Inagaki Yuji, Susko Edward, Fast Naomi M, Roger Andrew J
Program in Evolutionary Biology, Canadian Institute for Advanced Research and Genome Atlantic, Department of Biochemistry and Molecular Biology, Dalhousie University, Halifax, Nova Scotia, Canada.
Mol Biol Evol. 2004 Jul;21(7):1340-9. doi: 10.1093/molbev/msh130. Epub 2004 Mar 19.
Microsporidia branch at the base of eukaryotic phylogenies inferred from translation elongation factor 1alpha (EF-1alpha) sequences. Because these parasitic eukaryotes are fungi (or close relatives of fungi), it is widely accepted that fast-evolving microsporidian sequences are artifactually "attracted" to the long branch leading to the archaebacterial (outgroup) sequences ("long-branch attraction," or "LBA"). However, no previous studies have explicitly determined the reason(s) why the artifactual allegiance of microsporidia and archaebacteria ("M + A") is recovered by all phylogenetic methods, including maximum likelihood, a method that is supposed to be resistant to classical LBA. Here we show that the M + A affinity can be attributed to those alignment sites associated with large differences in evolutionary site rates between the eukaryotic and archaebacterial subtrees. Therefore, failure to model the significant evolutionary rate distribution differences (covarion shifts) between the ingroup and outgroup sequences is apparently responsible for the artifactual basal position of microsporidia in phylogenetic analyses of EF-1alpha sequences. Currently, no evolutionary model that accounts for discrete changes in the site rate distribution on particular branches is available for either protein or nucleotide level phylogenetic analysis, so the same artifacts may affect many other "deep" phylogenies. Furthermore, given the relative similarity of the site rate patterns of microsporidian and archaebacterial EF-1alpha proteins ("parallel site rate variation"), we suggest that the microsporidian orthologs may have lost some eukaryotic EF-1alpha-specific nontranslational functions, exemplifying the extreme degree of reduction in this parasitic lineage.
根据翻译延伸因子1α（EF-1α）序列推断，微孢子虫在真核生物系统发育树的基部发生分支。由于这些寄生性真核生物是真菌（或真菌的近亲），人们普遍认为快速进化的微孢子虫序列被人为地“吸引”到通向古细菌（外类群）序列的长分支上（“长枝吸引”，或“LBA”）。然而，以前没有研究明确确定为什么包括最大似然法（一种被认为对经典LBA有抗性的方法）在内的所有系统发育方法都能恢复微孢子虫和古细菌的人为关联（“M + A”）。在这里，我们表明M + A亲和力可归因于那些与真核生物和古细菌亚树之间进化位点速率差异较大相关的比对位点。因此，未能对类群内和类群外序列之间显著的进化速率分布差异（共变位点转移）进行建模显然是微孢子虫在EF-1α序列系统发育分析中处于人为基部位置的原因。目前，无论是蛋白质还是核苷酸水平的系统发育分析，都没有考虑特定分支上位点速率分布离散变化的进化模型，所以同样的人为因素可能会影响许多其他“深层”系统发育。此外，鉴于微孢子虫和古细菌EF-1α蛋白的位点速率模式相对相似（“平行位点速率变异”），我们认为微孢子虫的直系同源物可能已经失去了一些真核生物EF-1α特有的非翻译功能，这体现了这个寄生谱系极端的简化程度。
