加拿大蒙特利尔大学和法国路易斯巴斯德大学的科学家联合研究发现，一种取名Lrh1的神秘基因，具有控制排卵的功能。该项发现对于研制新型避孕药物有着重要意义。研究报告发表在最新出版的《基因与发育》（Genes & Development）上。
两国科学家在研究中使用了已培育出的一种新型基因改良实验鼠，该鼠的Lrh1基因在卵巢中可以被有选择地阻断。他们发现，去除Lrh1基因的实验鼠可有效停止排卵。
加拿大蒙特利尔大学动物研究中心主任布鲁斯·默菲教授介绍，他们在研究中发现，Lrh1基因在控制排卵中发挥着重要作用。他表示，虽然迄今为止该基因在雌性动物怀孕过程中能够发挥何种作用还不十分清楚，但他们已发现了该基因控制排卵的机理，以及对受孕可能存在的潜在影响。
该项发现意味着科学家可以研发出新型的避孕药物，这种药物可以有选择地终止排卵。默菲教授认为，如果成功，这些新型避孕药物将比现有方法更加有效，而且副作用比目前主要采用的类固醇型避孕药物小。同时，该项发现还将有助于开发出可以激活Lrh1基因的药物，帮助那些不能怀孕的夫妇实现生孩子的愿望。（生物谷Bioon.com）
生物谷推荐原始出处：
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.
