Cell cycle transition from S-phase to G1 in Caulobacter is mediated by ancestral virulence regulators
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA230623 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1042920.fastq.gz | Fastqsanger.gz | |||
| SRR1042921.fastq.gz | Fastqsanger.gz | |||
| SRR1042922.fastq.gz | Fastqsanger.gz | |||
| SRR1042923.fastq.gz | Fastqsanger.gz | |||
| SRR1042924.fastq.gz | Fastqsanger.gz |
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Project description:We report that ancestral zinc-finger-domain transcriptional regulators, previously reported to control virulence/symbiosis, implement a cell cycle (SM-bM-^FM-^RG1) transcriptional switch. To unravel how this G1-phase transcriptional program is reinstated during a primitive cell cycle, we first defined G1-specific promoters in the model bacterium Caulobacter crescentus by comparative ChIP-Seq analysis. We then exploited one such promoter as genetic proxy, to identify two conserved developmental regulator paralogs, MucR1/2, that constitute a quadripartite and homeostatic regulatory module directing the switch from SM-bM-^FM-^RG1-phase transcription. Surprisingly, MucR orthologs that regulate virulence and symbiosis gene transcription in Brucella, Agrobacterium or Sinorhizobium support the G1 transcriptional switch in Caulobacter. Pan-genomic ChIP-Seq analyses in Sinorhizobium and Caulobacter show that this module targets orthologous genes. Thus, this ancestral bacterial lineage from which eukaryotic organelles descended may coordinate virulence/symbiosis with other cell cycle functions using a primordial transcription factor fold that is now primarily found in the eukaryotic domain of life. Examination of 5 transcripton factor binding in two different species
2014-05-25 | E-GEOD-52849 | biostudies-arrayexpress
Project description:We report that ancestral zinc-finger-domain transcriptional regulators, previously reported to control virulence/symbiosis, implement a cell cycle (S→G1) transcriptional switch. To unravel how this G1-phase transcriptional program is reinstated during a primitive cell cycle, we first defined G1-specific promoters in the model bacterium Caulobacter crescentus by comparative ChIP-Seq analysis. We then exploited one such promoter as genetic proxy, to identify two conserved developmental regulator paralogs, MucR1/2, that constitute a quadripartite and homeostatic regulatory module directing the switch from S→G1-phase transcription. Surprisingly, MucR orthologs that regulate virulence and symbiosis gene transcription in Brucella, Agrobacterium or Sinorhizobium support the G1 transcriptional switch in Caulobacter. Pan-genomic ChIP-Seq analyses in Sinorhizobium and Caulobacter show that this module targets orthologous genes. Thus, this ancestral bacterial lineage from which eukaryotic organelles descended may coordinate virulence/symbiosis with other cell cycle functions using a primordial transcription factor fold that is now primarily found in the eukaryotic domain of life.
2014-05-25 | GSE52849 | GEO
Project description:Zinc-finger domain transcriptional regulators regulate a myriad of functions in eukaryotes. Interestingly, ancestral versions (MucR) from Alpha-proteobacteria control bacterial virulence/symbiosis. Whether virulence regulators can also control cell cycle transcription is unknown. Here we report that MucR proteins implement a hitherto elusive primordial S→G1 transcriptional switch. After charting G1-specific promoters in the cell cycle model Caulobacter crescentus by comparative ChIP-seq, we use one such promoter as genetic proxy to unearth two MucR paralogs, MucR1/2, as constituents of a quadripartite and homeostatic regulatory module directing the S→G1 transcriptional switch. Surprisingly, MucR orthologues that regulate virulence and symbiosis gene transcription in Brucella, Agrobacterium or Sinorhizobium support this S→G1 switch in Caulobacter. Pan-genomic ChIP-seq analyses in Sinorhizobium and Caulobacter show that this module indeed targets orthologous genes. We propose that MucR proteins and possibly other virulence regulators primarily control bacterial cell cycle (G1-phase) transcription, rendering expression of target (virulence) genes periodic and in tune with the cell cycle.
| S-EPMC4083442 | biostudies-literature
Project description:Cell fate determination in the asymmetric bacterium Caulobacter crescentus (Caulobacter) is triggered by the localization of the developmental regulator SpmX to the old (stalked) cell pole during the G1-S transition. While SpmX is required to localize and activate the cell fate-determining kinase DivJ at the stalked pole in Caulobacter, it is also required for organelle (stalk) positioning in the cousin Asticaccaulis. We unearth the conserved s54-dependent transcriptional activator regulator TacA as global regulator in Caulobacter whose activation by phosphorylation is indirectly down-regulated by SpmX. Using a combination of forward genetics and cytological screening we uncover a previously uncharacterized and polarized component (SpmY) of the TacA phosphorylation control system, and we show that the SpmY function and localization is conserved. Thus, we demonstrate that SpmX organizes a site-specific, ancestral and multi-functional regulatory hub whose function includes the coordinated control of two co-oscillating global transcriptional regulators, CtrA and TacA.
