Koniukhov B V, Iakovlev M I
Biull Eksp Biol Med. 1986 Jun;101(6):738-40.
The aim of the present study was to determine the cellular site of eyeless-I (ey-I) and eyeless-2 (ey-2) gene action, causing anophthalmia or microphthalmia. Eye primordia from 10-day-old embryos of ZRDCT-AN and CC57BR (control) mice were cultured in vitro for 3 or 6 days. In 59 out of 77 cultured mutant eye primordia neural retina was disturbed. In 9 mutant eye primordia the disturbed neural retina was 4-6 times thinner than in the control. However, lens differentiation was similar to that in the control, epithelial and fibrous components were observed. Thus, mutant genes eyeless inhibit the growth of primordial retina, causing secondary developmental defects of the lens and other eye structures.
本研究的目的是确定导致无眼症或小眼症的无眼-1(ey-1)和无眼-2(ey-2)基因作用的细胞位点。将ZRDCT-AN和CC57BR(对照)小鼠10日龄胚胎的眼原基进行体外培养3天或6天。在77个培养的突变眼原基中,有59个神经视网膜受到干扰。在9个突变眼原基中,受干扰的神经视网膜比对照薄4至6倍。然而,晶状体分化与对照相似,观察到上皮和纤维成分。因此,无眼突变基因抑制原始视网膜的生长,导致晶状体和其他眼结构的继发性发育缺陷。