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Src42A is required for E-cadherin dynamics at cell junctions during Drosophila axis elongation
Lenin Chandran1, Wilko Backer2, Raphael Schleutker2
1Developmental Genetics, Institut für Biologie, Universität Kassel, 34132 Kassel, Germany.
Development (Cambridge, England)
|January 11, 2023
Summary
Src42A kinase regulates cell junction remodeling in Drosophila gastrulation by controlling E-cadherin localization and mechanical tension at cell interfaces.
Area of Science:
- Cell Biology
- Developmental Biology
- Biochemistry
Background:
- Src kinases are crucial for regulating cell adhesion and junction dynamics.
- Understanding the precise roles of specific Src family kinases in developmental processes like gastrulation is essential.
Purpose of the Study:
- To investigate the function of Src42A in junction remodeling during Drosophila gastrulation.
- To elucidate the molecular mechanisms by which Src42A influences cell intercalation and adhesion.
Main Methods:
- Maternal RNA interference (RNAi) for Src42A knockdown.
- CRISPR-Cas9-induced germline mosaics in Drosophila.
- Analysis of tyrosine phosphorylation at bicellular and tricellular junctions.
- Assessment of E-cadherin localization and planar polarity.
Main Results:
- Src42A is required for tyrosine phosphorylation at bicellular and tricellular junctions.
- Src42A regulates junction contraction during cell intercalation.
- Src42A knockdown leads to compromised E-cadherin planar polarity and accumulation at tricellular junctions.
- Src42A functions in conjunction with Abl kinase.
Conclusions:
- Src42A plays a dual role in establishing mechanical tension and acting as a signaling factor at tricellular junctions.
- Src42A controls E-cadherin residence time, impacting junction remodeling during gastrulation.
- These findings provide insights into the regulation of cell adhesion and tissue morphogenesis.
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