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首页> 外文期刊>Cell biology international. >Cloning, sequencing and expression of a cDNA encoding the mouse L35a ribosomal protein during differentiation of murine erythroleukemia (MEL) cells.
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Cloning, sequencing and expression of a cDNA encoding the mouse L35a ribosomal protein during differentiation of murine erythroleukemia (MEL) cells.

机译：鼠红白血病（MEL）细胞分化过程中编码小鼠L35a核糖体蛋白的cDNA的克隆，测序和表达。

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摘要

In a previous study we reported that ribosomal protein S5 gene is suppressed in differentiating and not in proliferating or apoptotic murine erythroleukaemia (MEL) cells (Vizirianakis et al., 1999). We wish to report here the isolation, characterisation and expression of the full length cDNA for another ribosomal protein, the L35a (rpL35a), in MEL cells. This cDNA shares significant structural homology in both DNA and protein levels to genes encoding the rat and human L35a ribosomal proteins. Northern blot hybridisation analysis has shown that the steady-state level of rpL35a mRNA is progressively reduced during differentiation of MEL cells along the erythrocytic maturation pathway induced by DMSO or UDP-4, two structurally unrelated inducers of differentiation. However, in cells where differentiation was inhibited by N(6)-methyladenosine, the level of rpL35a RNA transcripts was not affected. In addition, rpL35a gene expression was not altered in apoptotic MEL cells. Furthermore, the suppression of L35a gene was not correlated to any change in DNA methylation at CCGG sites located at the rpL35a gene locus in undifferentiated and differentiated MEL cells, as we observed for the rpS5 gene. Overall, these data suggest that the expression of ribosomal genes, the L35a of 60S ribosomal subunit and the S5 of 40S ribosomal subunit, are regulated by a common mechanism in differentiating MEL cells, leading to the observed decrease in ribosomal function. Copyright 2001 Academic Press.
机译：在先前的研究中，我们报道了核糖体蛋白S5基因在分化中受到抑制，而在鼠类红细胞白血病（MEL）细胞的增殖或凋亡中却没有受到抑制（Vizirianakis等，1999）。我们希望在此报告MEL细胞中另一种核糖体蛋白L35a（rpL35a）的全长cDNA的分离，表征和表达。该cDNA在DNA和蛋白质水平上与编码大鼠和人L35a核糖体蛋白的基因具有显着的结构同源性。 Northern杂交杂交分析表明，在MEL细胞沿DMSO或UDP-4诱导的红细胞成熟途径分化的过程中，rpL35a mRNA的稳态水平逐渐降低，这是两种结构上无关的分化诱导剂。但是，在分化受N（6）-甲基腺苷抑制的细胞中，rpL35a RNA转录本的水平不受影响。此外，凋亡的MEL细胞中rpL35a基因表达没有改变。此外，正如我们观察到的rpS5基因一样，L35a基因的抑制与未分化和分化的MEL细胞中位于rpL35a基因位点的CCGG位点的DNA甲基化的任何变化都不相关。总体而言，这些数据表明核糖体基因，60S核糖体亚基的L35a和40S核糖体亚基的S5的表达受分化MEL细胞中的共同机制调节，导致观察到的核糖体功能下降。版权所有2001，学术出版社。

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