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WDR13  expresses from the X chromosome and has a highly conserved coding sequence. There have been multiple associations of  WDR13  with memory. However, its detailed function in context of brain and behavior remains unknown. We characterized the behavioral phenotype of 2 month old male mice lacking the homolog of  WDR13  gene ( Wdr13  −/0 ). Taking cue from analysis of its expression in the brain, we chose hippocampus for molecular studies to delineate its function.  Wdr13  −/0  mice spent less time in the central area of the open field test (OFT) and with the novel object in novel object recognition test (NOR) as compared to the wild-type. However, these mice didn't show any significant changes in total time spent in arms or in frequency of arm entries in elevated plus maze (EPM). In the absence of  Wdr13 , there was a significant upregulation of synaptic proteins, viz., SYN1, RAB3A, CAMK2A etc. accompanied with increased spine density of hippocampal CA1 neurons and better spatial memory in mice as measured by increased time spent in the target quadrant of Morris water maze (MWM) during probe test. Parallel study from our lab has established c-JUN, ER α/β, and HDAC 1,3,7 as interacting partners of WDR13. WDR13 represses transcription from AP1 (c-JUN responsive) and Estrogen Receptor Element (ERE) promoters. We hypothesized that absence of  Wdr13  would result in de-regulated expression of a number of genes including multiple synaptic genes leading to the observed phenotype. Knocking down  Wdr13  in Neuro2a cell lines led to increased transcripts of  Camk2a  and  Nrxn2  consistent with  in-vivo  results. Summarily, our data provides functional evidence for the role of  Wdr13  in brain.

frontiers in molecular neuroscience

Implication of Genetic Deletion of Wdr13 in Mice: Mild Anxiety, Better Performance in Spatial Memory Task, with Upregulation of Multiple Synaptic Proteins