Goodenough D A, Simon A M, Paul D L
Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Novartis Found Symp. 1999;219:226-35; discussion 235-40. doi: 10.1002/9780470515587.ch14.
A targeted disruption of the gene encoding the gap junction protein connexin37 (Cx37; alpha 4) results in female infertility. Mutant follicles are not observed to develop beyond early antral stages, and there is a lack of both observable mature Graafian follicles and ovulation. The oocytes are unable to acquire meiotic competence. Following oocyte failure, the residual follicular cells do not undergo atresia but rather transdifferentiate into luteal cells, resulting in a mutant ovary populated with numerous, inappropriate corpora lutea. These results indicate that the Cx37-containing gap junctions formed between oocyte and follicular cells permit bidirectional signalling between the two cell types. These junctions are required for oocyte growth and development during preantral stages of the follicle, and for the inhibition of follicle cell luteinization. An additional role for these junctions may be to permit transfer of cytoplasmic signals required to hold oocytes in meiotic arrest. Since the mutant follicles never acquire meiotic competence, this latter role for gap junctional communication cannot be tested in this model.
编码缝隙连接蛋白连接蛋白37（Cx37；α4）的基因发生靶向破坏会导致雌性不育。未观察到突变卵泡发育超过早期窦状卵泡阶段，并且既没有可观察到的成熟格拉夫卵泡，也没有排卵现象。卵母细胞无法获得减数分裂能力。卵母细胞功能衰竭后，残留的卵泡细胞不会发生闭锁，而是转分化为黄体细胞，导致突变卵巢中充满大量不适当的黄体。这些结果表明，卵母细胞与卵泡细胞之间形成的含Cx37缝隙连接允许两种细胞类型之间进行双向信号传导。这些连接对于卵泡窦前期卵母细胞的生长和发育以及抑制卵泡细胞黄体化是必需的。这些连接的另一个作用可能是允许传递将卵母细胞维持在减数分裂阻滞状态所需的细胞质信号。由于突变卵泡从未获得减数分裂能力，因此在该模型中无法测试缝隙连接通讯的后一种作用。
