Learning the cell cycle with a game: Virtual experiments in cell biology

Cell Cycle Learn (CCL) is a learning game designed for undergraduate students in Biology to learn common knowledge about the cell-division cycle along with practical skills related with setting up an experiment and the scientific method in general. In CCL, learners are guided through the process of formulating hypotheses, conducting virtual experiments and analysing the results in order to validate or invalidate the hypotheses. The game has been designed in the University of Toulouse and introduced last year as part of the curriculum of a cellular biology class. This paper presents early results of an evaluation of the game enabled by questionnaires filled by the participants and game data collected during the training sessions. The results demonstrate with examples that both types of data can be used to assess the game's utility

Phosphorylation de BCL-2 en réponse au traitement par le paclitaxel (mécanismes moléculaires impliqués et conséquences sur sa fonction anti-apoptotique)

TOULOUSE3-BU Sciences (315552104) / SudocSudocFranceF

Up-regulation of cdc2 protein during paclitaxel-induced apoptosis

International audienceMicrotubule damages induced by paclitaxel inhibit proteasome-dependent degradation of cyclin B, resulting in a sustained activation of cyclin B/cdc2 kinase and a cell cycle arrest in mitosis. It has been previously shown that this kinase activity is also required for paclitaxel-induced apoptosis. We found here that paclitaxel increased cdc2 mRNA and protein levels and led to an accumulation of cdc2 in the active dephosphorylated form in NIH-OVCAR-3 cells. The addition of cycloheximide inhibited the paclitaxel-induced increase in cdc2 protein level, further indicating that paclitaxel stimulates cdc2 synthesis. This increase in cdc2 synthesis is a consequence of paclitaxel-induced arrest in mitosis. Indeed, dual analysis of DNA and cdc2 protein contents indicated that cdc2 up-regulation occurred in cells arrested with a G2/M DNA content. Furthermore, no up-regulation of cdc2 protein was observed when paclitaxel-treated cells were prevented from entering mitosis by treatment with purvalanol A, a cyclin-dependent kinase (CDK) inhibitor, or stimulated to exit mitosis with 2-AP, a non-specific kinase inhibitor. In addition, when paclitaxel-induced apoptosis was inhibited by Bcl-2 over-expression, cdc2 up-regulation did not occur, leading to a lower level of activation of the cyclin B/cdc2 complex. Taken together, these results indicated that paclitaxel-induced cdc2 protein synthesis participates in a positive feedback loop designed to increase the activity of cyclin B/cdc2 kinase and thus may play a role in paclitaxel-induced apoptosis

Phosphorylation and Proteasome-Dependent Degradation of Bcl-2 in Mitotic-Arrested Cells after Microtubule Damage

International audienc