University of Cambridge > Talks.cam > Genetics Seminar  > Asymmetry in Drosophila neuroblasts: centrosomes & mRNA.

Asymmetry in Drosophila neuroblasts: centrosomes & mRNA.

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Host: Yuu Kimata

Asymmetric cell division can be seen as a tumor suppressor condition in stem cells. If this delicately balanced process is perturbed, cell fate information might not be correctly transmitted to the resulting daughter cells letting them to derail from their normal developmental routes. We are interested in the control of asymmetry in Drosophila neuroblast, the stem cells that generate the adult CNS during larval life. We particularly focus on the polarity of the cytoskeleton, notably microtubules and centrosomes and analyse the role they play in establishing and maintaining neuroblast polarity.

Neuroblasts have an extremely short cell cycle and go through repeated rounds of rapid polarization and depolarization of the cell cortex, while the axis of cell polarity remains stable between different cell cycles. How the orientation of this neuroblast polarity axis is set and remembered between the different cell cycles is not known. We have previously found a role for centrosomes and the interphase microtubule network in this process but their precise contribution remains unclear.

One interesting possibility is that the microtubule network positions cues that function as landmarks to orient the cell polarity axis. Intriguingly many transcripts of genes that are involved in asymmetric cell division have been reported to localize to the apical side of neuroblasts. Given the tight time constraints of the neuroblasts cell cycle, we reasoned that spatially controlled translation of localizes mRNAs might contribute to establish cell polarity in neuroblasts. How mRNAs are maintained apically and if their localization contributes to establishing neuroblast polarity remains unclear. I will report on a surprising localization pattern of one transcript during the larval neuroblasts cell cycle, its connection to centrosomes and what we learned so far about the molecular mechanism behind this, which we uncovered in great part by tracing mRNAs in neuroblasts by live microscopy.

This talk is part of the Genetics Seminar series.

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