期刊
NEURON
卷 69, 期 6, 页码 1069-1084出版社
CELL PRESS
DOI: 10.1016/j.neuron.2011.02.018
关键词
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资金
- Federation of European Biochemical Societies (FEBS)
- Medical Research Council (MAC)
- Australian CJ Martin Fellowship [310616]
- Medical Research Council [U117570528]
- Wellcome Trust [086947/Z/08/Z]
- King's College London
- Royal Society
- BBSRC [BB/E004083/2]
- Wellcome Trust [086947/Z/08/Z] Funding Source: Wellcome Trust
- BBSRC [BB/E004083/2, BB/E004083/1] Funding Source: UKRI
- MRC [MC_U117570528] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/E004083/1, BB/E004083/2] Funding Source: researchfish
- Medical Research Council [MC_U117570528] Funding Source: researchfish
Little is known of the intracellular machinery that controls the motility of newborn neurons. We have previously shown that this proneural protein Neurog2 promotes the migration of nascent cortical neurons by inducing the expression of the atypical Rho GTPase Rnd2. Here, we show that another proneural factor, Ascl1, promotes neuronal migration in the cortex through direct regulation of a second Rnd family member, Rnd3. Both Rnd2 and Rnd3 promote neuronal migration by inhibiting RhoA signaling, but they control distinct steps of the migratory process, multipolar to bipolar transition in the intermediate zone and locomotion in the cortical plate, respectively. Interestingly, these divergent functions directly result from the distinct subcellular distributions of the two Rnd proteins. Because Rnd proteins also regulate progenitor divisions and neurite outgrowth, we propose that proneural factors, through spatiotemporal regulation of Rnd proteins, integrate the process of neuronal migration with other events in the neurogenic program.
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