Data from: Evolution of novel wood decay mechanisms in Agaricales revealed by the genome sequences of Fistulina hepatica and Cylindrobasidium torrendii

Wood decay mechanisms in Agaricomycotina have been traditionally separated in two categories termed white and brown rot. Recently the accuracy of such a dichotomy has been questioned. Here, we present the genome sequences of the white rot fungus Cylindrobasidium torrendii and the brown rot fungus Fistulina hepatica both members of Agaricales, combining comparative genomics and wood decay experiments. Cylindrobasidium torrendii is closely related to the white-rot root pathogen Armillaria mellea, while F. hepatica is related to Schizophyllum commune, which has been reported to cause white rot. Our results suggest that C. torrendii and S. commune are intermediate between white-rot and brown-rot fungi, but at the same time they show characteristics of decay that resembles soft rot. Both species cause weak wood decay and degrade all wood components but leave the middle lamella intact. Their gene content related to lignin degradation is reduced, similar to brown-rot fungi, but both have maintained a rich array of genes related to carbohydrate degradation, similar to white-rot fungi. These characteristics appear to have evolved from white-rot ancestors with stronger ligninolytic ability. Fistulina hepatica shows characteristics of brown rot both in terms of wood decay genes found in its genome and the decay that it causes. However, genes related to cellulose degradation are still present, which is a plesiomorphic characteristic shared with its white-rot ancestors. Four wood degradation-related genes, homologs of which are frequently lost in brown-rot fungi, show signs of pseudogenization in the genome of F. hepatica. These results suggest that transition towards a brown rot lifestyle could be an ongoing process in F. hepatica. Our results reinforce the idea that wood decay mechanisms are more diverse than initially thought and that the dichotomous separation of wood decay mechanisms in Agaricomycotina into white rot and brown rot should be revisited.

伞菌亚门（Agaricomycotina）的木材腐朽机制传统上被划分为白腐与褐腐两大类。近年来，该二分法的准确性已受到学界质疑。本研究结合比较基因组学与木材腐朽实验，报道了两种伞菌目（Agaricales）真菌的全基因组序列：白腐真菌柱孢革菌（Cylindrobasidium torrendii）与褐腐真菌牛舌菌（Fistulina hepatica）。柱孢革菌与白腐根病原菌蜜环菌（Armillaria mellea）亲缘关系紧密；而牛舌菌则与裂褶菌（Schizophyllum commune）亲缘关系相近，后者已被报道可引发白腐。

本研究结果显示，柱孢革菌与裂褶菌处于白腐真菌与褐腐真菌的过渡类群，同时兼具软腐腐朽的特征。两种真菌均仅引发微弱的木材腐朽，可降解所有木材组分，但完整保留胞间层（middle lamella）的结构。二者与木质素降解相关的基因丰度较低，与褐腐真菌特征一致；但同时保留了大量与碳水化合物降解相关的基因，这一点又与白腐真菌相似。这类特征推测起源于具备更强木质素分解能力的白腐祖先类群。

牛舌菌无论从其基因组携带的木材腐朽相关基因，还是实际引发的腐朽模式来看，均表现出褐腐真菌的特征。但其仍保留了与纤维素降解相关的基因，这是与白腐祖先类群共有的祖征（plesiomorphic characteristic）。在牛舌菌的基因组中，有4个木材降解相关基因出现了假基因化（pseudogenization）的迹象——这类基因的同源序列在褐腐真菌中常发生丢失。上述结果表明，牛舌菌向褐腐生活方式演化的过程可能仍在进行中。

本研究进一步证实，木材腐朽机制的多样性远超最初的认知，且伞菌亚门的木材腐朽机制二分法划分（白腐与褐腐）亟待重新审视。