FGF SIGNALING AND ZINC FINGER PROTEINS IN GONAD DEVELOPMENT AND REPRODUCTION

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 我们的研究兴趣是确定导致男性和女性不孕不育的因素。我们最初的项目是利用Ptcme/MES和Sufu+/-；Ptc1me/MES来研究Hedgehog信号分子Patted 1和融合抑制因子Ptc1me在卵巢发育中的潜在作用。由于这些突变小鼠存在轻微的卵巢缺陷，我们已经将重点转移到其他分子的研究上，包括FGFRs和雄性生殖细胞表达的锌指蛋白在利用突变小鼠模型进行生殖过程中的研究。这些突变小鼠的产生和功能分析将为人类不育或不育的发病机制提供洞察力。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Our research interest is to identify factors contributing to male and female subfertility and infertility. Our original project is to characterize the potential role of hedgehog signaling molecules patched 1 and suppressor of fused using Ptcmes/mes and Sufu+/-;Ptc1mes/mes in the ovarian development. Due to minor ovarian defects in those mutant mice, we have shifted our focus on the studies of other molecules including FGFRs and male germ cell-expressing zinc finger proteins in reproduction using mutant mouse models. Generation and functional analyses of these mutant mice will provide insight into the pathogenesis of human subfertility or infertility.