title: Host actin polymerization tunes the cell division cycle of an intracellular pathogen.
abstract: Growth and division are two of the most fundamental capabilities of a bacterial cell. While they are well described for model organisms growing in broth culture, very little is known about the cell division cycle of bacteria replicating in more complex environments. Using a D-alanine reporter strategy, we found that intracellular Listeria monocytogenes (Lm) spend a smaller proportion of their cell cycle dividing compared to Lm growing in broth culture. This alteration to the cell division cycle is independent of bacterial doubling time. Instead, polymerization of host-derived actin at the bacterial cell surface extends the non-dividing elongation period and compresses the division period. By decreasing the relative proportion of dividing Lm, actin polymerization biases the population toward cells with the highest propensity to form actin tails. Thus, there is a positive-feedback loop between the Lm cell division cycle and a physical interaction with the host cytoskeleton.
authors.affiliation: Department of Chemistry, University of California, Berkeley, Berkeley, CA 94720, USA.
authors.forename: M Sloan
authors.initials: MS
authors.lastname: Siegrist
authors.affiliation: Department of Chemistry, University of California, Berkeley, Berkeley, CA 94720, USA.
authors.forename: Arjun K
authors.initials: AK
authors.lastname: Aditham
authors.affiliation: Department of Molecular Biology, Umeå University, Umeå 901 87, Sweden; Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå University, Umeå 901 87, Sweden.
authors.forename: Akbar
authors.initials: A
authors.lastname: Espaillat
authors.affiliation: Department of Plant and Microbial Biology, University of California, Berkeley, Berkeley, CA 94720, USA.
authors.forename: Todd A
authors.initials: TA
authors.lastname: Cameron
authors.affiliation: Department of Chemistry, University of California, Berkeley, Berkeley, CA 94720, USA.
authors.forename: Sarah A
authors.initials: SA
authors.lastname: Whiteside
authors.affiliation: Department of Molecular Biology, Umeå University, Umeå 901 87, Sweden; Laboratory for Molecular Infection Medicine Sweden (MIMS), Umeå University, Umeå 901 87, Sweden.
authors.forename: Felipe
authors.initials: F
authors.lastname: Cava
authors.affiliation: Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA; Department of Molecular and Cell Biology, School of Public Health, University of California, Berkeley, Berkeley, CA 94720, USA.
authors.forename: Daniel A
authors.initials: DA
authors.lastname: Portnoy
authors.affiliation: Department of Chemistry, University of California, Berkeley, Berkeley, CA 94720, USA; Department of Molecular and Cell Biology, University of California, Berkeley, Berkeley, CA 94720, USA; Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA. Electronic address: crb@berkeley.edu.
authors.forename: Carolyn R
authors.initials: CR
authors.lastname: Bertozzi
mesh_terms: D008841:Actin Cytoskeleton / Q000378:metabolism; D000199:Actins / Q000378:metabolism*; D000818:Animals; D002455:Cell Division; D002460:Cell Line; D025461:Feedback, Physiological; D054884:Host-Pathogen Interactions; D008089:Listeria monocytogenes / Q000166:cytology* / Q000472:pathogenicity; D008264:Macrophages / Q000378:metabolism / Q000382:microbiology; D051379:Mice; D058105:Polymerization
chemical_list: D000199:Actins