How do sigma factors help regulate gene expression during the transition to stationary phase? O Sigma factors create extra nutrients by fixing CO2 and N2 in the air, thereby preventing the onset of stationary phase. O Different sigma factors recognize different promoters. Sigma factors that recognize stress response and catabolic metabolism promoters are expressed during stationary phase and the housekeeping sigma factor is downregulated. Thus, transcription shifts toward stress response and away from growth, O Sigma factors bind the ribosome and block it from translating certain MRNAS that no longer need to be translated in stationary phase O Sigma factors are transcriptional inhibitors, they stop transcription entirely so the bacteria don't waste energy on transcription during starvation O Stationary phase is caused by rifampin treatment, and sigma factors block rifampin activity. thereby preventing the onset of stationary phase.

Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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**How do sigma factors help regulate gene expression during the transition to stationary phase?**

1. Sigma factors create extra nutrients by fixing CO2 and N2 in the air, thereby preventing the onset of stationary phase.

2. Different sigma factors recognize different promoters. Sigma factors that recognize stress response and catabolic metabolism promoters are expressed during stationary phase and the housekeeping sigma factor is downregulated. Thus, transcription shifts toward stress response and away from growth.

3. Sigma factors bind the ribosome and block it from translating certain mRNAs that no longer need to be translated in stationary phase.

4. Sigma factors are transcriptional inhibitors, they stop transcription entirely so the bacteria don’t waste energy on transcription during starvation.

5. Stationary phase is caused by rifampin treatment, and sigma factors block rifampin activity, thereby preventing the onset of stationary phase.
Transcribed Image Text:**How do sigma factors help regulate gene expression during the transition to stationary phase?** 1. Sigma factors create extra nutrients by fixing CO2 and N2 in the air, thereby preventing the onset of stationary phase. 2. Different sigma factors recognize different promoters. Sigma factors that recognize stress response and catabolic metabolism promoters are expressed during stationary phase and the housekeeping sigma factor is downregulated. Thus, transcription shifts toward stress response and away from growth. 3. Sigma factors bind the ribosome and block it from translating certain mRNAs that no longer need to be translated in stationary phase. 4. Sigma factors are transcriptional inhibitors, they stop transcription entirely so the bacteria don’t waste energy on transcription during starvation. 5. Stationary phase is caused by rifampin treatment, and sigma factors block rifampin activity, thereby preventing the onset of stationary phase.
Chloramphenicol and linezolid have the same mechanism of action in the ribosome. However, Figure 2 in the Marks, 2016 paper shows that they affect ribosome stalling in slightly different ways. So, CHL inhibits ribosomes the most when there is either an alanine or a serine at the +1 site of the peptidyl tRNA and an aspartate at the 0 site of the peptidyl tRNA, while LZD inhibits the most only when there is an alanine at the -1 site, and the other sites have little effect. Which of the following is the best explanation for this difference?

A) CHL and LZD have different chemical structures. They will relieve ribosome stalling more effectively the more tightly they bind to the peptidyltransferase center, which causes ribosome stalling. CHL probably binds nearly as tightly when there is a serine as when there is an alanine, whereas LZD’s different structure means it probably only binds very tightly when there is an alanine.

B) CHL and LZD have different chemical structures. They will inhibit ribosomes more effectively the more tightly they bind to the peptidyltransferase center. CHL probably binds nearly as tightly when there is a serine at the +1 site as when there is an alanine, whereas LZD’s different structure means it probably only binds very tightly when there is an alanine at the -1 site.

C) CHL and LZD have different chemical structures. They will stall ribosome more, the more loosely they bind to the peptidyltransferase center. CHL probably binds nearly as tightly when there is a serine at the +1 site as when there is an alanine, whereas LZD’s different structure means it probably only binds loosely when there is an alanine at the -1 site.

D) CHL and LZD have different chemical structures. They will inhibit ribosome more effectively when they bind at the decoding center. CHL probably binds nearly as tightly when there is a serine at the +1 site as when there is an alanine codon at the -1 decoding site.

The explanation options describe different ways in which the chemical structures of CHL and LZD may affect their ribosome binding capabilities, impacting how they stall or inhibit ribosome activity based on the amino acid composition of specific sites on the peptidyl
Transcribed Image Text:Chloramphenicol and linezolid have the same mechanism of action in the ribosome. However, Figure 2 in the Marks, 2016 paper shows that they affect ribosome stalling in slightly different ways. So, CHL inhibits ribosomes the most when there is either an alanine or a serine at the +1 site of the peptidyl tRNA and an aspartate at the 0 site of the peptidyl tRNA, while LZD inhibits the most only when there is an alanine at the -1 site, and the other sites have little effect. Which of the following is the best explanation for this difference? A) CHL and LZD have different chemical structures. They will relieve ribosome stalling more effectively the more tightly they bind to the peptidyltransferase center, which causes ribosome stalling. CHL probably binds nearly as tightly when there is a serine as when there is an alanine, whereas LZD’s different structure means it probably only binds very tightly when there is an alanine. B) CHL and LZD have different chemical structures. They will inhibit ribosomes more effectively the more tightly they bind to the peptidyltransferase center. CHL probably binds nearly as tightly when there is a serine at the +1 site as when there is an alanine, whereas LZD’s different structure means it probably only binds very tightly when there is an alanine at the -1 site. C) CHL and LZD have different chemical structures. They will stall ribosome more, the more loosely they bind to the peptidyltransferase center. CHL probably binds nearly as tightly when there is a serine at the +1 site as when there is an alanine, whereas LZD’s different structure means it probably only binds loosely when there is an alanine at the -1 site. D) CHL and LZD have different chemical structures. They will inhibit ribosome more effectively when they bind at the decoding center. CHL probably binds nearly as tightly when there is a serine at the +1 site as when there is an alanine codon at the -1 decoding site. The explanation options describe different ways in which the chemical structures of CHL and LZD may affect their ribosome binding capabilities, impacting how they stall or inhibit ribosome activity based on the amino acid composition of specific sites on the peptidyl
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