SpdR, a Response Regulator Required for Stationary-Phase Induction of
            <i>Caulobacter crescentus cspD</i>

Silva, Carolina A. P. T. da; Balhesteros, Heloise; Mazzon, Ricardo Ruiz; Marques, Marilis V.

doi:10.1128/jb.00440-10

Cited by 15 publications

(30 citation statements)

References 52 publications

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“…6, C. crescentus cells start to remove DnaA protein well before they stop growing. C. crescentus clearly has a complex stationary-phase program(s) (48)(49)(50)(51)(52), and DnaA is not just a replication factor: DnaA is also a global regulator of many genes (36). In light of our results, we propose that HdaA is not only a RIDA component but also a key component of the programs that prepare cells for survival in the stationary phase.…”

Section: Discussionmentioning

confidence: 83%

The Caulobacter crescentus Homolog of DnaA (HdaA) Also Regulates the Proteolysis of the Replication Initiator Protein DnaA

Wargachuk

Marczynski

2015

J Bacteriol

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It is not known how diverse bacteria regulate chromosome replication. Based on Escherichia coli studies, DnaA initiates replication and the homolog of DnaA (Hda) inactivates DnaA using the RIDA (regulatory inactivation of DnaA) mechanism that thereby prevents extra chromosome replication cycles. RIDA may be widespread, because the distantly related Caulobacter crescentus homolog HdaA also prevents extra chromosome replication (J. While most bacteria use the DnaA protein to initiate chromosome replication (1-3), bacteria responding to diverse environmental pressures probably evolved many different mechanisms to regulate DnaA and thereby adjust replication control to their specific needs (3-5). The model Gram-negative bacterium Caulobacter crescentus is found in nutrient-poor freshwater lakes and streams (6). C. crescentus evolved to divide asymmetrically, and it produces a motile "swarmer cell" and a nonmotile "stalked cell" after each cell division (6-8). Chromosome replication is coupled to this dimorphic cell division since only the stalked cells initiate chromosome replication, and the swarmer cells differentiate into stalked cells before they replicate their chromosomes (9-13). CtrA is a global response regulator protein that binds to and represses the C. crescentus origin of chromosome replication in the swarmer cells (10,(14)(15)(16). Competitive binding between CtrA and DnaA is a key mechanism of replication control that blocks replication in swarmer cells while allowing replication in the stalked cells (10,17). In addition to this dimorphic control, C. crescentus chromosome replication occurs once and only once per cell division cycle (18). However, CtrA activity does not block extra rounds of chromosome replication prior to cell division (16,19).Escherichia coli uses at least three mechanisms to block extra rounds of chromosome replication. As reviewed by Katayama and coworkers (20), E. coli possesses two mechanisms that restrict DnaA binding to the origin of replication (oriC) and one mechanism, termed RIDA (regulatory inactivation of DnaA), that inactivates DnaA. Of these three mechanisms, RIDA is the dominant mechanism in E. coli (20,21). E. coli DnaA binds ATP or ADP, but only the active DnaA-ATP form can initiate oriC replication. RIDA prevents overreplication by producing the inactive DnaA-ADP form. This is essentially a negative-feedback mechanism that Citation Wargachuk R, Marczynski GT. 2015. The Caulobacter crescentus homolog of DnaA (HdaA) also regulates the proteolysis of the replication initiator protein DnaA.

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Section: Discussionmentioning

confidence: 83%

The Caulobacter crescentus Homolog of DnaA (HdaA) Also Regulates the Proteolysis of the Replication Initiator Protein DnaA

Wargachuk

Marczynski

2015

J Bacteriol

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“…In Caulobacter crescentus , expression of cspD is inversely correlated to the growth rate. In addition to (p)ppGpp, induction in stationary phase is mediated by the response regulator SpdR (da Silva et al ., 2010). All these findings raise the interesting possibility that the role for Lon is much more relevant for the degradation of CspD than for its induction.…”

Section: Discussionmentioning

confidence: 99%

The Escherichia coli replication inhibitor CspD is subject to growth‐regulated degradation by the Lon protease

