells in this way willallow the investigator to see the shapes of the Pax6−eye cells more easily than if they did not expressGFP. Diagram a Pax6 gene construct that wouldenable her to do this experiment.
Explain the role/importance of the localization of GTPase-activating protein (Ran- GAP) in BOTH nuclear export and import. What would occur if there was a loss of function mutation in Ran-GAP? What would occur if Ran-GAP was localized in the nucleus?
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)…
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…