Neuron-Glia interactions through the heartless fgf receptor signaling pathway mediate morphogenesis of drosophila astrocytes

Wilm Tobias Stork, Amy Sheehan, Ozge E. Tasdemir-Yilmaz, Marc Freeman

Research output: Contribution to journalArticle

85 Citations (Scopus)

Abstract

Astrocytes are critically important for neuronal circuit assembly and function. Mammalian protoplasmic astrocytes develop a dense ramified meshwork of cellular processes to form intimate contacts with neuronal cell bodies, neurites, and synapses. This close neuron-glia morphological relationship is essential for astrocyte function, but it remains unclear how astrocytes establish their intricate morphology, organize spatial domains, and associate with neurons and synapses invivo. Here we characterize a Drosophila glial subtype that shows striking morphological and functional similarities to mammalian astrocytes. We demonstrate that the Fibroblast growth factor (FGF) receptor Heartless autonomously controls astrocyte membrane growth, and the FGFs Pyramus and Thisbe direct astrocyte processes to ramify specifically in CNS synaptic regions. We further show that the shape and size of individual astrocytes are dynamically sculpted through inhibitory or competitive astrocyte-astrocyte interactions and Heartless FGF signaling. Our data identify FGF signaling through Heartless as a key regulator of astrocyte morphological elaboration invivo.

Original languageEnglish (US)
Pages (from-to)388-403
Number of pages16
JournalNeuron
Volume83
Issue number2
DOIs
StatePublished - Jul 16 2014
Externally publishedYes

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Morphogenesis
Neuroglia
Astrocytes
Drosophila
Neurons
Fibroblast Growth Factors
Synapses
Fibroblast Growth Factor Receptors
Neurites
Membranes

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Neuron-Glia interactions through the heartless fgf receptor signaling pathway mediate morphogenesis of drosophila astrocytes. / Stork, Wilm Tobias; Sheehan, Amy; Tasdemir-Yilmaz, Ozge E.; Freeman, Marc.

In: Neuron, Vol. 83, No. 2, 16.07.2014, p. 388-403.

Research output: Contribution to journalArticle

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