The previously accepted model of the chloramphenicol action was that it inhibited all ribosomes equally. Why were the authors of the Marks, 2016 paper skeptical of this model? Choose all that are correct. Because they had observed that certain bacteria were resistant to chloramphenicol, and this proves that chloramphenicol stalls ribosomes at certain sites within those bacteria. Because certain MRNA templates had been observed to be inhibited by chloramphenicol more strongly than others Because chloramphenicol induces expression of chloramphenicol resistance proteins through translational arrest at specific codons in the leader ORFS of chloramphenicol resistance genes, which suggests there is preferential stalling at certain sites. Because chloramphenicol induces expression of chloramphenicol resistance proteins - therefore, these proteins must be able to be translated during chloramphenicol treatment. Because chloramphenicol binds the decoding center of the 30S subunit, and there are always different tRNAS there, which could interact with chloramphenicol differently.

The previously accepted model of the chloramphenicol action was that it inhibited all ribosomes equally. Why were the authors of the Marks, 2016 paper skeptical of this model? Choose all that are correct. Because they had observed that certain bacteria were resistant to chloramphenicol, and this proves that chloramphenicol stalls ribosomes at certain sites within those bacteria. Because certain MRNA templates had been observed to be inhibited by chloramphenicol more strongly than others Because chloramphenicol induces expression of chloramphenicol resistance proteins through translational arrest at specific codons in the leader ORFS of chloramphenicol resistance genes, which suggests there is preferential stalling at certain sites. Because chloramphenicol induces expression of chloramphenicol resistance proteins - therefore, these proteins must be able to be translated during chloramphenicol treatment. Because chloramphenicol binds the decoding center of the 30S subunit, and there are always different tRNAS there, which could interact with chloramphenicol differently.

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,...

See similar textbooks

Similar questions

Pls help ASAP
Ferritin levels are controlled in cells to ensure that free iron levels do not surpass a toxic threshold. Its levels must never be too high or it will titrate too much iron and jeapardize critical cellular iron-dependent enzyme activities. How is this achieved? Choose one. a) Elements present in the 5' UTR contribute to its translational block in low iron conditions. b) The Ferritin mRNA is under IRE-BP control so that in high iron conditions IRE-BP is not in its active conformation an has no negative effect on Ferritin mRNA translation c) IRE-BP can effectively bind to destablizing elements in the 3'UTR of the Ferritin mRNA, thus drastically reducing the half life of the transcript 4) a and b only 5) a, b and c
You plan to synthesize a peptide to be used as a vaccine to treat melanoma, a particularly aggressive form of skin cancer. Normally, gp100, a protein on the surface of melanocytes, activates cell growth when it is bound by its ligand. Activation of the growth pathway depends on the presence of threonine in the ligand. The effective peptide vaccine will mimic the natural ligand, but won’t cause cell growth and division. Below is the sequence of the natural ligand: LDMKTAG In order to ensure your newly designed peptide vaccine does not cause cell growth upon binding, you must substitute the Threonine residue at position 5. What amino acid would you replace it with, bearing in mind that the peptide should still be similar enough to bind to the gp100 protein in the surface of melanocytes. Explain your choice. Your vaccine will be administered as a topical cream, and you require your peptide to have an overall neutral charge in order to be functional. At what pH should you formulate…
Consider the mechanism of the enzyme RNase:  What would happen to the Km (i.e., would it increase, decrease, or stay the same) if the his12 was mutated to a lysine? Explain.  What would happen to the Kcat (i.e., would it increase, decrease, or stay the same) if the his12 was mutated to a valine? Explain.
A newly identified protein from the cells of the Panopyra plant on Pandora was shown to inhibit translation of its target genes by binding to the 5’ UTR of the mRNA and preventing ribosome binding. A possible way this inhibition may be relieved by an sRNA would be: Group of answer choices a)The sRNA acts as a silencer, suppressing the inhibitory protein and allowing translation to take place. b)The sRNA acts as a decoy, sequestering the inhibitory protein and allowing translation to take place. c)The sRNA acts as a marker, flagging the inhibitory protein for ubiquitination and allowing translation to take place.
Searching the yeast Saccharomyces cerevisiae genome, researchers found approximately 4,000 DNA sites with a sequence which could potentially bind the yeast transcription factor GAL4. GAL4 activates the transcription of galactose genes. Yet there are only 10 GAL4-binding sites which control the genes necessary for galactose metabolism. The GAL4 binding sequence is CGGAT#AGAAGC*GCCG, where # is T, C or G, and * is C or T. In one chromatin immunoprecipitation experiment (ChIP), yeast growing on galactose were lysed, and subjected to cross-linking reagents which cross-linked transcription factors and activators to DNA. Next the DNA was sheared into small fragments, and antibodies to GAL4 were added. These antibodies coprecipitated the GAL4 and the DNA it was cross-linked to. The cross-linking was then chemically reversed, and the DNA was isolated, cloned into a library of plasmids and sequenced. Results showed that only 10 different DNA sequences had GAL4 bound. Since the…
In the absence of cladosporin, explain the initiation steps in the synthesis of lysyl-tRNA synthetase enzyme or protein in the bacterial cell, with the involvement of all initiation factors, each site in the ribosome, any important conserved sequence, subunits of ribosomes, initiation codon, charged tRNA containing what amino acid, whether it requires ATP or GTP
The diagram below shows a closeup of regulatory proteins binding to one of the UASG elements near the GAL7, GALI0, and GALI genes, which code for the protein products needed for yeast to use the sugar galactose. The red triangle symbolizes an "effector" molecule that binds to Gal80p. In this hypothesis (which has since been shown to be incorrect), what could be happening to Gal80p when it is bound to the effector molecule that causes it to change its position and uncover the Gal4p transcriptional activation domain. Hint: think about what effector molecules do upon binding to proteins such as the the Lac repressor protein or the CAP protein. Galactose absent, glucose absent Gal80p. _Activation domain Gal4p dimer -Binding domain UASG Galactose present, glucose absent Activation domain Gal80p- Binding domain UASG For the toolbar, press ALT+F10 (PC) or ALT+FN+F10 (Mac).
The structure of a prodrug used for treating people with HIV virus (human immunodeficiency virus) and AIDS is shown below. This molecule is a precursor of a protease inhibitor that competitively inhibits HIV protease due to its resemblance to the proteolytic site of the enzyme. Which process in the viral life cycle does this inhibitor target directly ? Group of answer choices a. viral protein processing for making new viruses b. viral mRNA synthesis c. viral DNA integration into the host cell DNA d. viral DNA synthesis
Given the following diagram of how protein AWESOME1 binds to it's target DNA, describe the potential effects of each of the 5 mutations shown below. The wild-type sequence of a helix #1 is also shown in the blue box, and all the mutations are in helix #1 (see numbers for identifying particular residues). a helix #1 R(1)-V-I-L-Y-F-W-I-M-Y-F-S-H-Y-W-R(16) #1 Predict the consequence of the following mutations: 1) Arg(1) to Glu 2) Arg(1) to Ala 3) Phe(6) to lle 4) Trp(7) to Phe 5) Met(9) to Pro in