Maf acts downstream of ComGA to arrest cell division in competent cells of B. subtilis

Authors

  • Kenneth Briley Jr,

    1. Department of Microbiology and Molecular Genetics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103, USA.
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    • Present address: Department of Microbiology, University of Pennsylvania, Philadelphia, PA, USA.

  • Peter Prepiak,

    1. Public Health Research Institute Center of the New Jersey Medical School, Newark, NJ 07103, USA
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  • Miguel J. Dias,

    1. Public Health Research Institute Center of the New Jersey Medical School, Newark, NJ 07103, USA
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  • Jeanette Hahn,

    1. Department of Microbiology and Molecular Genetics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103, USA.
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  • David Dubnau

    Corresponding author
    1. Department of Microbiology and Molecular Genetics, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, NJ 07103, USA.
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E-mail dubnauda@umdnj.edu; Tel. (+1) 973 854 3400; Fax (+1) 973 854 3453.

Summary

Transformable (competent) cells of Bacillus subtilis are blocked in cell division because the traffic ATPase ComGA prevents the formation of FtsZ rings. Although ComGA-deficient cells elongate and form FtsZ rings, cell division remains blocked at a later stage and the cells become mildly filamented. Here we show that the highly conserved protein Maf is synthesized predominantly in competent cells under the direct control of the transcription factor ComK and is solely responsible for the later block in cell division. In vivo and in vitro data show that Maf binds to both ComGA and DivIVA. A point mutation in maf that interferes with Maf binding to DivIVA also interferes with the ability of Maf to inhibit cell division. Based on these findings, we propose that Maf and ComGA mediate mechanisms for the inhibition of cell division in competent cells with Maf acting downstream of ComGA. We further suggest that Maf must interact with DivIVA to inhibit cell division.

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