Similar Datasets
Project description:Alphaproteobacteria commonly produce a polar adhesin that is anchored to the exterior of the cell envelope. In Caulobacter crescentus, this adhesin enables permanent attachment to solid surfaces and is known as the holdfast. An ensemble of two-component signal transduction (TCS) proteins control C. crescentus holdfast biogenesis by indirectly regulating expression of HfiA, a potent holdfast inhibitor. We designed a genetic screen to identify regulators of hfiA that function downstream of the TCS adhesion regulatory system. This screen identified a hypothetical protein that we have named RtrC. Though the primary structure of RtrC does not match any defined sequence family, we demonstrate that RtrC directly binds and regulates dozens of sites on the C. crescentus chromosome via a pseudo-palindromic motif. Among these binding sites is the hfiA promoter where RtrC functions to repress transcription and thereby activate holdfast biogenesis. RtrC forms an OR-gated type I coherent feedforward loop with the DNA-binding response regulator SpdR and the adhesion regulator RtrB. This type of network motif is known to buffer gene expression against transient loss of regulating signals. We further demonstrate that, in addition to promoting adhesion, RtrC expression influences cell motility in soft agar. We conclude that the formerly hypothetical gene, rtrC, encodes a transcription factor that functions downstream of the C. crescentus TCS adhesion control system to regulate holdfast biogenesis and motility.
2022-04-27 | GSE201497 | GEO
Project description:Alphaproteobacteria commonly produce a polar adhesin that is anchored to the exterior of the cell envelope. In Caulobacter crescentus, this adhesin enables permanent attachment to solid surfaces and is known as the holdfast. An ensemble of two-component signal transduction (TCS) proteins control C. crescentus holdfast biogenesis by indirectly regulating expression of HfiA, a potent holdfast inhibitor. We designed a genetic screen to identify regulators of hfiA that function downstream of the TCS adhesion regulatory system. This screen identified a hypothetical protein that we have named RtrC. Though the primary structure of RtrC does not match any defined sequence family, we demonstrate that RtrC directly binds and regulates dozens of sites on the C. crescentus chromosome via a pseudo-palindromic motif. Among these binding sites is the hfiA promoter where RtrC functions to repress transcription and thereby activate holdfast biogenesis. RtrC forms an OR-gated type I coherent feedforward loop with the DNA-binding response regulator SpdR and the adhesion regulator RtrB. This type of network motif is known to buffer gene expression against transient loss of regulating signals. We further demonstrate that, in addition to promoting adhesion, RtrC expression influences cell motility in soft agar. We conclude that the formerly hypothetical gene, rtrC, encodes a transcription factor that functions downstream of the C. crescentus TCS adhesion control system to regulate holdfast biogenesis and motility.
2022-04-27 | GSE201498 | GEO
Project description:A cryptic transcription factor regulates Caulobacter crescentus adhesion
| PRJNA832104 | ENA
Project description:A cryptic transcription factor regulates Caulobacter crescentus adhesion [RNA-seq]
| PRJNA832111 | ENA
Project description:A cryptic transcription factor regulates Caulobacter crescentus adhesion [ChIP-seq]
| PRJNA832112 | ENA
Project description:Alphaproteobacteria commonly produce an adhesin that is anchored to the exterior of the envelope at one cell pole. In Caulobacter crescentus this adhesin, known as the holdfast, facilitates attachment to solid surfaces and cell partitioning to air-liquid interfaces. An ensemble of two-component signal transduction (TCS) proteins controls C. crescentus holdfast biogenesis by indirectly regulating expression of HfiA, a potent inhibitor of holdfast synthesis. We performed a genetic selection to discover direct hfiA regulators that function downstream of the adhesion TCS system and identified rtrC, a hypothetical gene. rtrC transcription is directly activated by the adhesion TCS regulator, SpdR. Though its primary structure bears no resemblance to any defined protein family, RtrC binds and regulates dozens of sites on the C. crescentus chromosome via a pseudo-palindromic sequence. Among these binding sites is the hfiA promoter, where RtrC functions to directly repress transcription and thereby activate holdfast development. Either RtrC or SpdR can directly activate transcription of a second hfiA repressor, rtrB. Thus, environmental regulation of hfiA transcription by the adhesion TCS system is subject to control by an OR-gated type I coherent feedforward loop; these regulatory motifs are known to buffer gene expression against fluctuations in regulating signals. We have further assessed the functional role of rtrC in holdfast-dependent processes, including surface adherence to a cellulosic substrate and formation of pellicle biofilms at air-liquid interfaces. Strains harboring insertional mutations in rtrC have a diminished adhesion profile in a competitive cheesecloth binding assay and a reduced capacity to colonize pellicle biofilms in select media conditions. Our results add to an emerging understanding of the regulatory topology and molecular components of a complex bacterial cell adhesion control system.
| S-EPMC9648850 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2011-04-20 | GSE25999 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2023-08-25 | GSE241057 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series
2016-08-06 | E-GEOD-71961 | biostudies-arrayexpress
Project description:Bacteria carry out sophisticated developmental programs to colonize exogenous surfaces. The rotary flagellum, a dynamic machine that drives motility, is a key regulator of surface colonization. The specific signals recognized by flagella and the pathways by which those signals are transduced to coordinate adhesion remain subjects of debate. Mutations that disrupt flagellar assembly in the dimorphic bacterium Caulobacter crescentus stimulate the production of a polysaccharide adhesin called the holdfast. Using a genomewide phenotyping approach, we compared surface adhesion profiles in wild-type and flagellar mutant backgrounds of C. crescentus We identified a diverse set of flagellar mutations that enhance adhesion by inducing a hyperholdfast phenotype and discovered a second set of mutations that suppress this phenotype. Epistasis analysis of the flagellar signaling suppressor (fss) mutations demonstrated that the flagellum stimulates holdfast production via two genetically distinct pathways. The developmental regulator PleD contributes to holdfast induction in mutants disrupted at both early and late stages of flagellar assembly. Mutants disrupted at late stages of flagellar assembly, which assemble an intact rotor complex, induce holdfast production through an additional process that requires the MotAB stator and its associated diguanylate cyclase, DgcB. We have assigned a subset of the fss genes to either the stator- or pleD-dependent networks and characterized two previously unidentified motility genes that regulate holdfast production via the stator complex. We propose a model through which the flagellum integrates mechanical stimuli into the C. crescentus developmental program to coordinate adhesion.IMPORTANCE Understanding how bacteria colonize solid surfaces is of significant clinical, industrial and ecological importance. In this study, we identified genes that are required for Caulobacter crescentus to activate surface attachment in response to signals from a macromolecular machine called the flagellum. Genes involved in transmitting information from the flagellum can be grouped into separate pathways, those that control the C. crescentus morphogenic program and those that are required for flagellar motility. Our results support a model in which a developmental and a mechanical signaling pathway operate in parallel downstream of the flagellum and converge to regulate adhesion. We conclude that the flagellum serves as a signaling hub by integrating internal and external cues to coordinate surface colonization and emphasize the role of signal integration in linking complex sets of environmental stimuli to individual behaviors.
| S-EPMC7885107 | biostudies-literature