Microbiology: An Evolving Science (Fourth Edition)
4th Edition
ISBN: 9780393615098
Author: John W. Foster, Joan L. Slonczewski
Publisher: W. W. Norton & Company
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Chapter 10.3, Problem 2TQ
Summary Introduction
To review:
The growth of fur mutant on succinate based on the regulatory circuit of small RNA (ribonucleic acid) RyhB, the iron regulatory protein Fur, and succinate dehydrogenase.
Introduction:
The small regulatory RNAs are the noncoding molecules of RNA that play an important role in cellular processes like activation and inhibition. These are composed of several stem loop structures. These RNAs play a crucial role in the regulation of genes through various mechanisms.
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Briefly explain how heme regulates the expression of globin genes in cells that synthesize hemoglobin.
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).
Here we utilize a novel, well-characterized, endogenous mitochondrial mutation in the ATP6 gene of Drosophila melanogaster with a nearly complete loss of ATP synthase activity. These Drosophila mutants have a missense mutation in ATP6 (G to A transition resulting in a glycine to glutamate change at position 116 in the protein), the mitochondrial gene encoding subunit 6 of the F1Fo-ATP synthase(complex V of the respiratory chain. ATP6 allows for the hydrogen ion translocation required for the rotation of the Fo motor and the production of ATP from ADP. Drosophila ATP61 mutants model human mitochondrial encephalomyopathy and demonstrate phenotypes associated with degenerative disease, including: reduced longevity, mitochondrial pathology, progressive neural dysfunction, tissue degeneration and locomotor impairment.
ATP61 Drosophila mutants exhibit a stereotyped phenotypic progression that is analogous to the symptomatic progression reported for many human mitochondrial disease…
Chapter 10 Solutions
Microbiology: An Evolving Science (Fourth Edition)
Ch. 10.1 - Prob. 1TQCh. 10.2 - Prob. 1TQCh. 10.2 - Prob. 2TQCh. 10.2 - Prob. 3TQCh. 10.2 - Prob. 4TQCh. 10.2 - Prob. 5TQCh. 10.3 - Prob. 1TQCh. 10.3 - Prob. 2TQCh. 10.4 - Prob. 1TQCh. 10.5 - Prob. 1TQ
Ch. 10.5 - Prob. 2TQCh. 10.6 - Prob. 1TQCh. 10 - Prob. 1RQCh. 10 - Prob. 2RQCh. 10 - Prob. 3RQCh. 10 - Prob. 4RQCh. 10 - Prob. 5RQCh. 10 - Prob. 6RQCh. 10 - Prob. 7RQCh. 10 - Prob. 8RQCh. 10 - Prob. 9RQCh. 10 - Prob. 10RQCh. 10 - Prob. 11RQCh. 10 - Prob. 12RQCh. 10 - Prob. 13RQCh. 10 - Prob. 14RQCh. 10 - Prob. 1TQCh. 10 - Prob. 2TQCh. 10 - Prob. 3TQCh. 10 - Prob. 4TQ
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- What effect does binding of the IRF protein to the IRE in the mRNA encoding ferritin have on the production of ferritin? Briefly explain why this effect is observed.arrow_forwardCTP synthetase catalyzes the glutamine-dependent conversion of UTP to CTP. The enzyme is allosterically inhibited by the product, CTP. Mammalian cells defective in this allosteric inhibition are found to have a complex phenotype: They require thymidine in the growth medium, they have unbalanced nucleotide pools, and they have an elevated spontaneous mutation rate. Explain the likely basis for these observations.arrow_forwardwhat is the nature and likely location(s) of a mutant that would, 1)allow constitutive expression of the lac gene? 2)prevent the cell from responding to lactose ( genes are not induced when exposed to lactose)? 3) not allow the cell to utilize lactose even when the genes are inducedarrow_forward
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- A species of bacteria can synthesize the amino acid histidine, so they do not require histidine in their growth medium. A key enzyme, which we will call histidine synthetase, is necessary for histidine biosynthesis. When these bacteria are given histidine in their growth medium, they stop synthesizing histidine intracellularly. Based on this observation alone, propose three different regulatory mechanisms to explain why histidine biosynthesis ceases when histidine is in the growth medium. To explore this phenomenon further, you measure the amount of intracellular histidine synthetase protein when cells are grown in the presence and absence of histidine. In both conditions, the amount of this protein is identical. Which mechanism of regulation is consistent with this observation?arrow_forwardConsider the following simple regulatory pathways. Assume the full pathway is shown. A- E- B- F- C- G- D- 1 A H- 2 B || L You identify several null mutations (a complete deletion of the gene). For each mutant (indicated with a - sign), determine whether the final product (I, J, K or L) is inducible, uninducible, or constitutive. 3 C 4 D- [Choose ] [Choose ] [Choose ] [Choose ] [Choose ] [Choose ] [Choose ] E [Choose ] F G I H || J Karrow_forwardWhy do E. coli cells with a defective lacZ gene fail to show galactoside permease activity after the addition of lactose in the absence of glucose?arrow_forward
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