1. Methylation of DNA and acetylation of histones are directly correlated. 2. Histone demethylation and acetylation are both for gene inactivation. OA.Only the first statement is true. OB.Only the second statement is true. OC. Both statements are true. OD. Both statements are false.
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- I. The retinoic acid receptor (RAR) is a transcription factor that is similar to steroid hormone receptors. Thesubstance (ligand) that binds to this receptor is retinoicacid. One of the genes whose transcription is activatedby retinoic acid binding to the receptor is myoD. Thediagram that follows shows a schematic view of theRAR proteins produced by genes into which one oftwo different 12-base double-stranded oligonucleotides had been inserted in the ORF. The insertion site(a–m) associated with each mutant protein is indicatedwith the appropriate letter on the polypeptide map.For constructs encoding proteins a–e, oligonucleotide 1(5′ TTAATTAATTAA 3′ read off either strand) wasinserted into the RAR gene. For constructs encoding proteins f–m, oligonucleotide 2 (5′ CCGGCCGGCCGG 3′)was inserted into the gene.NH2 f g h i j k l m COOHa b c d eThe wild-type RAR protein can both bind DNA and activate transcription weakly in the absence of retinoic acid(RA) and strongly in RA’s presence. Each…5. How the modification and histone interaction with DNA brought to transcriptional silencing. Use Saccharomyces cerevisiae as example to explain the question. Write a short essay. Please answer asap and in short and content should not be palgarised please1a. Provide a paper published in a scientific journal between January 2018 and September 2022 that addresses the role of an example of histone modification in affecting expression of a gene by altering histone acetylation/chromatin state of the DNA encoding that gene.
- When chromatin is condensed, transcription cannot happen. Why not? RNA cannot access the promoter region of the gene DNA helicase cannot access the RNA strand RNA polymerase cannot access the DNA strand Transcription factors cannot access the termination region of the gene1a. Provide a paper published in a scientific journal between January 2018 and September 2022 that addresses the role of an example of histone modification in affecting expression of a gene by altering histone acetylation/chromatin state of the DNA encoding that gene. What organism and/or cell type did the authors do their study in?1. Histone methylation can have many different effects on gene expression. In some cases, histone methylation is associated with activation of transcription, whereas in other cases it can trigger the formation of heterochromatin and a decrease in transcription. If histone methylation has been detected in the region of gene YFG in yeast, describe an experiment that could distinguish whether the methylation is important to activate or repress transcription of gene YFG. al 6 2. An E. coli strain of chromosomal genotype lacl* lacP" lacO* lacz* lacY*. You wish to transform this strain into a wild-type lac operon by the addition of an extra piece of DNA (plasmid). a. What regulatory region(s), gene or genes would you add on this extra DNA that would make this strain express the lac operon genes as wild type? b. How would you design this plasmid if you want the strain of E. coli to express the lac operon genes even if lactose is absent in the medium (constitutively)?
- 4e. You also study the expression of 3 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'..TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3’ 3'...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5’ promoter i. Mutant A has a single base pair substitution with the T/A being replaced with C/G base pair at position 35 (position denoted by the * in the sequence above). ii. Mutant B has a 2 G/C pairs inserted between position 19 and 20 (position denoted by the ^ in the sequence above).4e. You also study the expression of 3 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'...TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3' 3' ...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5' * promoter1. In a couple of sentences, explain how eukaryotic activator proteins (that are usually gene-specific transcription factors) can enhance transcription even when bound to sequences hundreds or thousands of nucleotide pairs away from a gene’s promoter. 2. Describe three common characteristics of transcription factors. The characteristics may relate to structure, or mechanism of action (PLEASE ANSWER BOTH PLEASE)
- 1. Trithorax group proteins silence genes by* a. trimethylating histone 3 at lysine residue 2. b. trimethylating histone 4 at lysine residue 2. c. trimethylating histone 3 at lysine residue 4. d. trimethylating histone 4 at lysine residue 4. 2. Bonding of which ligand does NOT result to transcription activation?* a. fibroblast growth factor b. jagged protein c. TGF-β family d. Wnt family2. Which ONE of these statements on chromatin modification is UNTRUE? O DNA is methylated on the cytosine of CpG sequences in the DNA O Histone acetyl transferases transfer an acetyl group to lysines in histones O Bromodomain proteins bind to acetylated histones O Histone lysine methyltransferases (KMTS) are epigenetic erasers O Epigenetic changes can contribute to cancer evolution NE1. Explain the anti-apoptotic role of telomerase and telomeres. In which cell type telomerase is normally expressed? Understand the pathway of cellular response to DNA damage; main players of this pathway such as p53 and p21, how they get activated and what is their function in the pathway. 2. Explain role of Apoptosis during embryo development and during metamorphosis. 3. Explain the main players of apoptosis – caspases (their active site, what site they target during cleavage, role of initiator caspases vs executioner caspases).