title: Parental and sexual conflicts over the Peg3 imprinted domain.
abstract: In the current study, the imprinting control region of the mouse Peg3 domain was deleted to test its functional impact on animal growth and survival. The paternal transmission of the deletion resulted in complete abolition of the transcription of two paternally expressed genes, Peg3 and Usp29, causing the reduced body weight of the pups. In contrast, the maternal transmission resulted in the unexpected transcriptional up-regulation of the remaining paternal allele of both Peg3 and Usp29, causing the increased body weight and survival rates. Thus, the imprinted maternal allele of the ICR may be a suppressor antagonistic to the active paternal allele of the ICR, suggesting a potential intralocus allelic conflict. The opposite outcomes between the two transmissions also justify the functional compromise that the maternal allele has become epigenetically repressed rather than genetically deleted during mammalian evolution. The mice homozygous for the deletion develop normally but with a skewed sex ratio, one male per litter, revealing its sex-biased effect. Overall, the Peg3 locus may have evolved to an imprinted domain to cope with both parental and sexual conflicts driven by its growth-stimulating paternal versus growth-suppressing maternal alleles.
authors.affiliation: Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA.
authors.forename: Hongzhi
authors.initials: H
authors.lastname: He
authors.affiliation: Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA.
authors.forename: Bambarendage P U
authors.initials: BP
authors.lastname: Perera
authors.affiliation: Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA.
authors.forename: An
authors.initials: A
authors.lastname: Ye
authors.affiliation: Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA.
authors.forename: Joomyeong
authors.initials: J
authors.lastname: Kim
mesh_terms: D000483:Alleles; D000818:Animals; D005075:Biological Evolution; D044127:Epigenesis, Genetic / Q000235:genetics; D005260:Female; D018392:Genomic Imprinting / Q000235:genetics*; D051741:Kruppel-Like Transcription Factors / Q000235:genetics*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D018345:Mice, Knockout; D000072417:Protein Domains / Q000235:genetics*; D017384:Sequence Deletion / Q000235:genetics; D015996:Survival Rate; D014158:Transcription, Genetic / Q000235:genetics; D064570:Ubiquitin-Specific Proteases / Q000235:genetics; D015854:Up-Regulation / Q000235:genetics
chemical_list: D051741:Kruppel-Like Transcription Factors; C097901:Peg3 protein, mouse; D064570:Ubiquitin-Specific Proteases