生物谷報(bào)道:日本的一個(gè)研究小組1月6日在《自然—遺傳學(xué)》(Nature Genetics)雜志網(wǎng)絡(luò)版上發(fā)表論文說,他們發(fā)現(xiàn)了胎盤正常工作的一個(gè)必要基因,,它很可能來源于哺乳動(dòng)物祖先感染的病毒,。
哺乳動(dòng)物的胎兒通過胎盤的毛細(xì)血管從母體獲取營養(yǎng)。東京醫(yī)科齒科大學(xué),、東海大學(xué)等機(jī)構(gòu)的科學(xué)家聯(lián)合研究發(fā)現(xiàn),,實(shí)驗(yàn)鼠和人體內(nèi)都存在一種名為“Peg11”的基因,這種基因上殘留的一些痕跡說明,,該基因很可能從遠(yuǎn)古病毒的DNA(脫氧核糖核酸)轉(zhuǎn)而編入了鼠和人類的DNA,。
日本專家剔除了實(shí)驗(yàn)鼠的“Peg11”基因,或者讓這個(gè)基因異常發(fā)揮作用,,結(jié)果發(fā)現(xiàn)都會(huì)造成實(shí)驗(yàn)鼠胎盤毛細(xì)血管結(jié)構(gòu)異常,,交換營養(yǎng)物質(zhì)的能力下降,最終導(dǎo)致胎兒因發(fā)育不良而胎死腹中,,或者出生后夭折,。
日本專家認(rèn)為,這項(xiàng)研究可幫助診斷一些不明原因的發(fā)育障礙,,并有助于了解原始哺乳動(dòng)物的進(jìn)化過程,。(來源:新華網(wǎng) 錢錚)
生物谷推薦原始出處:
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: [email protected]
Correspondence to: Fumitoshi Ishino1 e-mail: [email protected]