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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Targeted knockdown of Cerkl, a retinal dystrophy gene, causes mild affectation of the retinal ganglion cell layer
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Targeted knockdown of Cerkl, a retinal dystrophy gene, causes mild affectation of the retinal ganglion cell layer

机译：视网膜营养不良基因Cerkl的靶向敲低会引起视网膜神经节细胞层的轻度感染

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摘要

In order to approach the function of the retinal dystrophy . CERKL gene we generated a novel knockout mouse model by cre-mediated targeted deletion of the . Cerkl first exon and proximal promoter. The excised genomic region (2.3. kb) encompassed the first . Cerkl exon, upstream sequences including the proximal promoter and the initial segment of the first intron. The . Cerkl-/- mice were viable and fertile. The targeted . Cerkl deletion resulted in a knockdown more than a knockout model, given that alternative promoters (unreported at that time) directed basal expression of . Cerkl (35%). . In situ hybridizations and immunohistochemistry showed that this remnant expression was moderate in the photoreceptors and weak in the ganglion and inner cell layers. Morphological characterization of the . Cerkl-/- retinas did not show any gross structural changes, even at 12. months of age. However, some clear and consistent signals of gliosis and retinal stress were detected by the statistically significant increase of i) the glial fibrillary antigen protein (GFAP) expression, and ii) apoptosis, as detected by TUNEL. Remarkably, consistent non-progressive perturbation (from birth up to 12. months of age) of ganglion cells was supported by the decrease of the Brn3a marker expression as well as the reduced oscillatory potentials in the electroretinographic recordings. In conclusion, the . Cerkl-/- knockdown shows a mild retinal phenotype, with increased levels of cellular stress and apoptosis indicators, and clear signs of functional alteration at the ganglion cell layer, but no detectable morphological changes.
机译：为了接近视网膜营养不良的功能。 CERKL基因我们通过cre介导的靶向缺失产生了一种新型的基因敲除小鼠模型。 Cerkl是第一个外显子和近端启动子。切除的基因组区域（2.3。kb）包含第一个。 Cerk1外显子，上游序列包括近端启动子和第一个内含子的起始片段。的。 Cerk1 //-小鼠是活的和可育的。有针对性的。鉴于替代启动子（当时未报道）指导Cerk1的基础表达，Cerkl缺失导致的敲除多于敲除模型。 Cerkl（35％）。 。原位杂交和免疫组化显示，该残余表达在感光细胞中中等，在神经节和内细胞层中弱。 。的形态特征。即使在12个月大时，Cerkl-/-视网膜也未显示任何明显的结构变化。但是，通过TUNEL检测，i）胶质纤维原蛋白蛋白（GFAP）表达和ii）凋亡在统计学上显着增加，从而检测出一些清晰一致的胶质增生和视网膜应力信号。值得注意的是，神经节细胞的一致的非渐进性扰动（从出生到12个月大），受到Brn3a标志物表达的减少以及视网膜电图记录中振荡电位的降低的支持。总之，。 Cerk1-/-敲低显示轻度的视网膜表型，具有增加的细胞应激和凋亡指示剂水平，并且在神经节细胞层具有明显的功能改变迹象，但是没有可检测的形态学改变。

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