Premium
Replication fork passage drives asymmetric dynamics of a critical nucleoid‐associated protein in Caulobacter
Author(s) -
AriasCartin Rodrigo,
Dobihal Genevieve S,
Campos Manuel,
Surovtsev Ivan V,
Parry Bradley,
JacobsWagner Christine
Publication year - 2016
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201695513
Subject(s) - caulobacter crescentus , biology , nucleoid , dna replication , chromosome segregation , control of chromosome duplication , cell division , genetics , microbiology and biotechnology , cell cycle , seqa protein domain , chromosome , dna , origin of replication , origin recognition complex , eukaryotic dna replication , gene , cell , escherichia coli
In bacteria, chromosome dynamics and gene expression are modulated by nucleoid‐associated proteins ( NAP s), but little is known about how NAP activity is coupled to cell cycle progression. Using genomic techniques, quantitative cell imaging, and mathematical modeling, our study in Caulobacter crescentus identifies a novel NAP (GapR) whose activity over the cell cycle is shaped by DNA replication. GapR activity is critical for cellular function, as loss of GapR causes severe, pleiotropic defects in growth, cell division, DNA replication, and chromosome segregation. GapR also affects global gene expression with a chromosomal bias from origin to terminus, which is associated with a similar general bias in GapR binding activity along the chromosome. Strikingly, this asymmetric localization cannot be explained by the distribution of GapR binding sites on the chromosome. Instead, we present a mechanistic model in which the spatiotemporal dynamics of GapR are primarily driven by the progression of the replication forks. This model represents a simple mechanism of cell cycle regulation, in which DNA ‐binding activity is intimately linked to the action of DNA replication.