生物谷报道:日本的一个研究小组1月6日在《自然—遗传学》(Nature Genetics)杂志网络版上发表论文说,他们发现了胎盘正常工作的一个必要基因,它很可能来源于哺乳动物祖先感染的病毒。
哺乳动物的胎儿通过胎盘的毛细血管从母体获取营养。东京医科齿科大学、东海大学等机构的科学家联合研究发现,实验鼠和人体内都存在一种名为“Peg11”的基因,这种基因上残留的一些痕迹说明,该基因很可能从远古病毒的DNA(脱氧核糖核酸)转而编入了鼠和人类的DNA。
日本专家剔除了实验鼠的“Peg11”基因,或者让这个基因异常发挥作用,结果发现都会造成实验鼠胎盘毛细血管结构异常,交换营养物质的能力下降,最终导致胎儿因发育不良而胎死腹中,或者出生后夭折。
日本专家认为,这项研究可帮助诊断一些不明原因的发育障碍,并有助于了解原始哺乳动物的进化过程。(来源:新华网 钱铮)
生物谷推荐原始出处:
Nature Genetics
Published online: 6 January 2008 | doi:10.1038/ng.2007.51
Role of retrotransposon-derived imprinted gene, Rtl1, in the feto-maternal interface of mouse placenta
Yoichi Sekita1, Hirotaka Wagatsuma2, Kenji Nakamura3, Ryuichi Ono1, Masayo Kagami4, Noriko Wakisaka1,5, Toshiaki Hino3, Rika Suzuki-Migishima3, Takashi Kohda1, Atsuo Ogura6, Tsutomu Ogata4, Minesuke Yokoyama3,7, Tomoko Kaneko-Ishino5 & Fumitoshi Ishino1
Eutherian placenta, an organ that emerged in the course of mammalian evolution, provides essential architecture, the so-called feto-maternal interface, for fetal development by exchanging nutrition, gas and waste between fetal and maternal blood. Functional defects of the placenta cause several developmental disorders, such as intrauterine growth retardation in humans and mice. A series of new inventions and/or adaptations must have been necessary to form and maintain eutherian chorioallantoic placenta, which consists of capillary endothelial cells and a surrounding trophoblast cell layer(s)1. Although many placental genes have been identified2, it remains unknown how the feto-maternal interface is formed and maintained during development, and how this novel design evolved. Here we demonstrate that retrotransposon-derived Rtl1 (retrotransposon-like 1), also known as Peg11 (paternally expressed 11), is essential for maintenance of the fetal capillaries, and that both its loss and its overproduction cause late-fetal and/or neonatal lethality in mice.
Department of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kandasurugadai, Chiyoda-ku, Tokyo 101-0062, Japan.
Graduate School of Bioscience and Biotechnology, Tokyo Institute of Technology, 4259 Nagatsuta-cho, Midori-ku, Yokohama 226-8501, Japan.
Mitsubishi Kagaku Institute of Life Sciences, 11 Minamiooya, Machida, Tokyo 194-8511, Japan.
Department of Endocrinology and Metabolism, National Research Institute for Child Health and Development, 2-10-1 Okura, Setagaya-ku, Tokyo 157-8535, Japan.
School of Health Sciences, Tokai University, Bohseidai, Isehara, Kanagawa 259-1193, Japan.
BioResource Center, RIKEN, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan.
Present address: Brain Research Institute, Niigata University, 1-757 Asahimachi-dori, Niigata 951-8585, Japan.
Correspondence to: Tomoko Kaneko-Ishino5 e-mail: tkanekoi@is.icc.u-tokai.ac.jp
Correspondence to: Fumitoshi Ishino1 e-mail: fishino.epgn@mri.tmd.ac.jp