加拿大蒙特利爾大學(xué)和法國路易斯巴斯德大學(xué)的科學(xué)家聯(lián)合研究發(fā)現(xiàn)，一種取名Lrh1的神秘基因,，具有控制排卵的功能,。該項發(fā)現(xiàn)對于研制新型避孕藥物有著重要意義。研究報告發(fā)表在最新出版的《基因與發(fā)育》（Genes & Development）上,。
兩國科學(xué)家在研究中使用了已培育出的一種新型基因改良實驗鼠,，該鼠的Lrh1基因在卵巢中可以被有選擇地阻斷。他們發(fā)現(xiàn),，去除Lrh1基因的實驗鼠可有效停止排卵,。
加拿大蒙特利爾大學(xué)動物研究中心主任布魯斯·默菲教授介紹，他們在研究中發(fā)現(xiàn),，Lrh1基因在控制排卵中發(fā)揮著重要作用,。他表示，雖然迄今為止該基因在雌性動物懷孕過程中能夠發(fā)揮何種作用還不十分清楚,，但他們已發(fā)現(xiàn)了該基因控制排卵的機理,，以及對受孕可能存在的潛在影響。
該項發(fā)現(xiàn)意味著科學(xué)家可以研發(fā)出新型的避孕藥物,，這種藥物可以有選擇地終止排卵,。默菲教授認為，如果成功,，這些新型避孕藥物將比現(xiàn)有方法更加有效,，而且副作用比目前主要采用的類固醇型避孕藥物小。同時,，該項發(fā)現(xiàn)還將有助于開發(fā)出可以激活Lrh1基因的藥物,，幫助那些不能懷孕的夫婦實現(xiàn)生孩子的愿望。（生物谷Bioon.com）
生物谷推薦原始出處：
Genes & Development,，22:1871-1876, 2008,，Rajesha Duggavathi, Bruce D. Murphy and Kristina Schoonjans
Liver receptor homolog 1 is essential for ovulation
Rajesha Duggavathi1,2, David H. Volle1, Chikage Mataki1, Maria C. Antal3, Nadia Messaddeq3, Johan Auwerx1,3,4,7, Bruce D. Murphy2,6, and Kristina Schoonjans1,4,5
1 Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS/INSERM/ULP, 67404 Illkirch, France; 2 Centre de Recherche en Reproduction Animale, Faculté de Médecine Vétérinaire, St-Hyacinthe, Québec J2S 7C6, Canada; 3 Institut Clinique de la Souris, 67404 Illkirch, France; 4 Ecole Polytechnique Fédérale de Lausanne, CH-1015 Lausanne, Switzerland
Female fertility requires normal ovarian follicular growth and ovulation. The nuclear receptor liver receptor homolog 1 has been implicated in processes as diverse as bile acid metabolism, steroidogenesis, and cell proliferation. In the ovary, Lrh1 is expressed exclusively in granulosa and luteal cells. Using somatic targeted mutagenesis, we show that mice lacking Lrh1 in granulosa cells are sterile, due to anovulation. The preovulatory stimulus fails to elicit cumulus expansion, luteinization, and follicular rupture in these mice. Multiple defects, including severely reduced transactivation of the Lrh1 target gene, nitric oxide synthase 3, leads to increased intrafollicular estradiol levels in the absence of Lrh1. This further causes dysfunction of prostaglandin and hyaluronic acid cascades and interrupts cumulus expansion. Lack of Lrh1 also interferes with progesterone synthesis because of failure of normal expression of the Lrh1 targets, steroidogenic acute regulatory protein and cytochrome P450 side-chain cleavage. In addition, expression of extracellular matrix proteases essential for ovulation is compromised. These results demonstrate that Lrh1 is a regulator of multiple mechanisms essential for maturation of ovarian follicles and for ovulation. Lrh1 is therefore a key modulator of female fertility and a potential target for contraception.
