Embryology Unit, Children's Medical Research Institute, Westmead, Australia.
Dev Dyn. 2010 Nov;239(11):2851-9. doi: 10.1002/dvdy.22417.
Mouse embryos lacking Lhx1 (Lim1) activity display defective gastrulation and are deficient of primordial germ cells (PGCs) (Tsang et al. [2001] International Journal of Developmental Biology 45:549-555). To dissect the specific role of Lhx1 in germ cell development, we studied embryos with conditional inactivation of Lhx1 activity in epiblast derivatives, which, in contrast to completely null embryos, develop normally through gastrulation before manifesting a head truncation phenotype. Initially, PGCs are localized properly to the definitive endoderm of the posterior gut in the conditional mutant embryos, but they depart from the embryonic gut prematurely. The early exit of PGCs from the gut is accompanied by the failure to maintain a strong expression of Ifitm1 in the mesoderm enveloping the gut, which may mediate the repulsive activity that facilitates the retention of PGCs in the hindgut during early organogenesis. Lhx1 therefore may influence the localization of PGCs by modulating Ifitm1-mediated repulsive activity.
缺失 Lhx1（Lim1）活性的小鼠胚胎显示出严重的原肠胚形成缺陷，并且缺乏原始生殖细胞（PGCs）（Tsang 等人，[2001]国际发育生物学杂志 45:549-555）。为了剖析 Lhx1 在生殖细胞发育中的具体作用，我们研究了条件性灭活 Lhx1 活性的胚胎，这些胚胎与完全缺失的胚胎不同，它们在表现出头部截断表型之前，能够正常通过原肠胚形成。最初，条件性突变胚胎中的 PGCs 会正确地定位于后肠的限定内胚层，但它们会过早地离开胚胎肠道。PGCs 过早地从肠道中退出伴随着 Ifitm1 在环绕肠道的中胚层中表达的减弱，这可能介导了排斥活性，该活性有助于在早期器官发生过程中保持 PGCs 在 Hindgut 中的滞留。因此，Lhx1 可能通过调节 Ifitm1 介导的排斥活性来影响 PGCs 的定位。
