CD44 regulates dendrite morphogenesis through Src tyrosine kinase-dependent positioning of the Golgi apparatus | Zendy

Anna Skupien | Zendy; Anna Konopka | Zendy; Paweł Trzaskoma | Zendy; Josephine Labus | Zendy; Adam Gorlewicz | Zendy; Lukasz Swiech | Zendy; Matylda Babraj | Zendy; Hubert Doleżyczek | Zendy; Izabela Figiel | Zendy; Evgeni Ponimaskin | Zendy; Jakub Włodarczyk | Zendy; Jacek Jaworski | Zendy; Grzegorz M. Wilczyński | Zendy; Joanna Dzwonek | Zendy

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CD44 regulates dendrite morphogenesis through Src tyrosine kinase-dependent positioning of the Golgi apparatus

Author(s) -

Anna Skupien,

Anna Konopka,

Paweł Trzaskoma,

Josephine Labus,

Adam Gorlewicz,

Lukasz Swiech,

Matylda Babraj,

Hubert Doleżyczek,

Izabela Figiel,

Evgeni Ponimaskin,

Jakub Włodarczyk,

Jacek Jaworski,

Grzegorz M. Wilczyński,

Joanna Dzwonek

Publication year - 2014

Publication title -

journal of cell science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.384

H-Index - 278

eISSN - 1477-9137

pISSN - 0021-9533

DOI - 10.1242/jcs.154542

Subject(s) - biology , microbiology and biotechnology , proto oncogene tyrosine protein kinase src , dendrite (mathematics) , receptor tyrosine kinase , golgi apparatus , extracellular matrix , cd44 , signal transduction , in vitro , biochemistry , geometry , mathematics , endoplasmic reticulum

The acquisition of proper dendrite morphology is a crucial aspect of neuronal development towards the formation of a functional network. The role of the extracellular matrix and its cellular receptors in this process has remained enigmatic. We report that the CD44 adhesion molecule, the main hyaluronan receptor, is localized in dendrites and plays a crucial inhibitory role in dendritic tree arborization in vitro and in vivo. This novel function is exerted by the activation of Src tyrosine kinase, leading to the alteration of Golgi morphology. The mechanism operates during normal brain development, but its inhibition might have a protective influence on dendritic trees under toxic conditions, during which the silencing of CD44 expression prevents dendritic shortening induced by glutamate exposure. Overall, our results indicate a novel role for CD44 as an essential regulator of dendritic arbor complexity in both health and disease.

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