NDLI: Sirh7/Ldoc1 knockout mice exhibit placental P4 overproduction and delayed parturition.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Naruse, Mie Ono, Ryuichi Irie, Masahito Nakamura, Kenji Furuse, Tamio Hino, Toshiaki Oda, Kanako Kashimura, Misho Yamada, Ikuko Wakana, Shigeharu Yokoyama, Minesuke Ishino, Fumitoshi Kaneko-Ishino, Tomoko
Description	Country affiliation: Japan Author Affiliation: Naruse M ( Department of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan School of Health Sciences, Tokai University, Bohseidai, Isehara, Kanagawa 259-1193, Japan.); Ono R ( Department of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan.); Irie M ( Department of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan School of Health Sciences, Tokai University, Bohseidai, Isehara, Kanagawa 259-1193, Japan.); Nakamura K ( Mitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan Faculty of Medicine, Tokai University, Bohseidai, Isehara, Kanagawa 259-1193, Japan.); Furuse T ( Technology and Development Team for Mouse Phenotype Analysis, The Japan Mouse Clinic, RIKEN BRC, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.); Hino T ( Mitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan Department of Biological Sciences, Asahikawa Medical University, 2-1-1-1 Midorigaoka-higashi, Asahikawa 078-8510, Japan.); Oda K ( Mitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Niigata 951-8585, Japan.); Kashimura M ( Technology and Development Team for Mouse Phenotype Analysis, The Japan Mouse Clinic, RIKEN BRC, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.); Yamada I ( Technology and Development Team for Mouse Phenotype Analysis, The Japan Mouse Clinic, RIKEN BRC, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.); Wakana S ( Technology and Development Team for Mouse Phenotype Analysis, The Japan Mouse Clinic, RIKEN BRC, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.); Yokoyama M ( Mitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Niigata 951-8585, Japan.); Ishino F ( Department of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan Global Center of Excellence Program for International Research Center for Molecular Science in Tooth and Bone Diseases, Tokyo Medical and Dental University, 1-); Kaneko-Ishino T ( School of Health Sciences, Tokai University, Bohseidai, Isehara, Kanagawa 259-1193, Japan fishino.epgn@mri.tmd.ac.jp tkanekoi@is.icc.u-tokai.ac.jp.)
Abstract	Sirh7/Ldoc1 [sushi-ichi retrotransposon homolog 7/leucine zipper, downregulated in cancer 1, also called mammalian retrotransposon-derived 7 (Mart7)] is one of the newly acquired genes from LTR retrotransposons in eutherian mammals. Interestingly, Sirh7/Ldoc1 knockout (KO) mice exhibited abnormal placental cell differentiation/maturation, leading to an overproduction of placental progesterone (P4) and placental lactogen 1 (PL1) from trophoblast giant cells (TGCs). The placenta is an organ that is essential for mammalian viviparity and plays a major endocrinological role during pregnancy in addition to providing nutrients and oxygen to the fetus. P4 is an essential hormone in the preparation and maintenance of pregnancy and the determination of the timing of parturition in mammals; however, the biological significance of placental P4 in rodents is not properly recognized. Here, we demonstrate that mouse placentas do produce P4 in mid-gestation, coincident with a temporal reduction in ovarian P4, suggesting that it plays a role in the protection of the conceptuses specifically in this period. Pregnant Sirh7/Ldoc1 knockout females also displayed delayed parturition associated with a low pup weaning rate. All these results suggest that Sirh7/Ldoc1 has undergone positive selection during eutherian evolution as a eutherian-specific acquired gene because it impacts reproductive fitness via the regulation of placental endocrine function.
File Format	HTM / HTML
ISSN	09501991
e-ISSN	14779129
DOI	10.1242/dev.114520
Journal	Development
Issue Number	24
Volume Number	141
Language	English
Publisher	The Company of Biologists
Publisher Date	2014-12-01
Publisher Place	Great Britain (UK)
Access Restriction	Open
Subject Keyword	Discipline Developmental Discipline Biology Parturition Metabolism Placenta Placental Lactogen Progesterone Animals Dna Primers Genetics Genotype In Situ Hybridization Mice Mice, Knockout Mifepristone Polymerase Chain Reaction Pregnancy Real-time Polymerase Chain Reaction Reverse Transcriptase Polymerase Chain Reaction Time Factors Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Developmental Biology Molecular Biology

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