The VAPB-PTPIP51 endoplasmic reticulum-mitochondria tethering proteins are present in neuronal synapses and regulate synaptic activity

Literals

• dcterms:title
  • The VAPB-PTPIP51 endoplasmic reticulum-mitochondria tethering proteins are present in neuronal synapses and regulate synaptic activity
• dcterms:creator
  • Gómez-Suaga P.
• dcterms:contributor
  • Gomez-Suaga P., Perez-Nievas B.G., Glennon E.B., Lau D.H.W., Paillusson S., Morotz G.M., Cali T., Pizzo P., Noble W., Miller C.C.J.
• ou:bibtex
  • @article{ef6b11fac32044e99169644c18924cea, title = 'The VAPB-PTPIP51 endoplasmic reticulum-mitochondria tethering proteins are present in neuronal synapses and regulate synaptic activity', abstract = 'Signaling between the endoplasmic reticulum (ER) and mitochondria regulates a number of key neuronal functions. This signaling involves close physical contacts between the two organelles that are mediated by “tethering proteins” that function to recruit regions of ER to the mitochondrial surface. The ER protein, vesicle-associated membrane protein-associated protein B (VAPB) and the mitochondrial membrane protein, protein tyrosine phosphatase interacting protein-51 (PTPIP51), interact to form one such tether. Recently, damage to ER-mitochondria signaling involving disruption of the VAPB-PTPIP51 tethers has been linked to the pathogenic process in Parkinson{\textquoteright}s disease, fronto-temporal dementia (FTD) and related amyotrophic lateral sclerosis (ALS). Loss of neuronal synaptic function is a key feature of Parkinson{\textquoteright}s disease and FTD/ALS but the roles that ER-mitochondria signaling and the VAPB-PTPIP51 tethers play in synaptic function are not known. Here, we demonstrate that the VAPB-PTPIP51 tethers regulate synaptic activity. VAPB and PTPIP51 localise and form contacts at synapses, and stimulating neuronal activity increases ER-mitochondria contacts and the VAPB-PTPIP51 interaction. Moreover, siRNA loss of VAPB or PTPIP51 perturbs synaptic function and dendritic spine morphology. Our results reveal a new role for the VAPB-PTPIP51 tethers in neurons and suggest that damage to ER-mitochondria signaling contributes to synaptic dysfunction in Parkinson{\textquoteright}s disease and FTD/ALS.', keywords = 'Amyotrophic lateral sclerosis, Endoplasmic reticulum, Frontotemporal dementia, Mitochondria, PTPIP51, Parkinson{\textquoteright}s disease, Synapse, VAPB', author = 'Patricia G{\'o}mez-Suaga and P{\'e}rez-Nievas, {Beatriz G.} and Glennon, {Elizabeth B.} and Lau, {Dawn H. W.} and Sebastien Paillusson and M{\'o}rotz, {G{\'a}bor M.} and Tito Cal{\`i} and Paola Pizzo and Wendy Noble and Miller, {Christopher C. J.}', year = '2019', month = mar, day = '6', doi = '10.1186/s40478-019-0688-4', language = 'English', volume = '7', journal = 'Acta Neuropathologica Communications', issn = '2051-5960', publisher = 'BioMed Central', number = '1', }
• ou:tipoPublicacion
  • Article
• bibo:doi
  • 10.1186/s40478-019-0688-4
• bibo:eissn
  • 2051-5960
• fabio:hasPublicationYear
  • 2019
• ou:eid
  • 2-s2.0-85062604945
• vivo:identifier
  • 2019-2743
• bibo:page_range
  • 35
• dcterms:publisher
  • Acta neuropathologica communications
• vcard:url
  • https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85062604945&origin=inward
• ou:urlOrcid
  • https://kclpure.kcl.ac.uk/portal/en/publications/ef6b11fa-c320-44e9-9169-644c18924cea
• ou:urlScopus
  • https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85062604945&origin=inward
• ou:vecesCitado
  • 88
• bibo:volume
  • 7

Typed Literals

• ou:openaccess
  • True (xsd:boolean)

Relations

• ou:publicadaEnRevista
  • Acta Neuropathologica Communications

Inverse Relations

• Has related: ou:tienePublicacion
  • PATRICIA MARÍA GÓMEZ SUAGA