Langklotz

Narberhaus²

2011

Molecular Microbiology

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SummaryPost-translational proteolysis-dependent regulation of critical cellular processes is a common feature in bacteria. The Escherichia coli Lon protease is involved in the control of the SOS response, acid tolerance and nutritional deprivation. Moreover, Lon plays a role in the regulation of toxin-antitoxin (TA) systems and thereby is linked to persister cell induction. Persister cells represent a small subpopulation that has reversibly switched to a dormant and non-dividing state without genomic alterations. Formation of persister cells permits viability upon nutritional depletion and severe environmental stresses. CspD is a replication inhibitor, which is induced in stationary phase or upon carbon starvation and increases the production of persister cells. It has remained unknown how CspD activity is counteracted when growth is resumed. Here we report that CspD is subject to proteolysis by the Lon protease both in vivo and in vitro. Turnover of CspD by Lon is strictly adjusted to the growth rate and growth phase of E. coli, reflecting the necessity to control CspD levels according to the physiological conditions.

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“…We have named this kinase skaH (sensor kinase associated hybrid) for reasons we describe in a later section. spdS is the transmembrane sensor kinase component of the SpdS-SpdR TCS, which has been reported to regulate genes involved in stationary phase adaptation in C. crescentus [39,40] (Fig 2C). Homologs of SpdS-SpdR in other species are more commonly known as RegB-RegA, and have been reported to detect changes in cellular redox state, and regulate a variety of energy generating and energy consuming processes (Reviewed in [41]).…”

Section: Cc_3560 (Skah) and Spdr Regulate Hfia Transcription And Adhementioning

confidence: 97%

Regulation of bacterial surface attachment by a network of sensory transduction proteins

Ruiz

Fiebig²,

Crosson

2019

Preprint

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Bacteria are often attached to surfaces in natural ecosystems. A surface-associated lifestyle can have advantages, but shifts in the physiochemical state of the environment may result in conditions in which attachment has a negative fitness impact. Therefore, bacterial cells employ numerous mechanisms to control the transition from an unattached to a sessile state. The Caulobacter crescentus protein HfiA is a potent developmental inhibitor of the secreted polysaccharide adhesin known as the holdfast, which enables permanent attachment to surfaces. Multiple environmental cues influence expression of hfiA, but mechanisms of hfiA regulation remain largely undefined. Through a forward genetic selection, we have discovered a multi-gene network encoding a suite of twocomponent system (TCS) proteins and transcription factors that coordinately control hfiA transcription and surface adhesion. The hybrid HWE-family histidine kinase, SkaH, is central among these regulators and forms heteromeric complexes with the kinases, LovK and SpdS. The response regulator SpdR indirectly inhibits hfiA expression by activating two XRE-family transcription factors that directly bind the hfiA promoter to repress its transcription. This study provides evidence for a model in which a consortium of environmental sensors and transcriptional regulators integrate environmental cues at the hfiA promoter to control the attachment decision. Author summaryLiving on a surface within a community of cells confers a number of advantages to a bacterium. However, the transition from a free-living state to a surface-attached lifestyle should be tightly regulated to ensure that cells avoid adhering to toxic or resource-limited niches. Many bacteria build adhesive structures at their surfaces that enable attachment. We sought to discover genes that control development of the Caulobacter crescentus surface adhesin known as the holdfast. Our studies uncovered a network of signal transduction proteins that coordinately control the biosynthesis of the holdfast by regulating transcription of the holdfast inhibitor, hfiA. We conclude that C. crescentus uses a multi-component regulatory system to sense and integrate environmental information to determine whether to attach to a surface, or to remain in an unattached state.

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SpdR, a Response Regulator Required for Stationary-Phase Induction of Caulobacter crescentus cspD

Cited by 15 publications

References 52 publications

The Caulobacter crescentus Homolog of DnaA (HdaA) Also Regulates the Proteolysis of the Replication Initiator Protein DnaA

The Caulobacter crescentus Homolog of DnaA (HdaA) Also Regulates the Proteolysis of the Replication Initiator Protein DnaA

The Escherichia coli replication inhibitor CspD is subject to growth‐regulated degradation by the Lon protease

Regulation of bacterial surface attachment by a network of sensory transduction proteins

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