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Défense de thèse de doctorat en sciences biologiques : "Caulobacter crescentus"

Intrinsic dimorphism of Caulobacter crescentus as an adaptive strategy to toxic Cu-rich environment.

Catégorie : défense de thèse
Date : 11/12/2015 16:00 - 11/12/2015 18:00
Lieu : Amphithéâtre CH01, rue Grafé, 5000 Namur
Orateur(s) : Emeline LAWAREE
Organisateur(s) : Jean-Yves MATROULE
Jury

Martin THANBICHLER (Philipps Univ., Marburg), Max MERGEAY (ULB), Sébastien RIGALI (ULg), Frédéric SILVESTRE, président (UNamur), Jean-Yves MATROULE, promoteur (UNamur)

Résumé

Over time, bacteria have developed stress resistance mechanisms to cope with the unpredictability of their environment. Among them, developmental changes such as sporulation or biofilm formation are efficient stress responses but are time-consuming processes. With this in mind, the intrinsic dimorphism of C. crescentus could provide an immediate and non-inducible adaptation to environmental fluctuations.

In the first part of this thesis, we provide the first evidence of a prompt bacterial Fight-or-Flight response as the C. crescentus intrinsic dimorphism permits a dual response to a toxic Cu-rich environment. We demonstrate that the motile swarmer cell triggers a flight response from the Cu source. If maintained in a Cu-rich environment, the swarmer cell differentiates into a sessile stalked cell expressing a PcoAB-dependent Cu homeostasis system highly efficient to detoxify Cu. PcoA is a periplasmic Cu oxidase that oxidizes toxic Cu+ in the less toxic Cu2+, while PcoB is anchored in the outer membrane and likely acts as a Cu efflux pump.

Under stress conditions, it has been shown that C. crescentus is able to modulate its cell cycle progression as an adaptive stress process. In the second part of this thesis, we show that a Cu stress induces specifically a delay in the cell division. While we still do not have elucidated the exact molecular actors involved in this delay, we suggest that this modulation of C. crescentus cell cycle could allow time to repair DNA damage generated by an oxidative stress due to high cellular Cu level. However, supplementary experiments are needed to confirm this hypothesis.

La défense est publique.

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