Our goal is to gain a better understanding of how the events of cellular reorganization during M-phase are controlled, since any deregulation or response to stress conditions potentially drive to genetic instability as consequence of cell cycle checkpoint transgression and/or aneuploidy. The identification of the molecular keys involved in the regulation of the progression into M-Phase has not led so far to a model where these molecular pieces fit together in a coherent whole. Among these molecular pieces, the MPF (M-Phase Promoting Factor) plays a pivotal and universal role in M-phase progression, whereas its direct and indirect regulators (such as Myt1, Cdc25, MAPK/Erk and PKA) may diversely intervene according to different models ; indeed, there is a lack of understanding on how cell cycle is regulated by the wiring and rewiring of the network, through (i) non-canonical interaction and pathways that remain to be deciphered, (ii) feed-back and (iii) feed-forward loops. In addition, several parameters such as intensity, amplitude and localization of enzymatic activities are largely unknown.
The strategy we undertook several years ago is articulated around two goals :
1 - The development of quantitative and qualitative approaches of signaling pathways and their interconnections ;
2 - The disruption structure/function of M-Phase cell cycle regulators by gasotransmitters and contaminants.
The originality of our work relies on analyses of cellular phenomenon performed in single and/or living cells through the use of amphibian oocytes as heterologous system of expression and through a kinase-sensors approach.