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[小鼠中突变性无晶状体、坐立不安和眼部发育迟缓基因的相互作用]

[Interaction of the mutant aphakia, fidget and ocular retardation genes in mice].

作者信息

Koniukhov B V, Nonchev S G

出版信息

Genetika. 1982 Jul;18(7):1107-14.

PMID:6889550
Abstract

The phenogenetic analysis of the effects of aphakia (ak) gene and its interaction with the ocular retardation (or) and fidget (fi) genes suggests that the ak gene acts in the lens cells with the result of arresting lens fibre differentiation. In mice homozygous for ak, the lens failure leads to secondary retina defects, in particular, to formation of retinal folds. In ak/ak or/or mice, the lens and retina morphogenesis stops at the optic cup stage, the eye is strongly reduced in size and more affected, compared to the corresponding single homozygotes. Unlike ak/ak or/or, in the ak/ak fi/fi mice the eyes are more regular in shape than those in the ak/ak +/+ condition. The fi gene inhibition of the retina anlage growth leads to some improvement of the eye development in double ak/ak fi/fi homozygotes, due to the absence of extensive retina folding.

摘要

无晶状体(ak)基因的效应及其与小眼症(or)和多动(fi)基因相互作用的表型发生分析表明,ak基因在晶状体细胞中起作用,导致晶状体纤维分化停滞。在ak基因纯合的小鼠中,晶状体发育不全导致继发性视网膜缺陷,特别是视网膜褶皱的形成。在ak/ak or/or小鼠中,晶状体和视网膜形态发生在视杯阶段停止,与相应的单基因纯合子相比,眼睛大小显著减小且受影响更大。与ak/ak or/or不同,在ak/ak fi/fi小鼠中,眼睛形状比ak/ak +/+条件下的更规则。fi基因对视网膜原基生长的抑制导致双ak/ak fi/fi纯合子的眼睛发育有所改善,这是因为没有广泛的视网膜褶皱。

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