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Childhood malnutrition is a risk factor for mental disorders, such as major depression and anxiety. Evidence shows that similar early life adversities induce sex-dependent epigenetic reprogramming. However, little is known about how genes are specifically affected by early malnutrition and the implications for males and females respectively. One relevant target is neuropeptide Y (NPY), which regulates both stress and food-intake. We studied maternal low protein diet (LPD) during pregnancy/lactation in mice. Male, but not female, offspring of LPD mothers consistently displayed anxiety- and depression-like behaviors under acute stress. Transcriptome-wide analysis of the effects of acute stress in the amygdala, revealed a list of transcription factors affected by either sex or perinatal LPD. Among these immediate early genes (IEG), members of the  Early growth response  family ( Egr1 /2/4) were consistently upregulated by perinatal LPD in both sexes. EGR1 also bound the  NPY receptor Y1  gene ( Npy1r ), which co-occurred with sex-specific effects of perinatal LPD on both  Npy1r  DNA-methylation and gene transcription. Our proposed pathway connecting early malnutrition, sex-independent regulatory changes in  Egr1 , and sex-specific epigenetic reprogramming of its effector gene,  Npy1r , represents the first molecular evidence of how early life risk factors may generate sex-specific epigenetic effects relevant for mental disorders.

Perinatal Malnutrition Leads to Sexually Dimorphic Behavioral Responses with Associated Epigenetic Changes in the Mouse Brain