Postnatal Loss of Mef2c Results in Dissociation of Effects on Synapse Number and Learning and Memory.

ABSTRACT:

Background

Myocyte enhancer factor 2 (MEF2) transcription factors play critical roles in diverse cellular processes during central nervous system development. Studies attempting to address the role of MEF2 in brain have largely relied on overexpression of a constitutive MEF2 construct that impairs memory formation or knockdown of MEF2 function that increases spine numbers and enhances memory formation. Genetic deletion of individual MEF2 isoforms in brain during embryogenesis demonstrated that Mef2c loss negatively regulates spine numbers resulting in learning and memory deficits, possibly as a result of its essential role in development.

Methods

To investigate MEF2C function in brain further, we genetically deleted Mef2c during postnatal development in mice. We characterize

SUBMITTER: Adachi M 

PROVIDER: S-EPMC4826326 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature