Proteomic assessment of the role of N -acyl homoserine lactone in Shewanella putrefaciens spoilage

2017 ◽  
Vol 65 (5) ◽  
pp. 388-394 ◽  
Author(s):  
C. Zhang ◽  
S. Zhu ◽  
A.-N. Jatt ◽  
Y. Pan ◽  
M. Zeng
Keyword(s):  
Homoserine Lactone ◽  
Shewanella Putrefaciens ◽  
Acyl Homoserine Lactone

Role of N-acyl-homoserine lactone (AHL) based quorum sensing on biofilm formation on packing media in wastewater treatment process

RSC Advances ◽  
2016 ◽  
Vol 6 (14) ◽  
pp. 11128-11139 ◽  
Author(s):  
Huizhi Hu ◽  
Junguo He ◽  
Jian Liu ◽  
Huarong Yu ◽  
Jian Tang ◽  
...  
Keyword(s):  
Wastewater Treatment ◽  
Quorum Sensing ◽  
Biofilm Formation ◽  
Treatment Process ◽  
Single Species ◽  
Homoserine Lactone ◽  
Acyl Homoserine Lactone ◽  
Wastewater Treatment Process

Quorum sensing (QS) signaling has been extensively studied in granules and single species populations.

scholarly journals The Transcriptional Activator rfiA Is Quorum-Sensing Regulated by Cotranscription with the luxI Homolog pcoI and Is Essential for Plant Virulence in Pseudomonas corrugata

2009 ◽  
Vol 22 (12) ◽  
pp. 1514-1522 ◽  
Author(s):  
Grazia Licciardello ◽  
Iris Bertani ◽  
Laura Steindler ◽  
Patrizia Bella ◽  
Vittorio Venturi ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Homoserine Lactone ◽  
Acyl Homoserine Lactone ◽  
Dna Binding Domain ◽  
Pseudomonas Corrugata ◽  
Gram Negative ◽  
Rnd Transporter ◽  
Pith Necrosis ◽  
Rhodotorula Pilimanae

The gram-negative phytopathogen Pseudomonas corrugata has an acyl-homoserine lactone (AHL) quorum-sensing (QS) system called PcoI/PcoR that is involved in virulence on tomato. This work identifies, downstream of pcoI, a gene designated rfiA, which we demonstrate is directly linked to QS by cotranscription with pcoI. The deduced RfiA protein contains a DNA-binding domain characteristic of the LuxR family but lacks the autoinducer-binding terminus characteristic of the QS LuxR-family proteins. We also identified, downstream of rfiA, an operon designated pcoABC, encoding for the three components of a tripartite resistance nodulation-cell-division (RND) transporter system. The expression of pcoABC is regulated by RfiA. We found that lipodepsipeptide (LDP) production is cell density dependent and mutants of pcoI, pcoR, and rfiA are unable to inhibit the growth of the LDP-sensitive microorganisms Rhodotorula pilimanae and Bacillus megaterium. P. corrugata rfiA mutants were significantly reduced in their ability to cause necrosis development in tomato pith. In addition, it was established that PcoR in the absence of AHL also played a role in virulence on tomato. A model for the role of PcoI, PcoR, and RfiA in tomato pith necrosis is presented.

scholarly journals A Distinct QscR Regulon in the Pseudomonas aeruginosa Quorum-Sensing Circuit

2006 ◽  
Vol 188 (9) ◽  
pp. 3365-3370 ◽  
Author(s):  
Yannick Lequette ◽  
Joon-Hee Lee ◽  
Fouzia Ledgham ◽  
Andrée Lazdunski ◽  
E. Peter Greenberg
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Quorum Sensing ◽  
Opportunistic Pathogen ◽  
Homoserine Lactone ◽  
Acyl Homoserine Lactone ◽  
Signal Molecule ◽  
Control Of Gene Expression ◽  
Signaling Systems ◽  
Sensing Systems

