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Fungal Genet Biol. 2015 Mar;76:78-92. doi: 10.1016/j.fgb.2015.02.002. Epub 2015 Feb 12.

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

Author information

1
Department of Biology, Clark University, 950 Main St, Worcester 01610, MA, USA; MEMEG, Ecology Building Sölvegatan 37, 223 62, Lund, Sweden. Electronic address: dimitrios.floudas@biol.lu.se.
2
Department of Plant Pathology, University of Minnesota, 1991 Upper Buford Circle, St. Paul, MN 55108-6030, USA. Electronic address: bheld@umn.edu.
3
US Department of Energy (DOE) Joint Genome Institute, Walnut Creek, California, USA. Electronic address: RWRiley@lbl.gov.
4
Department of Biology, Clark University, 950 Main St, Worcester 01610, MA, USA; Institute of Biochemistry, Biological Research Centre of the Hungarian Academy of Sciences, Temesvári krt. 62, H-6726 Szeged, Hungary. Electronic address: cortinarius2000@gmail.com.
5
Department of Chemistry and Chemical Biology, Indiana University-Purdue University Indianapolis, LD326, 402 N Blackford St, Indianapolis, IN 46202, USA. Electronic address: gagek@iupui.edu.
6
Department of Chemistry and Chemical Biology, Indiana University-Purdue University Indianapolis, LD326, 402 N Blackford St, Indianapolis, IN 46202, USA. Electronic address: aransdel@gmail.com.
7
Department of Chemistry and Chemical Biology, Indiana University-Purdue University Indianapolis, LD326, 402 N Blackford St, Indianapolis, IN 46202, USA. Electronic address: hinayounus@rediffmail.com.
8
US Department of Energy (DOE) Joint Genome Institute, Walnut Creek, California, USA. Electronic address: JChow@lbl.gov.
9
US Department of Energy (DOE) Joint Genome Institute, Walnut Creek, California, USA. Electronic address: JLChiniquy@lbl.gov.
10
US Department of Energy (DOE) Joint Genome Institute, Walnut Creek, California, USA. Electronic address: ALipzen@lbl.gov.
11
US Department of Energy (DOE) Joint Genome Institute, Walnut Creek, California, USA. Electronic address: AJTritt@lbl.gov.
12
US Department of Energy (DOE) Joint Genome Institute, Walnut Creek, California, USA. Electronic address: HSun@lbl.gov.
13
US Department of Energy (DOE) Joint Genome Institute, Walnut Creek, California, USA. Electronic address: SHaridas@lbl.gov.
14
US Department of Energy (DOE) Joint Genome Institute, Walnut Creek, California, USA. Electronic address: klabutti@lbl.gov.
15
US Department of Energy (DOE) Joint Genome Institute, Walnut Creek, California, USA; Microbiology, Utrecht University, Padualaan 8, 3584 CH, Utrecht, The Netherlands. Electronic address: R.A.Ohm@uu.nl.
16
Institute for Forest Botany, University of Göttingen, Büsgenweg 2, 37077 Göttingen, Germany. Electronic address: ukuees@gwdg.de.
17
Department of Plant Pathology, University of Minnesota, 1991 Upper Buford Circle, St. Paul, MN 55108-6030, USA. Electronic address: robertb@umn.edu.
18
US Department of Energy (DOE) Joint Genome Institute, Walnut Creek, California, USA. Electronic address: IVGrigoriev@lbl.gov.
19
Department of Chemistry and Chemical Biology, Indiana University-Purdue University Indianapolis, LD326, 402 N Blackford St, Indianapolis, IN 46202, USA. Electronic address: rminto@iupui.edu.
20
Department of Biology, Clark University, 950 Main St, Worcester 01610, MA, USA. Electronic address: dhibbett@clarku.edu.

Abstract

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. C. 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. F. 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 toward 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.

KEYWORDS:

Brown rot; Genome sequencing; Pseudogenes; Reconciliation; White rot; Wood decay

PMID:
25683379
PMCID:
PMC4399860
DOI:
10.1016/j.fgb.2015.02.002
[Indexed for MEDLINE]
Free PMC Article

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