Chromosome-dependent transcription and cell width confinement drive nucleoid segregation and couple it to cell growth in the rod-shaped Escherichia coli.
ORAL
Abstract
Unlike eukaryotes, bacteria lack a cytoskeleton-based machinery to segregate their chromosomal DNA (nucleoid). Yet, Escherichia coli faithfully segregates its nucleoids across various growth rates. Here, we provide theoretical and experimental evidence that the biogenesis of the active translation complexes (polysomes) within the nucleoid, combined with the steric repulsion between the polysomes and the radially confined DNA mesh, constitutes a nucleoid segregation mechanism in E. coli. This mechanism manifests via the out-of-equilibrium accumulations of polysomes which correlate with nucleoid compaction and asymmetric positioning. Inhibition of chromosomal transcription or its redirection towards plasmids arrests nucleoid segregation, whereas maintenance of a rod-shaped morphology is important for the longitudinal and efficient segregation of replicated nucleoids. Since the proposed mechanism depends on the rates of nucleoid elongation and chromosomal gene expression, it inherently couples the timing of nucleoid segregation to cell growth.
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Presenters
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Alexandros Papagiannakis
Department of Biology, Stanford University, Stanford, CA 94305, USA
Authors
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Alexandros Papagiannakis
Department of Biology, Stanford University, Stanford, CA 94305, USA
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Qiwei Yu
Princeton University, Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton NJ 08544, USA
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Sander K Govers
Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA
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Wei-Hsiang Lin
Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA
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Ned S Wingreen
Princeton University, Department of Molecular Biology, Princeton University, Princeton NJ 08544, USA
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Christine Jacobs-Wagner
Department of Microbiology and Immunology, School of Medicine, Stanford, CA 94305, USA