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

• Published in: PLoS genetics 2016-05, Vol.12 (5), p.e1006053-e1006053
• Main Authors: Denizot, Anne-Lyse, Besson, Vanessa, Correra, Rosa Maria, Mazzola, Alessia, Lopes, Izolina, Courbard, Jean-Remy, Marazzi, Giovanna, Sassoon, David A
• Format: Article
• Language: English
• Subjects: Advantages; Alleles; Animal behavior; Animals; Biology and Life Sciences; Breastfeeding & lactation; Defects; Epigenesis, Genetic; Epigenetics; Exons; Female; Gene expression; Gene Expression Regulation; Gene mutation; Genetic aspects; Genetics; Genomic Imprinting - genetics; Humans; Hypotheses; Kruppel-Like Transcription Factors - biosynthesis; Kruppel-Like Transcription Factors - genetics; Lactation - genetics; Life Sciences; Mammals; Maternal Behavior; Medicine and Health Sciences; Metabolism; Mice; Mutant Proteins - biosynthesis; Mutant Proteins - genetics; Neurons - metabolism; Observations; Parenting; Physical Sciences; Physiological aspects; Research and Analysis Methods; Rodents; Statistical analysis; Stem cells; Umbilical cord
• ISSN: 1553-7404; 1553-7390; 1553-7404
• DOI: 10.1371/journal.pgen.1006053

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.