ABSTRACT The opportunistic pathogen Pseudomonas aeruginosa possesses two complete acyl-homoserine lactone (acyl-HSL) signaling systems. One system consists of LasI and LasR, which generate a 3-oxododecanoyl-homoserine lactone signal and respond to that signal, respectively. The other system is RhlI and RhlR, which generate butanoyl-homoserine lactone and respond to butanoyl-homoserine lactone, respectively. These quorum-sensing systems control hundreds of genes. There is also an orphan LasR-RhlR homolog, QscR, for which there is no cognate acyl-HSL synthetic enzyme. We previously reported that a qscR mutant is hypervirulent and showed that QscR transiently represses a few quorum-sensing-controlled genes. To better understand the role of QscR in P. aeruginosa gene regulation and to better understand the relationship between QscR, LasR, and RhlR control of gene expression, we used transcription profiling to identify a QscR-dependent regulon. Our analysis revealed that QscR activates some genes and represses others. Some of the repressed genes are not regulated by the LasR-I or RhlR-I systems, while others are. The LasI-generated 3-oxododecanoyl-homoserine lactone serves as a signal molecule for QscR. Thus, QscR appears to be an integral component of the P. aeruginosa quorum-sensing circuitry. QscR uses the LasI-generated acyl-homoserine lactone signal and controls a specific regulon that overlaps with the already overlapping LasR- and RhlR-dependent regulons.

Realizing the role of N-acyl-homoserine lactone-mediated quorum sensing in nitrification and denitrification: A review

Chemosphere ◽  
2021 ◽  
Vol 274 ◽  
pp. 129970
Author(s):  
Na Wang ◽  
Jie Gao ◽  
Ying Liu ◽  
Qiuying Wang ◽  
Xuliang Zhuang ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Homoserine Lactone ◽  
Acyl Homoserine Lactone ◽  
Nitrification And Denitrification

Performance and role of N-acyl-homoserine lactone (AHL)-based quorum sensing (QS) in aerobic granules

2014 ◽  
Vol 26 (8) ◽  
pp. 1615-1621 ◽  
Author(s):  
Yaochen Li ◽  
Junping Lv ◽  
Chen Zhong ◽  
Wen Hao ◽  
Yaqin Wang ◽  
...  
Keyword(s):  
Quorum Sensing ◽  
Homoserine Lactone ◽  
Aerobic Granules ◽  
Acyl Homoserine Lactone

scholarly journals Virulence of Burkholderia mallei Quorum-Sensing Mutants

2013 ◽  
Vol 81 (5) ◽  
pp. 1471-1478 ◽  
Author(s):  
Charlotte Majerczyk ◽  
Loren Kinman ◽  
Tony Han ◽  
Richard Bunt ◽  
E. Peter Greenberg
Keyword(s):  
Quorum Sensing ◽  
Homoserine Lactone ◽  
Mouse Lung ◽  
Depth Information ◽  
Acyl Homoserine Lactone ◽  
Burkholderia Mallei ◽  
Content Type ◽  
Homoserine Lactones ◽  
Acyl Homoserine Lactones

ABSTRACTManyProteobacteriause acyl-homoserine lactone-mediated quorum-sensing (QS) to activate specific sets of genes as a function of cell density. QS often controls the virulence of pathogenic species, and in fact a previous study indicated that QS was important forBurkholderia malleimouse lung infections. To gain in-depth information on the role of QS inB. malleivirulence, we constructed and characterized a mutant ofB. malleistrain GB8 that was unable to make acyl-homoserine lactones. The QS mutant showed virulence equal to that of its wild-type parent in an aerosol mouse infection model, and growth in macrophages was indistinguishable from that of the parent strain. Furthermore, we assessed the role of QS inB. malleiATCC 23344 by constructing and characterizing a mutant strain producing AiiA, a lactonase enzyme that degrades acyl-homoserine lactones. Although acyl-homoserine lactone levels in cultures of this strain are very low, it showed full virulence. Contrary to the previous report, we conclude that QS is not required for acuteB. malleiinfections of mice. QS may be involved in some stage of chronic infections in the natural host of horses, or the QS genes may be remnants of the QS network inB. pseudomalleifrom which this host-adapted pathogen evolved.

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