The polarity protein Angiomotin p130 controls dendritic spine maturation

Michael Wigerius; Dylan Quinn; Antonios Diab; Leanne Clattenburg; Annette Kolar; Jiansong Qi; Stefan R. Krueger; James P. Fawcett

doi:10.1083/jcb.201705184

The polarity protein Angiomotin p130 controls dendritic spine maturation

Michael Wigerius, Dylan Quinn, Antonios Diab, Leanne Clattenburg, Annette Kolar, Jiansong Qi, Stefan R. Krueger, James P. Fawcett

Medicine

Résultat de recherche: Article › examen par les pairs

13 Citations (Scopus)

Résumé

The actin cytoskeleton is essential for the structural changes in dendritic spines that lead to the formation of new synapses. Although the molecular mechanisms underlying spine formation are well characterized, the events that drive spine maturation during development are largely unknown. In this study, we demonstrate that Angiomotin (AMOT-130) is necessary for spine stabilization. AMOT-130 is enriched in mature dendritic spines and functions to stabilize the actin cytoskeleton by coupling F-actin to postsynaptic protein scaffolds. These functions of AMOT are transiently restricted during postnatal development by phosphorylation imposed by the kinase Lats1. Our study proposes that AMOT-130 is essential for normal spine morphogenesis and identifies Lats1 as an upstream regulator in this process. Moreover, our findings may link AMOT-130 loss and the related spine defects to neurological disorders.

Langue d'origine	English
Pages (de-à)	715-730
Nombre de pages	16
Journal	Journal of Cell Biology
Volume	217
Numéro de publication	2
DOI	https://doi.org/10.1083/jcb.201705184
Statut de publication	Published - févr. 1 2018

Note bibliographique

Funding Information:
This work was supported in part by funding from the Natural Sciences and Engineering Research Council of Canada to J.P. Fawcett (RGPIN-2017-05146) and S.R. Krueger (RGPIN-2011-326821), the Canadian Institutes of Health Research (MOP 341174), and a Research Scholar Award from the EJLB Foundation (to J.P. Fawcett). J.P. Fawcett was supported by the Canada Research Chairs Program through this work. The authors declare no competing financial interests.

Publisher Copyright:
© 2018 Wigerius et al.

ASJC Scopus Subject Areas

Cell Biology

Accès au document

10.1083/jcb.201705184

Autres fichiers et liens

Citer

@article{71a3bf5229334c11a783c0f712a5f284,

title = "The polarity protein Angiomotin p130 controls dendritic spine maturation",

abstract = "The actin cytoskeleton is essential for the structural changes in dendritic spines that lead to the formation of new synapses. Although the molecular mechanisms underlying spine formation are well characterized, the events that drive spine maturation during development are largely unknown. In this study, we demonstrate that Angiomotin (AMOT-130) is necessary for spine stabilization. AMOT-130 is enriched in mature dendritic spines and functions to stabilize the actin cytoskeleton by coupling F-actin to postsynaptic protein scaffolds. These functions of AMOT are transiently restricted during postnatal development by phosphorylation imposed by the kinase Lats1. Our study proposes that AMOT-130 is essential for normal spine morphogenesis and identifies Lats1 as an upstream regulator in this process. Moreover, our findings may link AMOT-130 loss and the related spine defects to neurological disorders.",

author = "Michael Wigerius and Dylan Quinn and Antonios Diab and Leanne Clattenburg and Annette Kolar and Jiansong Qi and Krueger, {Stefan R.} and Fawcett, {James P.}",

note = "Funding Information: This work was supported in part by funding from the Natural Sciences and Engineering Research Council of Canada to J.P. Fawcett (RGPIN-2017-05146) and S.R. Krueger (RGPIN-2011-326821), the Canadian Institutes of Health Research (MOP 341174), and a Research Scholar Award from the EJLB Foundation (to J.P. Fawcett). J.P. Fawcett was supported by the Canada Research Chairs Program through this work. The authors declare no competing financial interests. Publisher Copyright: {\textcopyright} 2018 Wigerius et al.",

year = "2018",

month = feb,

day = "1",

doi = "10.1083/jcb.201705184",

language = "English",

volume = "217",

pages = "715--730",

journal = "Journal of Cell Biology",

issn = "0021-9525",

publisher = "Rockefeller University Press",

number = "2",

}

TY - JOUR

T1 - The polarity protein Angiomotin p130 controls dendritic spine maturation

AU - Wigerius, Michael

AU - Quinn, Dylan

AU - Diab, Antonios

AU - Clattenburg, Leanne

AU - Kolar, Annette

AU - Qi, Jiansong

AU - Krueger, Stefan R.

AU - Fawcett, James P.

N1 - Funding Information: This work was supported in part by funding from the Natural Sciences and Engineering Research Council of Canada to J.P. Fawcett (RGPIN-2017-05146) and S.R. Krueger (RGPIN-2011-326821), the Canadian Institutes of Health Research (MOP 341174), and a Research Scholar Award from the EJLB Foundation (to J.P. Fawcett). J.P. Fawcett was supported by the Canada Research Chairs Program through this work. The authors declare no competing financial interests. Publisher Copyright: © 2018 Wigerius et al.

PY - 2018/2/1

Y1 - 2018/2/1

N2 - The actin cytoskeleton is essential for the structural changes in dendritic spines that lead to the formation of new synapses. Although the molecular mechanisms underlying spine formation are well characterized, the events that drive spine maturation during development are largely unknown. In this study, we demonstrate that Angiomotin (AMOT-130) is necessary for spine stabilization. AMOT-130 is enriched in mature dendritic spines and functions to stabilize the actin cytoskeleton by coupling F-actin to postsynaptic protein scaffolds. These functions of AMOT are transiently restricted during postnatal development by phosphorylation imposed by the kinase Lats1. Our study proposes that AMOT-130 is essential for normal spine morphogenesis and identifies Lats1 as an upstream regulator in this process. Moreover, our findings may link AMOT-130 loss and the related spine defects to neurological disorders.

AB - The actin cytoskeleton is essential for the structural changes in dendritic spines that lead to the formation of new synapses. Although the molecular mechanisms underlying spine formation are well characterized, the events that drive spine maturation during development are largely unknown. In this study, we demonstrate that Angiomotin (AMOT-130) is necessary for spine stabilization. AMOT-130 is enriched in mature dendritic spines and functions to stabilize the actin cytoskeleton by coupling F-actin to postsynaptic protein scaffolds. These functions of AMOT are transiently restricted during postnatal development by phosphorylation imposed by the kinase Lats1. Our study proposes that AMOT-130 is essential for normal spine morphogenesis and identifies Lats1 as an upstream regulator in this process. Moreover, our findings may link AMOT-130 loss and the related spine defects to neurological disorders.

UR - http://www.scopus.com/inward/record.url?scp=85041641595&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85041641595&partnerID=8YFLogxK

U2 - 10.1083/jcb.201705184

DO - 10.1083/jcb.201705184

M3 - Article

C2 - 29317530

AN - SCOPUS:85041641595

SN - 0021-9525

VL - 217

SP - 715

EP - 730

JO - Journal of Cell Biology

JF - Journal of Cell Biology

IS - 2

ER -

The polarity protein Angiomotin p130 controls dendritic spine maturation

Résumé

Note bibliographique

ASJC Scopus Subject Areas

Accès au document

Autres fichiers et liens

Empreinte numérique

Citer