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Three mechanisms control E-cadherin localization to the zonula adherens
Innokenty Woichansky1, Carlo Antonio Beretta2,3, Nicola Berns1
1Department of Cell and Molecular Biology and Division of Signaling and Functional Genomics at the German Cancer Research Center (DKFZ), Medical Faculty Mannheim, Heidelberg University, Ludolf-Krehl-Strasse 13-17, D-68167 Mannheim, Germany.
Nature Communications
|March 11, 2016
Summary
Researchers discovered how E-cadherin (epithelial cadherin) reaches the zonula adherens in epithelial cells. Three distinct pathways were identified, involving membrane trafficking and recycling, crucial for cell adhesion and tissue development.
Area of Science:
- Cell Biology
- Developmental Biology
- Molecular Biology
Background:
- E-cadherin localization at the zonula adherens is essential for epithelial cell differentiation.
- The precise mechanisms governing E-cadherin transport and localization remain largely unknown.
Purpose of the Study:
- To genetically dissect the in vivo mechanisms of E-cadherin transport to the zonula adherens.
- To identify the key molecular players and pathways involved in E-cadherin localization.
Main Methods:
- Utilized the Drosophila follicular epithelium as an in vivo model system.
- Employed genetic dissection to analyze E-cadherin transport pathways.
- Investigated the roles of Rab11 and RabX1 in E-cadherin trafficking.
Main Results:
- Identified three distinct mechanisms for E-cadherin accumulation at the zonula adherens.
- Described two membrane trafficking pathways delivering E-cadherin to the plasma membrane.
- Demonstrated a Rab11-dependent pathway targeting E-cadherin directly to the zonula adherens.
- Revealed a RabX1-dependent pathway involving endocytosis and recycling of lateral E-cadherin to the zonula adherens.
- Showed apically directed plasma membrane flow contributes to E-cadherin transport.
Conclusions:
- Differential regulation of these E-cadherin transport pathways may control cell shape changes during morphogenesis.
- Misregulation of these pathways can lead to compromised cell adhesion and disrupted tissue architecture.
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