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dc.contributor.authorFuentes-Medel, Yuly F.
dc.contributor.authorAshley, James A.
dc.contributor.authorBarria, Romina
dc.contributor.authorMaloney, Rachel
dc.contributor.authorFreeman, Marc R.
dc.contributor.authorBudnik, Vivian
dc.date2022-08-11T08:09:29.000
dc.date.accessioned2022-08-23T16:32:21Z
dc.date.available2022-08-23T16:32:21Z
dc.date.issued2012-10-09
dc.date.submitted2013-01-23
dc.identifier.citationCurr Biol. 2012 Oct 9;22(19):1831-8. doi: 10.1016/j.cub.2012.07.063. <a href="http://dx.doi.org/10.1016/j.cub.2012.07.063">Link to article on publisher's site</a>
dc.identifier.issn0960-9822 (Linking)
dc.identifier.doi10.1016/j.cub.2012.07.063
dc.identifier.pmid22959350
dc.identifier.urihttp://hdl.handle.net/20.500.14038/37865
dc.description<p>First author Yuly Fuentes-Medel is a doctoral student in the Neuroscience Program in the Graduate School of Biomedical Sciences (GSBS) at UMass Medical School.</p>
dc.description.abstractGlial cells are crucial regulators of synapse formation, elimination, and plasticity [1, 2]. In vitro studies have begun to identify glial-derived synaptogenic factors [1], but neuron-glia signaling events during synapse formation in vivo remain poorly defined. The coordinated development of pre- and postsynaptic compartments at the Drosophila neuromuscular junction (NMJ) depends on a muscle-secreted retrograde signal, the TGF-beta/BMP Glass bottom boat (Gbb) [3, 4]. Muscle-derived Gbb activates the TGF-beta receptors Wishful thinking (Wit) and either Saxophone (Sax) or Thick veins (Tkv) in motor neurons [3, 4]. This induces phosphorylation of Mad (P-Mad) in motor neurons, its translocation into the nucleus with a co-Smad, and activation of transcriptional programs controlling presynaptic bouton growth [5]. Here we show that NMJ glia release the TGF-beta ligand Maverick (Mav), which likely activates the muscle activin-type receptor Punt to potently modulate Gbb-dependent retrograde signaling and synaptic growth. Loss of glial Mav results in strikingly reduced P-Mad at NMJs, decreased Gbb transcription in muscle, and in turn reduced muscle-to-motor neuron retrograde TGF-beta/BMP signaling. We propose that by controlling Gbb release from muscle, glial cells fine tune the ability of motor neurons to extend new synaptic boutons in correlation to muscle growth. Our work identifies a novel glia-derived synaptogenic factor by which glia modulate synapse formation in vivo.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=22959350&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3605899/
dc.subjectSynapses
dc.subjectNeuroglia
dc.subjectTransforming Growth Factor beta
dc.subjectDevelopmental Neuroscience
dc.titleIntegration of a retrograde signal during synapse formation by glia-secreted TGF-beta ligand
dc.typeJournal Article
dc.source.journaltitleCurrent biology : CB
dc.source.volume22
dc.source.issue19
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/neurobiology_pp/136
dc.identifier.contextkey3608530
html.description.abstract<p>Glial cells are crucial regulators of synapse formation, elimination, and plasticity [1, 2]. In vitro studies have begun to identify glial-derived synaptogenic factors [1], but neuron-glia signaling events during synapse formation in vivo remain poorly defined. The coordinated development of pre- and postsynaptic compartments at the Drosophila neuromuscular junction (NMJ) depends on a muscle-secreted retrograde signal, the TGF-beta/BMP Glass bottom boat (Gbb) [3, 4]. Muscle-derived Gbb activates the TGF-beta receptors Wishful thinking (Wit) and either Saxophone (Sax) or Thick veins (Tkv) in motor neurons [3, 4]. This induces phosphorylation of Mad (P-Mad) in motor neurons, its translocation into the nucleus with a co-Smad, and activation of transcriptional programs controlling presynaptic bouton growth [5]. Here we show that NMJ glia release the TGF-beta ligand Maverick (Mav), which likely activates the muscle activin-type receptor Punt to potently modulate Gbb-dependent retrograde signaling and synaptic growth. Loss of glial Mav results in strikingly reduced P-Mad at NMJs, decreased Gbb transcription in muscle, and in turn reduced muscle-to-motor neuron retrograde TGF-beta/BMP signaling. We propose that by controlling Gbb release from muscle, glial cells fine tune the ability of motor neurons to extend new synaptic boutons in correlation to muscle growth. Our work identifies a novel glia-derived synaptogenic factor by which glia modulate synapse formation in vivo.</p>
dc.identifier.submissionpathneurobiology_pp/136
dc.contributor.departmentGraduate School of Biomedical Sciences, Neuroscience Program
dc.contributor.departmentFreeman Lab
dc.contributor.departmentBudnik Lab
dc.contributor.departmentNeurobiology
dc.source.pages1831-8
dc.contributor.studentJames Ashley
dc.contributor.studentYuly Fuentes-Medel
dc.description.thesisprogramNeuroscience


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