Cell cycle transition from S-phase to G1 in Caulobacter is mediated by ancestral virulence regulators
Coralie Fumeaux,
Sunish Kumar Radhakrishnan,
Silvia Ardissone,
Laurence Théraulaz,
Antonio Frandi,
Daniel Martins,
Jutta Nesper,
Sören Abel,
Urs Jenal and
Patrick H. Viollier ()
Additional contact information
Coralie Fumeaux: Faculty of Medicine/CMU, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, Rue Michel Servet 1
Sunish Kumar Radhakrishnan: Faculty of Medicine/CMU, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, Rue Michel Servet 1
Silvia Ardissone: Faculty of Medicine/CMU, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, Rue Michel Servet 1
Laurence Théraulaz: Faculty of Medicine/CMU, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, Rue Michel Servet 1
Antonio Frandi: Faculty of Medicine/CMU, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, Rue Michel Servet 1
Daniel Martins: Faculty of Medicine/CMU, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, Rue Michel Servet 1
Jutta Nesper: Biozentrum of the University of Basel, Klingelbergstrasse 50/70
Sören Abel: Biozentrum of the University of Basel, Klingelbergstrasse 50/70
Urs Jenal: Biozentrum of the University of Basel, Klingelbergstrasse 50/70
Patrick H. Viollier: Faculty of Medicine/CMU, Institute of Genetics and Genomics in Geneva (iGE3), University of Geneva, Rue Michel Servet 1
Nature Communications, 2014, vol. 5, issue 1, 1-14
Abstract:
Abstract 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.
Date: 2014
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5081
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DOI: 10.1038/ncomms5081
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