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首页> 外文期刊>Genomics >Genome-scale relationships between cytosine methylation and dinucleotide abundances in animals.
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Genome-scale relationships between cytosine methylation and dinucleotide abundances in animals.

机译：动物中胞嘧啶甲基化和二核苷酸丰度之间的基因组规模关系。

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In mammalian genomes CpGs occur at one-fifth their expected frequency. This is accepted as resulting from cytosine methylation and deamination of 5-methylcytosine leading to TpG and CpA dinucleotides. The corollary that a CpG deficit should correlate with TpG excess has not hitherto been systematically tested at a genomic level. I analyzed genome sequences (human, chimpanzee, mouse, pufferfish, zebrafish, sea squirt, fruitfly, mosquito, and nematode) to do this and generally to assess the hypothesis that CpG deficit, TpG excess, and other data are accountable in terms of 5-methylcytosine mutation. In all methylated genomes local CpG deficit decreases with higher G + C content. Local TpG surplus, while positively associated with G + C level in mammalian genomes but negatively associated with G + C in nonmammalian methylated genomes, is always explicable in terms of the CpG trend under the methylation model. Covariance of dinucleotide abundances with G + C demonstrates that correlation analyses should control for G + C. Doing this reveals a strong negative correlation between local CpG and TpG abundances in methylated genomes, in accord with the methylation hypothesis. CpG deficit also correlates with CpT excess in mammals, which may reflect enhanced cytosine mutation in the context 5'-YCG-3'. Analyses with repeat-masked sequences show that the results are not attributable to repetitive elements.
机译：在哺乳动物基因组中，CpG的出现频率为预期频率的五分之一。这被认为是由于胞嘧啶甲基化和5-甲基胞嘧啶脱氨基而导致TpG和CpA二核苷酸的结果。迄今为止，尚未在基因组水平上系统测试CpG缺乏应与TpG过量相关的推论。我分析了基因组序列（人类，黑猩猩，小鼠，河豚，斑马鱼，海鞘，果蝇，蚊子和线虫）以进行此操作，并通常评估了CpG缺陷，TpG过量和其他数据按5负责的假设。 -甲基胞嘧啶突变。在所有甲基化的基因组中，局部CpG缺陷随着G + C含量的增加而降低。在哺乳动物基因组中，局部TpG过量与G + C水平呈正相关，而在非哺乳动物甲基化基因组中与G + C呈负相关，在甲基化模型下，CpG趋势始终可以解释。二核苷酸丰度与G + C的协方差表明，相关分析应控制G +C。这样做表明，甲基化基因组中本地CpG和TpG丰度之间存在很强的负相关性，符合甲基化假设。 CpG缺乏症也与哺乳动物的CpT过量有关，这可能反映了5'-YCG-3'背景下胞嘧啶突变的增强。使用重复屏蔽序列的分析表明，结果不归因于重复元素。

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