A C. elegans Ror receptor tyrosine kinase regulates cell motility and asymmetric cell division

Nature ◽  
10.1038/23722 ◽  
1999 ◽  
Vol 400 (6747) ◽  
pp. 881-885 ◽  
Author(s):  
Wayne C. Forrester ◽  
Megan Dell ◽  
Elliot Perens ◽  
Gian Garriga
Keyword(s):  
Cell Division ◽  
Tyrosine Kinase ◽  
Cell Motility ◽  
Receptor Tyrosine Kinase ◽  
Asymmetric Cell Division ◽  
C Elegans

The receptor tyrosine kinase HIR-1 coordinates HIF-independent responses to hypoxia and extracellular matrix injury

2018 ◽  
Vol 11 (550) ◽  
pp. eaat0138
Author(s):  
Roman Vozdek ◽  
Yong Long ◽  
Dengke K. Ma
Keyword(s):  
Extracellular Matrix ◽  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Large Scale ◽  
Hypoxia Inducible Factor ◽  
Metabolic Adaptation ◽  
Loss Of Function ◽  
Ecm Remodeling ◽  
C Elegans ◽  
Heme Peroxidases

Inadequate tissue oxygen, or hypoxia, is a central concept in the pathophysiology of ischemic disorders and cancer. Hypoxia promotes extracellular matrix (ECM) remodeling, cellular metabolic adaptation, and cancer cell metastasis. To discover new pathways through which cells respond to hypoxia, we performed a large-scale forward genetic screen inCaenorhabditis elegansand identified a previously uncharacterized receptor tyrosine kinase named HIR-1. Loss of function inhir-1phenocopied the impaired ECM integrity associated with hypoxia or deficiency in the oxygen-dependent dual oxidase, heme peroxidases, or cuticular collagens involved in ECM homeostasis. Genetic suppressor screens identified NHR-49 and MDT-15 as transcriptional regulators downstream of HIR-1. Furthermore,hir-1mutants showed defects in adapting to and recovering from prolonged severe hypoxia. We propose thatC. elegansHIR-1 coordinates hypoxia-inducible factor–independent responses to hypoxia and hypoxia-associated ECM remodeling through mechanisms that are likely conserved in other organisms.

scholarly journals Cortical localization of the G  protein GPA-16 requires RIC-8function during C. elegans asymmetric cell division

Development ◽  
2005 ◽  
Vol 132 (20) ◽  
pp. 4449-4459 ◽  
Author(s):  
K. Afshar ◽  
F. S. Willard ◽  
K. Colombo ◽  
D. P. Siderovski ◽  
P. Gonczy
Keyword(s):  
Cell Division ◽  
G Protein ◽  
Asymmetric Cell Division ◽  
C Elegans ◽  
Cortical Localization

scholarly journals Extracellular control of PAR protein localization during asymmetric cell division in the C. elegans embryo

Development ◽  
2010 ◽  
Vol 137 (19) ◽  
pp. 3337-3345 ◽  
Author(s):  
Y. Arata ◽  
J.-Y. Lee ◽  
B. Goldstein ◽  
H. Sawa
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
Protein Localization ◽  
C Elegans

scholarly journals Regulation of anterior cell-specific mec-3 expression during asymmetric cell division in C. elegans

1992 ◽  
Vol 194 (4) ◽  
pp. 289-302 ◽  
Author(s):  
Jeffrey C. Way ◽  
Jin-Quan Run ◽  
Alice Y. Wang
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
C Elegans

scholarly journals Receptor tyrosine kinase signaling required for integrin alpha v beta 5-directed cell motility but not adhesion on vitronectin.

1994 ◽  
Vol 127 (3) ◽  
pp. 859-866 ◽  
Author(s):  
R L Klemke ◽  
M Yebra ◽  
E M Bayna ◽  
D A Cheresh
Keyword(s):  
Cell Migration ◽  
Tyrosine Kinase ◽  
Cell Motility ◽  
Receptor Tyrosine Kinase ◽  
Kinase Inhibitors ◽  
Kinase Inhibitor ◽  
De Novo ◽  
Growth Factor Receptor ◽  
Dependent Manner ◽  
Pkc Activation

FG human pancreatic carcinoma cells adhere to vitronectin using integrin alpha v beta 5 yet are unable to migrate on this ligand whereas they readily migrate on collagen in an alpha 2 beta 1-dependent manner. We report here that epidermal growth factor receptor (EGFR) activation leads to de novo alpha v beta 5-dependent FG cell migration on vitronectin. The EGFR specific tyrosine kinase inhibitor tyrphostin 25 selectively prevents EGFR autophosphorylation thereby preventing the EGF-induced FG cell migration response on vitronectin without affecting constitutive migration on collagen. Protein kinase C (PKC) activation also leads to alpha v beta 5-directed motility on vitronectin; however, this is not blocked by tyrosine kinase inhibitors. In this case, PKC activation appears to be associated with and downstream of EGFR signaling since calphostin C, an inhibitor of PKC, blocks FG cell migration on vitronectin induced by either PKC or EGF. These findings represent the first report implicating a receptor tyrosine kinase in a specific integrin mediated cell motility event independent of adhesion.

scholarly journals C. elegans Brat homologs regulate PAR protein-dependent polarity and asymmetric cell division

2008 ◽  
Vol 321 (2) ◽  
pp. 368-378 ◽  
Author(s):  
Vincent Hyenne ◽  
Marianne Desrosiers ◽  
Jean-Claude Labbé
Keyword(s):  
Cell Division ◽  
Asymmetric Cell Division ◽  
C Elegans
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