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DNA double strand break repair in Escherichia coli perturbs cell division and chromosome dynamics


Autoři: Martin A. White aff001;  Elise Darmon aff001;  Manuel A. Lopez-Vernaza aff001;  David R. F. Leach aff001
Působiště autorů: Institute of Cell Biology, School of Biological Sciences, University of Edinburgh, The King’s Buildings, Edinburgh, United Kingdom aff001;  Department of Molecular and Cellular Biology, Harvard University, Cambridge MA, United States of America aff002
Vyšlo v časopise: DNA double strand break repair in Escherichia coli perturbs cell division and chromosome dynamics. PLoS Genet 16(1): e32767. doi:10.1371/journal.pgen.1008473
Kategorie: Research Article
doi: https://doi.org/10.1371/journal.pgen.1008473

Souhrn

To prevent the transmission of damaged genomic material between generations, cells require a system for accommodating DNA repair within their cell cycles. We have previously shown that Escherichia coli cells subject to a single, repairable site-specific DNA double-strand break (DSB) per DNA replication cycle reach a new average cell length, with a negligible effect on population growth rate. We show here that this new cell size distribution is caused by a DSB repair-dependent delay in completion of cell division. This delay occurs despite unperturbed cell size regulated initiation of both chromosomal DNA replication and cell division. Furthermore, despite DSB repair altering the profile of DNA replication across the genome, the time required to complete chromosomal duplication is invariant. The delay in completion of cell division is accompanied by a DSB repair-dependent delay in individualization of sister nucleoids. We suggest that DSB repair events create inter-sister connections that persist until those chromosomes are separated by a closing septum.

Klíčová slova:

Cell cycle and cell division – DNA repair – DNA replication – Fluorescence imaging – Genetic loci – Chromosomal DNA – Chromosome structure and function – Cytokinesis


Zdroje

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Štítky
Genetika Reprodukční medicína

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PLOS Genetics


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