GRE Subject Test: Biochemistry, Cell, and Molecular Biology › Gene Regulation
Histone acetyltransferases (HATs) transfer acetyl groups from acetyl CoA to lysine residues on histones. What is the purpose of this transfer?
Promote formation of euchromatin and increase gene expression
Facilitate phosphorylation of these lysines by kinases
Signal for ubiquitin-mediated degredation of histones
Prevent transcription factors from binding to DNA
Prevent DNA degredation by endonucleases
The correct answer is to promote formation of euchromatin and increase gene expression. Acetylation of histones "relaxes" DNA coiling around histones by reducing the affinity between histones and DNA. This allows transcription factors to bind promoter regions and promote increased gene expression via transcription.
Histone acetyltransferases (HATs) transfer acetyl groups from acetyl CoA to lysine residues on histones. What is the purpose of this transfer?
Promote formation of euchromatin and increase gene expression
Facilitate phosphorylation of these lysines by kinases
Signal for ubiquitin-mediated degredation of histones
Prevent transcription factors from binding to DNA
Prevent DNA degredation by endonucleases
The correct answer is to promote formation of euchromatin and increase gene expression. Acetylation of histones "relaxes" DNA coiling around histones by reducing the affinity between histones and DNA. This allows transcription factors to bind promoter regions and promote increased gene expression via transcription.
Inducible operons are bound by a repressor and turned off under normal conditions. How are these operons turned on?
An inducer molecule binds to and inactivates the repressor
An inducer molecule competes with the repressor for binding to the operator
An activator protein displaces the repressor on the operator
A second repressor protein binds to and represses the repressor
The transcription of the repressor protein is inactivated
Negatively regulated operons that are said to be inducible have their operator sequence bound by a repressor molecule normally. That leads to these operons being off normally. For these operons to be turned on and transcribed, a small molecule called an inducer has to bind to and inactivate the repressor protein.
Inducible operons are bound by a repressor and turned off under normal conditions. How are these operons turned on?
An inducer molecule binds to and inactivates the repressor
An inducer molecule competes with the repressor for binding to the operator
An activator protein displaces the repressor on the operator
A second repressor protein binds to and represses the repressor
The transcription of the repressor protein is inactivated
Negatively regulated operons that are said to be inducible have their operator sequence bound by a repressor molecule normally. That leads to these operons being off normally. For these operons to be turned on and transcribed, a small molecule called an inducer has to bind to and inactivate the repressor protein.
Mutations in two or more genes cause cell death, however, a mutation in only one of the genes is not lethal.
Which of the following best describes this phenomenon?
Synthetic lethality
Oncogene addiction
Oncogenic shock
Apoptosis
Secondary mutations
Synthetic lethality is the correct answer. The combinatorial effect of multiple mutated genes disrupts homeostasis in cells, inducing cell death. A mutation in only one gene can be compensated for in cells by altering the expression of other genes, such as turning on anti-apoptotic signaling pathways.
Oncogene addiction occurs when a tumor cell relies on the expression of a particular oncogene (mutated gene) for survival.
Oncogenic shock refers to an increase in pro-apoptotic signaling and a decrease in anti-apoptotic signaling upon removal of an oncoprotein.
Apoptosis refers to the process of programmed cell death.
Secondary mutations occur in a cancer cell that is treated with a therapeutic agent to promote resistance to that specific agent.
Mutations in two or more genes cause cell death, however, a mutation in only one of the genes is not lethal.
Which of the following best describes this phenomenon?
Synthetic lethality
Oncogene addiction
Oncogenic shock
Apoptosis
Secondary mutations
Synthetic lethality is the correct answer. The combinatorial effect of multiple mutated genes disrupts homeostasis in cells, inducing cell death. A mutation in only one gene can be compensated for in cells by altering the expression of other genes, such as turning on anti-apoptotic signaling pathways.
Oncogene addiction occurs when a tumor cell relies on the expression of a particular oncogene (mutated gene) for survival.
Oncogenic shock refers to an increase in pro-apoptotic signaling and a decrease in anti-apoptotic signaling upon removal of an oncoprotein.
Apoptosis refers to the process of programmed cell death.
Secondary mutations occur in a cancer cell that is treated with a therapeutic agent to promote resistance to that specific agent.
Where are promoters typically found in DNA?
Upstream of the coding region of a gene
Downstream of the coding region of a gene
In the middle of the coding region of a gene
In the 3' UTR
Promoters are the sites where transcription factors and RNA polymerase bind to initiate transcription. It makes sense that the promoter would be found upstream of a gene (i.e. before a gene). "Downstream of the coding region" and "in the middle of the coding region" are redundant answers, and neither describes a location where a promoter would normally be located. The 3' UTR describes a region of mRNA and, thus, has nothing to do with promoters.
Where are promoters typically found in DNA?
Upstream of the coding region of a gene
Downstream of the coding region of a gene
In the middle of the coding region of a gene
In the 3' UTR
Promoters are the sites where transcription factors and RNA polymerase bind to initiate transcription. It makes sense that the promoter would be found upstream of a gene (i.e. before a gene). "Downstream of the coding region" and "in the middle of the coding region" are redundant answers, and neither describes a location where a promoter would normally be located. The 3' UTR describes a region of mRNA and, thus, has nothing to do with promoters.
X-chromosome inactivation occurs in females in which one X-chromosome is silenced and transcriptionally inactivated. The X-inactive specific transcript (Xist) gene is responsible for mediating this inactivation.
What does Xist encode?
Long non-coding RNA
MicroRNA
Protein
Ribosomal RNA
Piwi-interacting RNA
The correct answer is long non-coding (lnc) RNA. Xist lncRNA coats the X-chromosome from which it is transcribed, effectively silencing that X-chromosome. MicroRNAs are small RNAs (~20 base pairs (bp)) and play a role in RNA silencing and post-transcriptional regulation of gene expression. Short interfering RNAs are double-stranded (20-25 bp) and play a role in post-transcriptional gene silencing. Piwi-interacting RNAs are small non-coding RNAs that interact with piwi proteins in epigenetic and post-transcriptional silencing of genetic elements such as retroposons. While MicroRNAs, siRNAs and Piwi-interacting RNAs all silence genes, the mechanism of X-chromosome inactivation requires Xist lncRNA.
X-chromosome inactivation occurs in females in which one X-chromosome is silenced and transcriptionally inactivated. The X-inactive specific transcript (Xist) gene is responsible for mediating this inactivation.
What does Xist encode?
Long non-coding RNA
MicroRNA
Protein
Ribosomal RNA
Piwi-interacting RNA
The correct answer is long non-coding (lnc) RNA. Xist lncRNA coats the X-chromosome from which it is transcribed, effectively silencing that X-chromosome. MicroRNAs are small RNAs (~20 base pairs (bp)) and play a role in RNA silencing and post-transcriptional regulation of gene expression. Short interfering RNAs are double-stranded (20-25 bp) and play a role in post-transcriptional gene silencing. Piwi-interacting RNAs are small non-coding RNAs that interact with piwi proteins in epigenetic and post-transcriptional silencing of genetic elements such as retroposons. While MicroRNAs, siRNAs and Piwi-interacting RNAs all silence genes, the mechanism of X-chromosome inactivation requires Xist lncRNA.