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The cluster of imprinted genes located in theDlk1–Dio3domain spanning 1 Mb plays an essential role in controlling pre- and postnatal growth and differentiation in mice and humans. The failure of parent-of-origin-dependent gene expression in this domain results in grave disorders, leading to death in some cases. However, little is known about the role of maternally expressed non-coding RNAs (ncRNAs) including many miRNAs and snoRNAs in this domain. In order to further understand the role of these ncRNAs, we createdGtl2-mutant mice harboring a 10 kb deletion in exons 1–5. The mutant mice exhibited a very unique inheritance mode: when the deletion was inherited from the mother (Mat-KO), the pups were born with normal phenotypes; however, all of them died within 4 weeks after birth, probably due to severely hypoplastic pulmonary alveoli and hepatocellular necrosis. Mice carrying the paternal deletion (Pat-KO) showed severe growth retardation and perinatal lethality. Interestingly, the homozygous mutants (Homo-KO) survived and developed into fertile adults. Our results show that these phenotypes occur due to altered expression of theDlk1–Dio3cluster genes including miRNAs and snoRNAs via thecisandtranseffects.

human molecular genetics

Deletion of               Gtl2              , imprinted non-coding RNA, with its differentially methylated region induces lethal parent-origin-dependent defects in mice