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Specific functions of the SOS response participate in survival to fluoroquinolones.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
書名/作者:	Specific functions of the SOS response participate in survival to fluoroquinolones.
作者:	Theodore, Alyssa D.
面頁冊數:	150 p.
附註:	Source: Dissertation Abstracts International, Volume: 76-09(E), Section: B.
Contained By:	Dissertation Abstracts International76-09B(E).
標題:	Microbiology.
標題:	Genetics.
ISBN:	9781321700015
摘要、提要註:	Persisters are bacterial cells that are able to tolerate antibiotic treatment without acquiring heritable resistance. It has previously been shown that the SOS-regulated toxin TisB induces persister formation by forming a channel in the inner membrane, dissipating the proton motive force and reducing the concentration of intracellular ATP. However, this mechanism is wasteful because depletion of the proton motive force will activate futile respiration and exhaust the cell's stored nutrients, leaving the cell unable to resuscitate. Previous studies have shown that DNA damage leads to the cessation of respiration, leading to the possibility that this phenomenon may complement the action of TisB. We are interested in discovering the cause of respiration shutdown, and identifying its role in survival to antibiotics. We have found that in both a recA deletion strain and lexA3 mutant strain DNA damage does not lead to cessation of respiration, indicating that this shutoff is dependent on an active SOS response. To identify the mechanism of respiration shutoff, two genetic screens were performed using an indicator of respiration to identify mutants lacking this shutoff phenotype. Analysis of the protein composition in respiring culture versus non-respiring cultures was performed using 2D gel electrophoresis. This information can be further used to increase our understanding on the mechanism behind this shutoff and its significance.
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3700150

Specific functions of the SOS response participate in survival to fluoroquinolones.
Theodore, Alyssa D.

Specific functions of the SOS response participate in survival to fluoroquinolones. - 150 p.

Source: Dissertation Abstracts International, Volume: 76-09(E), Section: B.

Thesis (Ph.D.)--Northeastern University, 2015.

This item is not available from ProQuest Dissertations & Theses.

Persisters are bacterial cells that are able to tolerate antibiotic treatment without acquiring heritable resistance. It has previously been shown that the SOS-regulated toxin TisB induces persister formation by forming a channel in the inner membrane, dissipating the proton motive force and reducing the concentration of intracellular ATP. However, this mechanism is wasteful because depletion of the proton motive force will activate futile respiration and exhaust the cell's stored nutrients, leaving the cell unable to resuscitate. Previous studies have shown that DNA damage leads to the cessation of respiration, leading to the possibility that this phenomenon may complement the action of TisB. We are interested in discovering the cause of respiration shutdown, and identifying its role in survival to antibiotics. We have found that in both a recA deletion strain and lexA3 mutant strain DNA damage does not lead to cessation of respiration, indicating that this shutoff is dependent on an active SOS response. To identify the mechanism of respiration shutoff, two genetic screens were performed using an indicator of respiration to identify mutants lacking this shutoff phenotype. Analysis of the protein composition in respiring culture versus non-respiring cultures was performed using 2D gel electrophoresis. This information can be further used to increase our understanding on the mechanism behind this shutoff and its significance.

ISBN: 9781321700015Subjects--Topical Terms:

182563
Microbiology.

Specific functions of the SOS response participate in survival to fluoroquinolones.
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245 1 0 $a Specific functions of the SOS response participate in survival to fluoroquinolones.
300 $a 150 p.
500 $a Source: Dissertation Abstracts International, Volume: 76-09(E), Section: B.
500 $a Adviser: Kim Lewis.
502 $a Thesis (Ph.D.)--Northeastern University, 2015.
506 $a This item is not available from ProQuest Dissertations & Theses.
520 $a Persisters are bacterial cells that are able to tolerate antibiotic treatment without acquiring heritable resistance. It has previously been shown that the SOS-regulated toxin TisB induces persister formation by forming a channel in the inner membrane, dissipating the proton motive force and reducing the concentration of intracellular ATP. However, this mechanism is wasteful because depletion of the proton motive force will activate futile respiration and exhaust the cell's stored nutrients, leaving the cell unable to resuscitate. Previous studies have shown that DNA damage leads to the cessation of respiration, leading to the possibility that this phenomenon may complement the action of TisB. We are interested in discovering the cause of respiration shutdown, and identifying its role in survival to antibiotics. We have found that in both a recA deletion strain and lexA3 mutant strain DNA damage does not lead to cessation of respiration, indicating that this shutoff is dependent on an active SOS response. To identify the mechanism of respiration shutoff, two genetic screens were performed using an indicator of respiration to identify mutants lacking this shutoff phenotype. Analysis of the protein composition in respiring culture versus non-respiring cultures was performed using 2D gel electrophoresis. This information can be further used to increase our understanding on the mechanism behind this shutoff and its significance.
520 $a This work also looks at the role of repair in antibiotic tolerance. The processes outlined above will stop growth and prevent further damage, however in order for these responses to be generated there must be DNA damage present for the SOS response to be induced. However, without an active repair system these cells would not be able to survive and resuscitate because of the incurred damage. Mutations resulting in deficiency in SOS induction and repair of DSBs either completely abolish or lead to extremely low persistence to FQs but do not affect persistence to other types of antibiotics, proving that repair is necessary even in TisB-dependent non-growing cells. We have analyzed knock-outs of all known SOS genes [1, 2] in order to identify other SOS functions crucial for persister formation. We have found that the absence of DinG, UvrD and RuvAB lead to a sharp decrease in the surviving fraction at high and low concentrations of the antibiotic, confirming that the repair processes these proteins catalyze are essential for persistence. In addition, the inactivation of recF leads to an increase in persistence, identifying the RecFOR recombination pathway as a poisoning mechanism. We have shown before that the persistence to FQs is a result of an induced, active process [3]. Here we confirm that all the cells get damaged and also show that the same repair mechanism is taking place in the entire population.
590 $a School code: 0160.
650 4 $a Microbiology. $3 182563
650 4 $a Genetics. $3 172221
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710 2 $a Northeastern University. $b Biology. $3 630010
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