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Research Paper |
Department of Bacteriology, Swedish Institute for Infectious Disease Control, 171 82, Solna, Sweden1
Department of Cell and Molecular Biology, Biomedical Center, Uppsala University, Box 596, S-751 24, Uppsala, Sweden2
Author for correspondence: Kurt Nordström. Tel: +46 18 471 45 26. Fax: +46 18 53 03 96. e-mail: Kurt.Nordstroem{at}icm.uu.se
The Min system of Escherichia coli directs cell division to the mid-cell by a mechanism that involves the dynamic localization of all of its three constituent proteins, MinC, MinD and MinE. Both the Min system and the nucleoid regulate cell division negatively and strains of E. coli lacking a functional Min system can divide at nucleoid-free cell poles in addition to the nucleoid-free region between newly segregated nucleoids. Interestingly, E. coli strains with a defective Min system have disturbed nucleoid segregation and the cause for this disturbance is not known. It is reported here that growth conditions promoting a higher frequency of polar divisions also lead to a more pronounced disturbance in nucleoid segregation. In strains with an intact Min system, expression of MinE, but not of MinD, from an inducible promoter was followed by impaired nucleoid segregation. These results suggest that the disturbed nucleoid segregation in min mutants is not caused by polar divisions per se, nor by impaired resolution of chromosome dimers in min mutants, leaving open the possibility that the Min system has a direct effect on nucleoid segregation. It is also shown how the disturbed nucleoid segregation can explain in part the unexpected finding that the clear majority of cells in min mutant populations contain 2n (n=0, 1, 2...) origins of replication.
Keywords: cell size, min mutants, minicells
a
Thomas
kerlund and Björn Gullbrand contributed equally to this work.
b
Present address: Department of Molecular and Cell Biology, Division of Biochemistry and Molecular Biology, University of California, Berkeley, CA 94720, USA.
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