Literature DB >> 16775001

Csk differentially regulates Src64 during distinct morphological events in Drosophila germ cells.

Alana M O'Reilly1, Anna C Ballew, Byron Miyazawa, Hugo Stocker, Ernst Hafen, Michael A Simon.   

Abstract

The Src family protein tyrosine kinases (SFKs) are crucial regulators of cellular morphology. In Drosophila, Src64 controls complex morphological events that occur during oogenesis. Recent studies have identified key Src64-dependent mechanisms that regulate actin cytoskeletal dynamics during the growth of actin-rich ring canals, which act as intercellular bridges between germ cells. By contrast, the molecular mechanisms that regulate Src64 activity levels and potential roles for Src64 in additional morphological events in the ovary have not been defined. In this report, we demonstrate that regulation of Src64 by Drosophila C-terminal-Src Kinase (Csk) contributes to the packaging of germline cysts by overlying somatic follicle cells during egg chamber formation. These results uncover novel roles for both Csk and Src64 in a dynamic event that involves adhesion, communication between cell types and control of cell motility. Strikingly, Src64 and Csk function in the germline to control packaging, not in migrating follicle cells, suggesting novel functions for this signaling cassette in regulating dynamic adhesion. In contrast to the role played by Csk in the regulation of Src64 activity during packaging, Csk is dispensable for ring canal growth control, indicating that distinct mechanisms control Src64 activity during different morphological events.

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Year:  2006        PMID: 16775001     DOI: 10.1242/dev.02423

Source DB:  PubMed          Journal:  Development        ISSN: 0950-1991            Impact factor:   6.868


  18 in total

1.  HtsRC-Mediated Accumulation of F-Actin Regulates Ring Canal Size During Drosophila melanogaster Oogenesis.

Authors:  Julianne A Gerdes; Katelynn M Mannix; Andrew M Hudson; Lynn Cooley
Journal:  Genetics       Date:  2020-09-03       Impact factor: 4.562

Review 2.  Subcellular Specialization and Organelle Behavior in Germ Cells.

Authors:  Yukiko M Yamashita
Journal:  Genetics       Date:  2018-01       Impact factor: 4.562

3.  Identifying cellular pathways modulated by Drosophila palmitoyl-protein thioesterase 1 function.

Authors:  Stephanie Saja; Haley Buff; Alexis C Smith; Tiffany S Williams; Christopher A Korey
Journal:  Neurobiol Dis       Date:  2010-03-03       Impact factor: 5.996

4.  A Pak-regulated cell intercalation event leading to a novel radial cell polarity is involved in positioning of the follicle stem cell niche in the Drosophila ovary.

Authors:  Stephanie Vlachos; Sharayu Jangam; Ryan Conder; Michael Chou; Todd Nystul; Nicholas Harden
Journal:  Development       Date:  2015-01-01       Impact factor: 6.868

5.  The Misshapen kinase regulates the size and stability of the germline ring canals in the Drosophila egg chamber.

Authors:  Ashley Kline; Travis Curry; Lindsay Lewellyn
Journal:  Dev Biol       Date:  2018-05-09       Impact factor: 3.582

6.  Reverse signaling by glycosylphosphatidylinositol-linked Manduca ephrin requires a SRC family kinase to restrict neuronal migration in vivo.

Authors:  Thomas M Coate; Tracy L Swanson; Philip F Copenhaver
Journal:  J Neurosci       Date:  2009-03-18       Impact factor: 6.167

7.  Src inhibits midline axon crossing independent of Frazzled/Deleted in Colorectal Carcinoma (DCC) receptor tyrosine phosphorylation.

Authors:  Michael P O'Donnell; Greg J Bashaw
Journal:  J Neurosci       Date:  2013-01-02       Impact factor: 6.167

8.  Differing Src signaling levels have distinct outcomes in Drosophila.

Authors:  Marcos Vidal; Stephen Warner; Renee Read; Ross L Cagan
Journal:  Cancer Res       Date:  2007-11-01       Impact factor: 12.701

9.  Precise levels of the Drosophila adaptor protein Dreadlocks maintain the size and stability of germline ring canals.

Authors:  Kara Stark; Olivia Crowe; Lindsay Lewellyn
Journal:  J Cell Sci       Date:  2021-04-27       Impact factor: 5.285

10.  Drosophila PRL-1 is a growth inhibitor that counteracts the function of the Src oncogene.

Authors:  Krystle T Pagarigan; Bryce W Bunn; Jake Goodchild; Travis K Rahe; Julie F Weis; Leslie J Saucedo
Journal:  PLoS One       Date:  2013-04-08       Impact factor: 3.240

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