scholarly journals Role of Translational Coupling in Robustness of Bacterial Chemotaxis Pathway

PLoS Biology ◽  
2009 ◽  
Vol 7 (8) ◽  
pp. e1000171 ◽  
Author(s):  
Linda Løvdok ◽  
Kajetan Bentele ◽  
Nikita Vladimirov ◽  
Anette Müller ◽  
Ferencz S. Pop ◽  
...  
2013 ◽  
Vol 79 (7) ◽  
pp. 2416-2423 ◽  
Author(s):  
Rita A. Luu ◽  
Benjamin J. Schneider ◽  
Christie C. Ho ◽  
Vasyl Nesteryuk ◽  
Stacy E. Ngwesse ◽  
...  

ABSTRACTThe phenylacetic acid (PAA) degradation pathway is a widely distributed funneling pathway for the catabolism of aromatic compounds, including the environmental pollutants styrene and ethylbenzene. However, bacterial chemotaxis to PAA has not been studied. The chemotactic strainPseudomonas putidaF1 has the ability to utilize PAA as a sole carbon and energy source. We identified a putative PAA degradation gene cluster (paa) inP. putidaF1 and demonstrated that PAA serves as a chemoattractant. The chemotactic response was induced during growth with PAA and was dependent on PAA metabolism. A functionalcheAgene was required for the response, indicating that PAA is sensed through the conserved chemotaxis signal transduction system. AP. putidaF1 mutant lacking the energy taxis receptor Aer2 was deficient in PAA taxis, indicating that Aer2 is responsible for mediating the response to PAA. The requirement for metabolism and the role of Aer2 in the response indicate thatP. putidaF1 uses energy taxis to detect PAA. We also revealed that PAA is an attractant forEscherichia coli; however, a mutant lacking a functional Aer energy receptor had a wild-type response to PAA in swim plate assays, suggesting that PAA is detected through a different mechanism inE. coli. The role of Aer2 as an energy taxis receptor provides the potential to sense a broad range of aromatic growth substrates as chemoattractants. Since chemotaxis has been shown to enhance the biodegradation of toxic pollutants, the ability to sense PAA gradients may have implications for the bioremediation of aromatic hydrocarbons that are degraded via the PAA pathway.


2002 ◽  
Vol 184 (20) ◽  
pp. 5772-5780 ◽  
Author(s):  
J. Praszkier ◽  
A. J. Pittard

ABSTRACT Replication of the IncB miniplasmid pMU720 requires synthesis of the replication initiator protein, RepA, whose translation is coupled to that of a leader peptide, RepB. The unusual feature of this system is that translational coupling in repBA has to be activated by the formation of a pseudoknot immediately upstream of the repA Shine-Dalgarno sequence. A small antisense RNA, RNAI, controls replication of pMU720 by interacting with repBA mRNA to inhibit expression of repA both directly, by preventing formation of the pseudoknot, and indirectly, by inhibiting translation of repB. The mechanism of translational coupling in repBA was investigated using the specialized ribosome system, which directs a subpopulation of ribosomes that carry an altered anti-Shine-Dalgarno sequence to translate mRNA molecules whose Shine-Dalgarno sequences have been altered to be complementary to the mutant anti-Shine-Dalgarno sequence. Our data indicate that translation of repA involves reinitiation by the ribosome that has terminated translation of repB. The role of the pseudoknot in this process and its effect on the control of copy number in pMU720 are discussed.


1975 ◽  
Vol 72 (11) ◽  
pp. 4640-4644 ◽  
Author(s):  
M. S. Springer ◽  
E. N. Kort ◽  
S. H. Larsen ◽  
G. W. Ordal ◽  
R. W. Reader ◽  
...  

2018 ◽  
Vol 86 (5) ◽  
pp. e00878-17 ◽  
Author(s):  
Kieran D. Collins ◽  
Shuai Hu ◽  
Helmut Grasberger ◽  
John Y. Kao ◽  
Karen M. Ottemann

ABSTRACT The epithelial layer of the gastrointestinal tract contains invaginations, called glands or crypts, which are colonized by symbiotic and pathogenic microorganisms and may function as designated niches for certain species. Factors that control gland colonization are poorly understood, but bacterial chemotaxis aids occupation of these sites. We report here that a Helicobacter pylori cytoplasmic chemoreceptor, TlpD, is required for gland colonization in the stomach. tlpD mutants demonstrate gland colonization defects characterized by a reduction in the percentage of glands colonized but not in the number of bacteria per gland. Consistent with TlpD's reported role in reactive oxygen species (ROS) avoidance, tlpD mutants showed hallmarks of exposure to high ROS. To assess the role of host-generated ROS in TlpD-dependent gland colonization, we utilized mice that lack either the ability to generate epithelial hydrogen peroxide or immune cell superoxide. tlpD gland colonization defects were rescued to wild-type H. pylori levels in both of these mutants. These results suggest that multiple types of innate immune-generated ROS production limit gland colonization and that bacteria have evolved specific mechanisms to sense and direct their motility in response to this signal and thus spread throughout tissue.


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