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p27(Kip1)参与分化中的鸡视网膜神经节细胞内复制的调控。

p27(Kip1) participates in the regulation of endoreplication in differentiating chick retinal ganglion cells.

作者信息

Ovejero-Benito María C, Frade José M

机构信息

a Department of Molecular , Cellular, and Developmental Neurobiology; Cajal Institute; IC-CSIC ; Madrid , Spain.

出版信息

Cell Cycle. 2015;14(14):2311-22. doi: 10.1080/15384101.2015.1044175. Epub 2015 May 6.

Abstract

Nuclear DNA duplication in the absence of cell division (i.e. endoreplication) leads to somatic polyploidy in eukaryotic cells. In contrast to some invertebrate neurons, whose nuclei may contain up to 200,000-fold the normal haploid DNA amount (C), polyploid neurons in higher vertebrates show only 4C DNA content. To explore the mechanism that prevents extra rounds of DNA synthesis in these latter cells we focused on the chick retina, where a population of tetraploid retinal ganglion cells (RGCs) has been described. We show that differentiating chick RGCs that express the neurotrophic receptors p75 and TrkB while lacking retinoblastoma protein, a feature of tetraploid RGCs, also express p27(Kip1). Two different short hairpin RNAs (shRNA) that significantly downregulate p27(Kip1) expression facilitated DNA synthesis and increased ploidy in isolated chick RGCs. Moreover, this forced DNA synthesis could not be prevented by Cdk4/6 inhibition, thus suggesting that it is triggered by a mechanism similar to endoreplication. In contrast, p27(Kip1) deficiency in mouse RGCs does not lead to increased ploidy despite previous observations have shown ectopic DNA synthesis in RGCs from p27(Kip1-/-) mice. This suggests that a differential mechanism is used for the regulation of neuronal endoreplication in mammalian versus avian RGCs.

摘要

在没有细胞分裂的情况下进行核DNA复制(即核内复制)会导致真核细胞出现体细胞多倍体现象。与一些无脊椎动物神经元不同,其细胞核中的DNA含量可能高达正常单倍体DNA量(C)的200,000倍,高等脊椎动物中的多倍体神经元仅显示4C的DNA含量。为了探究阻止这些细胞进行额外DNA合成轮次的机制,我们聚焦于鸡视网膜,其中已描述了一群四倍体视网膜神经节细胞(RGC)。我们发现,正在分化的鸡RGC表达神经营养受体p75和TrkB,同时缺乏视网膜母细胞瘤蛋白(四倍体RGC的一个特征),它们也表达p27(Kip1)。两种显著下调p27(Kip1)表达的不同短发夹RNA(shRNA)促进了分离出的鸡RGC中的DNA合成并增加了倍性。此外,Cdk4/6抑制并不能阻止这种强制的DNA合成,因此表明它是由一种类似于核内复制的机制触发的。相比之下,尽管先前的观察表明p27(Kip1 - / -)小鼠的RGC中存在异位DNA合成,但小鼠RGC中p27(Kip1)的缺乏并不会导致倍性增加。这表明在哺乳动物和禽类RGC中,用于调节神经元核内复制的机制存在差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dc1d/4614947/971129753835/kccy-14-14-1044175-g001.jpg

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