Tsankova, Anna and Pham, Tri Thanh and Garcia, David Salvador and Otte, Fabian and Cabernard, Clemens. (2017) Cell Polarity Regulates Biased Myosin Activity and Dynamics during Asymmetric Cell Division via Drosophila Rho Kinase and Protein Kinase N. Developmental Cell, 42 (2). pp. 143-155.e5.
Full text not available from this repository.
Official URL: http://edoc.unibas.ch/55760/
Downloads: Statistics Overview
Abstract
Cell and tissue morphogenesis depends on the correct regulation of non-muscle Myosin II, but how this motor protein is spatiotemporally controlled is incompletely understood. Here, we show that in asymmetrically dividing Drosophila neural stem cells, cell intrinsic polarity cues provide spatial and temporal information to regulate biased Myosin activity. Using live cell imaging and a genetically encoded Myosin activity sensor, we found that Drosophila Rho kinase (Rok) enriches for activated Myosin on the neuroblast cortex prior to nuclear envelope breakdown (NEB). After NEB, the conserved polarity protein Partner of Inscuteable (Pins) sequentially enriches Rok and Protein Kinase N (Pkn) on the apical neuroblast cortex. Our data suggest that apical Rok first increases phospho-Myosin, followed by Pkn-mediated Myosin downregulation, possibly through Rok inhibition. We propose that polarity-induced spatiotemporal control of Rok and Pkn is important for unequal cortical expansion, ensuring correct cleavage furrow positioning and the establishment of physical asymmetry.
Faculties and Departments: | 05 Faculty of Science > Departement Biozentrum > Former Organization Units Biozentrum > Growth and Development (Cabernard) |
---|---|
UniBasel Contributors: | Cabernard, Clemens |
Item Type: | Article, refereed |
Article Subtype: | Research Article |
Publisher: | Elsevier |
ISSN: | 1534-5807 |
e-ISSN: | 1878-1551 |
Note: | Publication type according to Uni Basel Research Database: Journal article |
Identification Number: |
|
Last Modified: | 20 Oct 2017 09:43 |
Deposited On: | 20 Oct 2017 09:43 |
Repository Staff Only: item control page