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Parental imprinting is a mammalian-specific form of epigenetic regulation in which one allele of a gene is silenced depending on its parental origin. Parentally imprinted genes have been shown to play a role in growth, metabolism, cancer, and behavior. Although the molecular mechanisms underlying parental imprinting have been largely elucidated, the selective advantage of silencing one allele remains unclear. The mutant phenotype of the imprinted gene,  Pw1/Peg3 , provides a key example to illustrate the hypothesis on a coadaptation between mother and offspring, in which  Pw1/Peg3  is required for a set of essential maternal behaviors, such as nursing, nest building, and postnatal care. We have generated a novel  Pw1/Peg3  mutant allele that targets the last exon for the PW1 protein that contains >90% of the coding sequence resulting in a loss of  Pw1/Peg3  expression. In contrast to previous reports that have targeted upstream exons, we observe that maternal behavior and lactation are not disrupted upon loss of  Pw1/Peg3 . Both paternal and homozygous  Pw1/Peg3  mutant females nurse and feed their pups properly and no differences are detected in either oxytocin neuron number or oxytocin plasma levels. In addition, suckling capacities are normal in mutant pups. Consistent with previous reports, we observe a reduction of postnatal growth. These results support a general role for  Pw1 / Peg3  in the regulation of body growth but not maternal care and lactation.

A Novel Mutant Allele of Pw1/Peg3 Does Not Affect Maternal Behavior or Nursing Behavior