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

Producción científica: Contribución a una revista › Artículo › revisión exhaustiva

13 Citas (Scopus)

Resumen

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.

Idioma original	English
Páginas (desde-hasta)	715-730
Número de páginas	16
Publicación	Journal of Cell Biology
Volumen	217
N.º	2
DOI	https://doi.org/10.1083/jcb.201705184
Estado	Published - feb. 1 2018

Nota bibliográfica

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

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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.",

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AU - Qi, Jiansong

AU - Krueger, Stefan R.

AU - Fawcett, James P.

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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.

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The polarity protein Angiomotin p130 controls dendritic spine maturation

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