• Xavier de Bolle's Research Group
  • Xavier de Bolle's Research Group
  • Xavier de Bolle's Research Group
  • Xavier de Bolle's Research Group

Research

In bacteria, the main model for cell cycle and differentiation is Caulobacter crescentus, a free living alpha-proteobacterium. This bacterium segregates its replicated chromosomes and generates two differentiated cell types at each division. Intense research allowed the characterization of a molecular regulation network controlling cell cycle and differentiation. We discovered that the Brucella abortus cell cycle is surprisingly silmilar to the C. crescentus cell cycle. We now investigate main events of the cell cycle (such as growth and chromosomes replication and segregation) and their regulation. Indeed, our previous data indicate that cell cycle is tightly controlled along a cellular infection. Moreover, cell division events are essential processes, that could become targets for therapy in the future.

In the course of a cellular infection, Brucella abortus is able to control its trafficking. The factors involed in the survival of the bacterium inside host cells are also investigated.

 

Selected publications over the last 5 years :

Francis N, Poncin K, Fioravanti A, Vassen V, Ong TAP, Rappez L, Letesson JJ, Biondi E, De Bolle X (2017) CtrA controls cell division and outer membrane composition of the pathogen Brucella abortus. Molecular Microbiology 103, 780-797.

https://www.ncbi.nlm.nih.gov/pubmed/27893179

De Bolle, X., Crosson, S., Matroule, J.-Y., Letesson, J.J. (2015) Brucella abortus cell cycle and infection are coordinated. Trends Microbiol. 23, 812-821.

http://www.ncbi.nlm.nih.gov/pubmed/26497941

Deghelt, M., Mullier, C., Sternon, J.F., Francis, N., Laloux, G., Dotreppe, D., Van der Henst, C., Jacobs-Wagner, C., Letesson, J.J., De Bolle, X. (2014) G1-arrested newborn cells are the predominant infectious form of the pathogen Brucella abortus. Nature Communications 5, 4366.

http://www.ncbi.nlm.nih.gov/pubmed/25006695

Van der Henst, C., de Barsy, M., Zorreguieta, A., Letesson, J.J., De Bolle, X. (2013) The Brucella pathogens are polarized bacteria. Microbes and Infection 15, 998-1004.

http://www.ncbi.nlm.nih.gov/pubmed/24141086

Van der Henst, C., Beaufays, F., Mignolet, J., Didembourg, C., Colinet, J., Hallet, B., Letesson, J.-J., De Bolle, X. (2012) The histidine kinase PdhS controls cell cycle progression of the pathogenic alphaproteobacterium Brucella abortus. J. Bacteriol. 194, 5305-5314.

http://www.ncbi.nlm.nih.gov/pubmed/22843843

Brown, P.J.B., de Pedro, M.A., Kysela, D.T., Van der Henst, C., Kim, J., De Bolle, X., Fuqua, C., Brun, Y. (2012) Polar growth in the Alphaproteobacterial order Rhizobiales. Proc Natl. Acad. Sci. USA 109, 1697-1701.

http://www.ncbi.nlm.nih.gov/pubmed/22307633

 

 

Cell cycle of Brucella abortus

We characterize Brucella abortus cell cycle using tools that allow the monitoring of basic cell processes (such as growth and chromosomes replication and segregation) at the single cell level. Growth can be followed by the incorporation of fluorescent compound on the surface of the bacteria (panel A). Incorporation of new envelope material thus generates zones of unlabeled envelope (see Publication of Brown et al., 2012).

Brucella abortus strains have two chromosomes, one large "classical" chromosome (I) with a ParAB segregation system, and a smaller chromosome (II) ressembling plasmids of the rhizosphere, having a RepABC system for the initiation of replication and segregation of chromosome II to the future daughter cells. The replication of each chromosome is starting at a region called the "origin". Using fluorescent fusions to ParB and RepB (panel B), we have shown that the replication and the segregation of the two chromosomal origin is ordered (replication of chromosome I is initiated first, panel C) and follows a typical localization pattern (panel D, see Publications Deghelt et al., 2014 and De Bolle et al., 2015).

Using these fluorescent tools, we discovered that Brucella abortus is mainly internalized in its G1 form (these bacteria did not initiate the replication of their chromosomes), and their arrest their growth and their replication for a large fraction of their trafficking inside endosomal compartments of the host cells (panel E, see Deghelt et al., 2014).