The contribution of stress protein duplication and deletion events to the evolution of the Aspergilli was studied. We performed a large-scale homology analysis of stress proteins and generated and analysed three stress defence system models based on Saccharomyces cerevisiae, Schizosaccharomyces pombe and Aspergillus nidulans. Although both yeast-based and A. nidulans-based models were suitable to trace evolutionary changes, the A. nidulans-based model performed better in mapping stress protein radiations. The strong Mantel correlation found between the positions of species in the phylogenetic tree on the one hand and either in the A. nidulans-based or S. cerevisiae-based models on the other hand demonstrated that stress protein expansions and reductions contributed significantly to the evolution of the Aspergilli. Interestingly, stress tolerance attributes correlated well with the number of orthologs only for a few stress proteins. Notable examples are Ftr1 iron permease and Fet3 ferro-O₂-oxidoreductase, elements of the reductive iron assimilation pathway, in the S. cerevisiae-based model, as well as MpkC, a HogA-like mitogen activated protein kinase in the A. nidulans-based model. In the case of the iron assimilation proteins, the number of orthologs showed a positive correlation with H₂O₂-induced stress tolerance while the number of MpkC orthologs correlated positively with Congo Red induced cell wall stress, sorbitol induced osmotic stress and H₂O₂ induced oxidative stress tolerances. For most stress proteins, changes in the number of orthologs did not correlate well with any stress tolerance attributes. As a consequence, stress tolerance patterns of the studied Aspergilli did not correlate with either the sets of stress response proteins in general or with the phylogeny of the species studied. These observations suggest that stress protein duplication and deletion events significantly contributed to the evolution of stress tolerance attributes of Aspergilli. In contrast, there are other processes, which may counterbalance the effects of stress gene duplications or deletions including (i) alterations in the structures of stress proteins leading to changes in their biological activities, (ii) varying biosynthesis of stress proteins, (iii) rewiring stress response regulatory networks or even (iv) acquiring new stress response genes by horizontal gene transfer. All these multilevel changes are indispensable for the successful adaptation of filamentous fungi to altering environmental conditions, especially when these organisms are entering new ecological niches.

研究了应激蛋白复制和缺失事件对曲霉进化的贡献。我们对应激蛋白进行了大规模的同源性分析，并生成并分析了基于酿酒酵母、粟酒裂殖酵母和构巢曲霉的三种应激防御系统模型。尽管基于酵母和构巢曲霉的模型都适合追踪进化变化，但基于构巢曲霉的模型在绘制应激蛋白辐射图方面表现更好。一方面在系统发育树中的物种位置与另一方面在基于构巢曲霉或基于酿酒酵母的模型中发现的强曼特尔相关性表明，应激蛋白的扩展和减少对进化做出了显着贡献曲霉属。有趣的是，仅对于少数应激蛋白，应激耐受属性与直向同源物的数量密切相关。值得注意的例子是 Ftr1 铁渗透酶和 Fet3 铁-O ₂ -氧化还原酶（酿酒酵母模型中还原性铁同化途径的元件），以及 MpkC（构巢曲霉中的 HogA 样促细胞分裂原激活蛋白激酶）基于模型。在铁同化蛋白的情况下，直系同源物的数量与H ₂ O ₂诱导的应激耐受性呈正相关，而MpkC直系同源物的数量与刚果红诱导的细胞壁应激、山梨醇诱导的渗透应激和H ₂ O呈正相关。 ₂诱导氧化应激耐受。 对于大多数应激蛋白来说，直向同源物数量的变化与任何应激耐受属性没有很好的相关性。因此，所研究的曲霉菌的应激耐受模式与一般应激反应蛋白组或所研究物种的系统发育无关。这些观察结果表明，应激蛋白的复制和缺失事件对曲霉菌的应激耐受特性的进化做出了显着贡献。相反，还有其他过程可以抵消应激基因重复或缺失的影响，包括（i）应激蛋白结构的改变导致其生物活性的变化，（ii）应激蛋白生物合成的变化，（iii）重新连接应激反应调节网络，甚至（iv）通过水平基因转移获得新的应激反应基因。所有这些多层次的变化对于丝状真菌成功适应不断变化的环境条件都是必不可少的，特别是当这些生物体进入新的生态位时。