The transcription factor, MEF2C, mediates a change in approximately one half of the expressed frontal cortical transcriptome controlling cellular metabolism and synaptic strength in response to acute loss of sleep.
Mice that lack the autism- and schizophrenia-linked gene MEF2C in cortical neurons have an imbalance of excitatory and inhibitory synapses, and impaired social and cognitive abilities.
In Drosophila, the loss of Frataxin causes iron accumulation in the nervous system, which in turn enhances sphingolipid synthesis and activation of PDK1 and Mef2, which leads to neurodegeneration.
Increasing periods of neuronal activity progressively weaken and then eliminate synapses through the activation of specific transcription factors and genes.
Maf and Mafb differentially regulate MGE-derived cortical and hippocampal interneuron subtype and regional fate in part through promoting the expression of Mef2c and Pnoc during mouse embryonic neurogenesis.
The regulatory programs governing skeletal muscle regeneration that are controlled by Klf5 in cooperation with MyoD and Mef2 provide a potential avenue for intervention into muscle regeneration through modulation of Klf5.
Second-order guidance, a novel mechanism by which an initial guidance cue controls expression of a second guidance receptor, is required for precise refinement of axon trajectories during PNS development.
