英语翻译The factors that regulate normal retinal development remain obscure.However,it is known that elements in the retinal pigmentepithelium are critical.When melanin is absent there is a reduction in rods,the central retina fails to develop fu

英语翻译The factors that regulate normal retinal development remain obscure.However,it is known that elements in the retinal pigmentepithelium are critical.When melanin is absent there is a reduction in rods,the central retina fails to develop fu
英语翻译
The factors that regulate normal retinal development remain obscure.However,it is known that elements in the retinal pigment
epithelium are critical.When melanin is absent there is a reduction in rods,the central retina fails to develop fully and there is a systematic distortion in the chiasmatic projection to the brain.It has been demonstrated using transgenic mice that the chiasmatic abnormality is controlled by the tyrosinase gene,which is the key enzyme in melanin synthesis.Here we examine whether the two retinal deficits are regulated by this gene.We have examined the distribution of photoreceptors in an albino mouse strain in which a functional tyrosinase gene has been inserted and compared these transgenics with albino and wild type mice.In albinos,rod photoreceptors were reduced by approximately 30%,but were normal in the transgenics.Cone numbers were unchanged.Cell density in the ganglion cell layer was examined in transgenic rabbits,in which albinism had also been rescued with the tyrosinase gene.Normal rabbits have a steep gradient in cell density between central and peripheral retina.Cell density was abnormally low in the central retina in albinos,but normal in the transgenics.Hence,the tyrosinase gene is responsible for each of the retinal deficits associated with albinism.However,it is not clear whether this is due to the absence of melanin or whether the key agent is an associated cell product.

英语翻译The factors that regulate normal retinal development remain obscure.However,it is known that elements in the retinal pigmentepithelium are critical.When melanin is absent there is a reduction in rods,the central retina fails to develop fu
调节视网膜正常发展的因素仍模糊不清.然而,众所周知,元素在视网膜色素
上皮细胞是至关重要的.当黑色素不在有减少燃料棒,中央视网膜未能充分发展,并有系统地扭曲交叉投射到大脑.它已被证明使用转基因小鼠的视交叉异常是由酪氨酸酶基因,这是关键酶黑色素合成.在这里,我们审查是否两个视网膜赤字受这种基因.我们审核了光感受器分布在白化小鼠品系中的一个职司酪氨酸酶的基因已插入和比较这些转基因白化,并与野生型小鼠.在白老鼠,感光棒分别减少了约30 ％ ,但正常的转基因.锥体人数不变.细胞密度的神经节细胞层进行了检查转基因兔,其中白化病也被救出的酪氨酸酶基因.正常兔有梯度陡峭的细胞密度在中央与周边视网膜.细胞密度过低中央视网膜的白化症,而是正常的转基因.因此,酪氨酸酶的基因是负责每个视网膜赤字与白化病.不过,目前尚不清楚这是否是由于缺乏黑色素,还是代理的关键是相关的细胞产品.