Journal
NEURON
Volume 66, Issue 1, Pages 69-84Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2010.03.019
Keywords
-
Categories
Funding
- Helen Hay Whitney Post-doctoral Fellowship
- Department of Pediatrics, University of Texas, Health Science Center at Houston
- Sigrid Juselius Foundation
- Stuart H.Q. & Victoria Quan Fellowship
- NIH MSTP
- NIH [HD029178]
- UNC-CH Reynolds Faculty Fellowship
- EC [QLG3-CT-2002-01266)]
- Telethon [GGP07181]
- Children's Hospital Boston [P30HD018655]
- NINDS [R01NS32457, P01 NS40043]
Ask authors/readers for more resources
Cortical development depends upon tightly controlled cell fate and cell survival decisions that generate a functional neuronal population, but the coordination of these two processes is poorly understood. Here we show that conditional removal of a key apical complex protein, Pals1, causes premature withdrawal from the cell cycle, inducing excessive generation of early-born postmitotic neurons followed by surprisingly massive and rapid cell death, leading to the abrogation of virtually the entire cortical structure. Pals1 loss shows exquisite dosage sensitivity, so that heterozygote mutants show an intermediate phenotype on cell fate and cell death. Loss of Pals1 blocks essential cell survival signals, including the mammalian target of rapamycin (mTOR) pathway, while mTORC1 activation partially rescues Pals1 deficiency. These data highlight unexpected roles of the apical complex protein Pals1 in cell survival through interactions with mTOR signaling.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available