Conjugative plasmid, a key agent determining bacterial behavior, survival, and evolution in natural environment

  报告题目: Conjugative plasmid, a key agent determining bacterial behavior, survival, and evolution in natural environment

报 告 人: Prof. Hideaki NOJIRI

报告人单位: Biotechnology Research Center,
The University of Tokyo

报告时间: 2016年7月4日（星期一）10:00 ~ 11:00 pm

报告地点: A203会议室

主 持 人: 刘双江 研究员

报告人摘要：Conjugative plasmid largely contributes to the rapid adaptation/evolution of bacteria in nature. To understand the process, it is important to clarify how plasmids affect the host cell physiology, and how much influence the modified host cell physiology has on host behavior and survival.

Through the studies on the carbazole degradation system of pseudomonads, an IncP-7 conjugative plasmid pCAR1 was isolated as a key player for distribution of carbazole degradative capacity (1). To understand the behavior of pCAR1-carrying Pseudomonas strains, we comprehensively surveyed the pCAR1 effects on host Pseudomonas strains by transcriptome and phenotype analyses (2-4). It was also clarified that three pCAR1-borne nucleoid-associated proteins play important roles in the interaction between pCAR1 and host chromosome, which determines the phenotypes of pCAR1 host (5-7). Especially, Pmr, a pCAR1-encoded MvaT protein, functions cooperatively with host chromosome-encoded homologues and is a key determinant of the pCAR1 effect on host cell physiology (5, 7). Recent studies also revealed that Pmr has different functions from MvaT proteins encoded on KT2440 chromosome (5). In addition, crystal structure of an N-terminal dimerization/oligomerization domain of KT2440 chromosome-encoded MvaT protein, TurB, provided cues to understand the functional differences between Pmr and chromosomal homologues (Suzuki-Minakuchi et al. submitted).

On the other hand, the effect of plasmid carriage severally affects the fate of host in environment. Investigation of the mutants of pCAR1-harboring P. putida KT2440 showing decreased fitness cost suggested that pCAR1 cost is mainly caused by constitutive expression of some host chromosomal genes induced by pCAR1 carriage and expression of CAR-degradative car genes from pCAR1 (Kubo et al. unpublished).

(1) BBB, 76, 1-18, 2012. (2) EM, 12, 1413-1426, 2010. (3) EM, 17, 134-155, 2015. (4) EM Rep., 8, 261-271, 2016. (5) JBac, 192, 4720-4731, 2010. (6) AEM, 81, 2869-2880, 2015. (7) AEM, 82, 832-842, 2016.

报告人简介：

EDUCATIONAL BACKGROUND:

1989,4 – 1991,3 Department of Agricultural Chemistry, Faculty of Agriculture, The University of Tokyo, Japan.

1991,4 – 1993,3 Master Course, Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Japan.

1993,4 – 1995,4 Doctor Course, Department of Biotechnology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Japan.
APPOINTMENT:

1995,5 – 1999,3 Assistant Professor, Biotechnology Research Center, The University of Tokyo.

1999,4 – 2002,1 Lecturer, Biotechnology Research Center, The University of Tokyo.

2002,2 – 2012,12 Associate Professor, Biotechnology Research Center, The University of Tokyo.

2013,1 – present Professor, Biotechnology Research Center, The University of Tokyo.

2014.9 – present Visiting Professor, Southwest University, China

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