A Calcium-Regulated MEF2 Sumoylation Switch Controls Postsynaptic Differentiation-Reference-Cited by-同舟云学术

A Calcium-Regulated MEF2 Sumoylation Switch Controls Postsynaptic Differentiation

Published:2006-02-17 Issue:5763 Volume:311 Page:1012-1017
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Shalizi Aryaman¹²³⁴,Gaudillière Brice¹²³⁴,Yuan Zengqiang¹²³⁴,Stegmüller Judith¹²³⁴,Shirogane Takahiro¹²³⁴,Ge Qingyuan¹²³⁴,Tan Yi¹²³⁴,Schulman Brenda¹²³⁴,Harper J. Wade¹²³⁴,Bonni Azad¹²³⁴

Affiliation:

1. Department of Pathology, Harvard Medical School, 77 Louis Pasteur Avenue, Boston, MA 02115, USA.

2. Program in Biological and Biomedical Sciences, Harvard Medical School, 77 Louis Pasteur Avenue, Boston, MA 02115, USA.

3. Cell Signaling Technology, Inc., 166B Cummings Center, Beverly, MA 01915, USA.

4. Howard Hughes Medical Institute, Departments of Structural Biology and Genetics and Tumor Cell Biology, St. Jude Children's Research Hospital, 332 North Lauderdale, Memphis, TN 38105–2794, USA.

Abstract

Postsynaptic differentiation of dendrites is an essential step in synapse formation. We report here a requirement for the transcription factor myocyte enhancer factor 2A (MEF2A) in the morphogenesis of postsynaptic granule neuron dendritic claws in the cerebellar cortex. A transcriptional repressor form of MEF2A that is sumoylated at lysine-403 promoted dendritic claw differentiation. Activity-dependent calcium signaling induced a calcineurin-mediated dephosphorylation of MEF2A at serine-408 and, thereby, promoted a switch from sumoylation to acetylation at lysine-403, which led to inhibition of dendritic claw differentiation. Our findings define a mechanism underlying postsynaptic differentiation that may modulate activity-dependent synapse development and plasticity in the brain.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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