Deaf1, short for Deformed epidermal autoregulatory factor-1, is a transcriptional regulator. It binds to unmethylated and variably spaced CpG dinucleotide motifs, with a consensus of a repeated TTCGGG motif [3]. It is involved in multiple pathways and has significant biological importance, being associated with autoimmune, neurological disorders, and muscle regeneration [1,3].

RNA-sequencing using hippocampal RNA from mice with conditional deletion of Deaf1 in the central nervous system showed that loss of Deaf1 activity results in altered expression of genes involved in neuronal function, dendritic spine maintenance, development, and activity, with reduced dendritic spines in hippocampal regions [2]. In muscle, Deaf1 is transcriptionally repressed by FOXOs and targets to Pik3c3 and Atg16l1 promoter regions to suppress their expression. Deaf1 depletion or overexpression in muscle stem cells leads to defects in muscle regeneration, highlighting its role in fine-tuning autophagy during muscle regeneration [1].

In conclusion, Deaf1 is crucial for normal neuronal function, dendritic spine maintenance, and muscle regeneration. Mouse models with conditional deletion of Deaf1 have provided insights into its role in neurological and muscle-related conditions, contributing to our understanding of the underlying molecular mechanisms in these disease areas [1,2].