Pedersen A K, Wiuf C, Christiansen F B
Institute of Biological Sciences, University of Aarhus, Denmark.
Mol Biol Evol. 1998 Aug;15(8):1069-81. doi: 10.1093/oxfordjournals.molbev.a026006.
A codon-based model designed to describe lentiviral evolution is developed. The model incorporates unequal base compositions in the three codon positions and selection against the CpG dinucleotide within codons to account for a deficit of this dinucleotide exhibited by lentiviral genes. The model is, to a large extent, able to account for the pattern of codon usage exhibited by the HIV1 genes gag, pol, and env, in spite of its parameter paucity. The model is extended to a similar model which operates on pentets (codons and their neighboring bases). The results obtained by the pentet model establish the importance of depression of CpGs across codon boundaries as well as within codons. The goodness of fit of the CpG depression model to the observed evolution in pairwise alignments of HIV1 sequences is assessed. The model provides a significantly better description of the observed evolution than the simpler models examined. The parameter estimates indicate that part of the unusually large biases in nucleotide frequencies observed in HIV1 genes is caused by selection against CpGs. We find that the estimates of expected numbers of substitutions, of transitions to transversions, and of synonymous to nonsynonymous substitution rates are robust to CpG depression, whereas the ratio of CpG-generating substitutions to other substitutions is strongly influenced by the choice of model.
开发了一种用于描述慢病毒进化的基于密码子的模型。该模型纳入了三个密码子位置中碱基组成的不均等性,并针对密码子内的CpG二核苷酸进行选择,以解释慢病毒基因中该二核苷酸的缺乏现象。尽管该模型参数较少,但在很大程度上能够解释HIV-1基因gag、pol和env所表现出的密码子使用模式。该模型扩展为一个对五联体(密码子及其相邻碱基)起作用的类似模型。五联体模型获得的结果确立了密码子边界间以及密码子内CpG抑制的重要性。评估了CpG抑制模型对HIV-1序列两两比对中观察到的进化的拟合优度。与所检验的更简单模型相比,该模型对观察到的进化提供了显著更好的描述。参数估计表明,HIV-1基因中观察到的核苷酸频率异常大的偏差部分是由针对CpG的选择引起的。我们发现,替换预期数、转换与颠换以及同义替换与非同义替换率的估计对CpG抑制具有稳健性,而产生CpG的替换与其他替换的比率受模型选择的强烈影响。