Abstract
Genome condensation is increasingly recognized as a generic stress response in bacteria. To better understand the physiological implications of this response, we used fluorescent markers to locate specific sites on Escherichia coli chromosomes following exposure to cytotoxic stress. We find that stress-induced condensation proceeds through a nonrandom, zipper-like convergence of sister chromosomes, which is proposed to rely on the recently demonstrated intrinsic ability of identical double-stranded DNA molecules to specifically identify each other. We further show that this convergence culminates in spatial proximity of homologous sites throughout chromosome arms. We suggest that the resulting apposition of homologous sites can explain how repair of double strand DNA breaks might occur in a mechanism that is independent of the widely accepted yet physiologically improbable genome-wide search for homologous templates. We claim that by inducing genome condensation and orderly convergence of sister chromosomes, diverse stress conditions prime bacteria to effectively cope with severe DNA lesions such as double strand DNA breaks.
Highlights
Genome-wide homology search is inconsistent with the emerging view of bacterial genome morphology
By using fluorescent markers to locate specific Escherichia coli chromosomal sites, we show that stress-induced genome condensation proceeds through an orderly convergence of segregated sister chromosomes rather than through random DNA collapse
Stressful Growth Conditions Result in a Nonrandom Genome Condensation and Convergence of Sister Chromosomes—In unstressed, exponentially growing E. coli cells, chromatin is spread over the entire cytoplasm (Fig. 2A; Table 2), as is the case for other bacterial strains such as Bacillus subtilis [29] and in archaea [33]
Summary
Genome-wide homology search is inconsistent with the emerging view of bacterial genome morphology. By using fluorescent markers to locate specific Escherichia coli chromosomal sites, we show that stress-induced genome condensation proceeds through an orderly convergence of segregated sister chromosomes rather than through random DNA collapse This convergence is suggested to initiate at the replication forks and to be mediated by the recently demonstrated ability of identical double-stranded DNA molecules to identify each other and generate robust complexes [34, 35]. The results reported here imply that genome condensation, triggered even by relatively moderate stressful conditions and cellular damage, primes bacteria to rapidly and effectively cope with highly detrimental DNA lesions such as DSBs. our observations are consistent with the notion that RecA plays an essential role in the identification of accurate homologous template as well as in the formation of a stable complex between presynaptic filaments and their repair templates [2, 3, 36, 37], these findings imply that, in contrast to the widespread conviction, RecA-dependent genome-wide search is not required for DSB homologous repair
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