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，这种二分法的准确性受到了质疑。本研究结合比较基因组学与木材腐朽实验，报道了两种隶属于伞菌目（Agaricales）的真菌的基因组序列：白腐真菌柱孢韧革菌（Cylindrobasidium torrendii）与褐腐真菌牛舌菌（Fistulina hepatica）。柱孢韧革菌与白腐根病原菌蜜环菌（Armillaria mellea）亲缘关系紧密，而牛舌菌则与被报道可引发白腐的裂褶菌（Schizophyllum commune）亲缘相近。本研究结果显示，柱孢韧革菌与裂褶菌处于白腐真菌与褐腐真菌的过渡类群，同时二者还表现出类似软腐的腐朽特征。两种真菌均可引发轻度木材腐朽，能降解所有木材组分，但仍可保留胞间层（middle lamella）的完整性。二者与木质素降解相关的基因丰度有所降低，这一点与褐腐真菌类似；但同时二者仍保留了大量与碳水化合物降解相关的基因，这又与白腐真菌一致。这些特征推测起源于具备更强木质素分解能力的白腐真菌祖先类群。牛舌菌无论从其基因组中携带的木材腐朽相关基因，还是其实际引发的腐朽类型来看，均表现出褐腐真菌的特征。但该菌仍保留了与纤维素降解相关的基因，这是其与白腐真菌祖先共有的祖征（plesiomorphic characteristic）。在褐腐真菌中常发生丢失的4个木材降解相关基因的同源基因，在牛舌菌的基因组中表现出假基因化（pseudogenization）的迹象。上述结果表明，牛舌菌正处于向褐腐生活方式演化的过程中。本研究结果进一步证实，木材腐朽机制的多样性远超此前认知，伞菌亚门的木材腐朽机制二分法（白腐与褐腐）亟需重新审视。