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dc.contributor.authorBialas, Allison R.en_US
dc.contributor.authorStevens, Bethen_US
dc.date.accessioned2014-07-07T17:03:55Z
dc.date.issued2014en_US
dc.identifier.citationBialas, Allison R., and Beth Stevens. 2014. “TGF-β Signaling Regulates Neuronal C1q Expression and Developmental Synaptic Refinement.” Nature neuroscience 16 (12): 1773-1782. doi:10.1038/nn.3560. http://dx.doi.org/10.1038/nn.3560.en
dc.identifier.issn1097-6256en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:12406754
dc.description.abstractImmune molecules, including complement proteins C1q and C3, have emerged as critical mediators of synaptic refinement and plasticity. Complement localizes to synapses and refines the developing visual system via C3-dependent microglial phagocytosis of synapses. Retinal ganglion cells (RGCs) express C1q, the initiating protein of the classical complement cascade, during retinogeniculate refinement; however, the signals controlling C1q expression and function remain elusive. Previous work implicated an astrocyte-derived factor in regulating neuronal C1q expression. Here we identify retinal TGF-β as a key regulator of neuronal C1q expression and synaptic pruning in the developing visual system. Mice lacking TGF-β receptor II (TGFβRII) in retinal neurons have reduced C1q expression in RGCs, reduced synaptic localization of complement, and phenocopy refinement defects observed in complement-deficient mice, including reduced eye specific segregation and microglial engulfment of RGC inputs. These data implicate TGF-β in regulating neuronal C1q expression to initiate complement- and microglia-mediated synaptic pruning.en
dc.language.isoen_USen
dc.relation.isversionofdoi:10.1038/nn.3560en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3973738/pdf/en
dash.licenseLAAen_US
dc.titleTGF-β Signaling Regulates Neuronal C1q Expression and Developmental Synaptic Refinementen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalNature neuroscienceen
dash.depositing.authorBialas, Allison R.en_US
dc.date.available2014-07-07T17:03:55Z
dc.identifier.doi10.1038/nn.3560*
dash.contributor.affiliatedRosen, Allison
dash.contributor.affiliatedStevens, Beth


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