2016-10-24 | GSE85186 | GEO
Project description:Caulobacter sp. YL-Caulobacter Genome sequencing
| PRJNA618228 | ENA
Project description:Coordination of cell cycle progression with central metabolism is fundamental to all cell types and likely underlies differentiation into dispersal cells in bacteria. How central metabolism is monitored to regulate cell cycle functions is poorly understood. A forward genetic selection for cell cycle regulators in the polarized alpha-proteobacterium Caulobacter crescentus unearthed the uncharacterized CitA citrate synthase, a TCA (tricarboxylic acid) cycle enzyme, as unprecedented checkpoint regulator of the G1→S transition. We show that loss of the CitA protein provokes a (p)ppGpp alarmone-dependent G1-phase arrest without apparent metabolic or energy insufficiency. While S-phase entry is still conferred when CitA is rendered catalytically inactive, the paralogous CitB citrate synthase has no overt role other than sustaining TCA cycle activity when CitA is absent. With eukaryotic citrate synthase paralogs known to fulfill regulatory functions, our work extends the moonlighting paradigm to citrate synthase coordinating central (TCA) metabolism with development and perhaps antibiotic tolerance in bacteria.
2020-03-19 | GSE144533 | GEO
Project description:We report gene expression responses of Caulobacter crescentus to osmotic upshock (150 mM sucrose). The goal of this study is compare the transcriptional responses of wild type, sigT deletion, and gsrN overexpression (gsrN++) strains. The data provide a high resolution view of how two major regulators of the general stress response (sigT and gsrN) shape transcription upon shift to a hyperosmotic environment.
2018-05-30 | GSE114971 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE25996: Expression data from Caulobacter crescentus starved for carbon GSE25997: Expression data from Caulobacter crescentus (syn. C. vibrioides) swarmer and stalked cells starved for carbon GSE25998: Expression data from WT, DSigT and DSigU Caulobacter crescentus (syn. C. vibrioides) starved for carbon Refer to individual Series
2011-04-20 | E-GEOD-25999 | biostudies-arrayexpress
Project description:Investigation of whole genome gene expression level changes in a Caulobacter crescentus NA1000 delta-CCNA_00382 (ccrM) mutant, compared to the wild-type strain. The mutations engineered into this strain render it incapable of methylating its genome on the adenine at GANTC motifs. References for strains : WT: Marks, M.E., Castro-Rojas, C.M., Teiling, C., Du, L., Kapatral, V., Walunas, T.L. and Crosson, S. (2010) The genetic basis of laboratory adaptation in Caulobacter crescentus. J Bacteriol, 192, 3678-3688; Collier, J. and Shapiro, L. (2009) Feedback control of DnaA-mediated replication initiation by replisome-associated HdaA protein in Caulobacter. J Bacteriol, 191, 5706-5716. DccrM: Gonzalez, D. and Collier, J. (2013) DNA methylation by CcrM activates the transcription of two genes required for the division of Caulobacter crescentus. Mol Microbiol, 88, 203-218. A six chip study using total RNA recovered from three separate wild-type cultures of Caulobacter crescentus NA1000 and three separate cultures of a triple mutant strain, Caulobacter crescentus NA1000 delta-CCNA_00382 (ccrM), in which the ccrM gene coding for a DNA methyltransferase methylating the adenine in GANTC motifs is truncated and its product inactive. Each chip measures the expression level of 3933 genes from Caulobacter crescentus NA1000 with 3 probes per gene and with three-fold technical redundancy.
2014-01-08 | E-GEOD-52375 | biostudies-arrayexpress
Project description:Gene transfer agents (GTAs) are prophage-like entities found in many bacterial genomes that cannot propagate themselves and instead package ~5-15 kbp fragments of the host genome that can be subsequently transferred to related recipient cells. Although suggested to facilitate horizontal gene transfer in the wild, no clear physiological role for GTAs has been elucidated. Here, we demonstrate that the a-proteobacterium Caulobacter crescentus produces bona fide GTAs. The production of Caulobacter GTAs is tightly regulated by a novel transcription factor, RogA, that represses gafYZ, which are direct activators of GTA gene transcription. Cells lacking rogA or expressing gafYZ produce GTAs harboring an ~8.3 kbp fragment of the genome that can, after cell lysis, promote transfer of DNA into recipient cells. Notably, we find that GTAs promote the survival of Caulobacter in stationary phase and following DNA damage by providing recipient cells a template for homologous recombination-based repair. This function may be broadly conserved in other GTA-producing organisms and explain the prevalence of this unusual horizontal gene transfer mechanism.
2022-04-30 | GSE184478 | GEO