Altered patterns of gene duplication and differential gene gain and loss in fungal pathogens.
BACKGROUND
Duplication, followed by fixation or random loss of novel genes, contributes to genome evolution. Particular outcomes of duplication events are possibly associated with pathogenic life histories in fungi. To date, differential gene gain and loss have not been studied at genomic scales in fungal pathogens, despite this phenomenon's known importance in virulence in bacteria and viruses.


RESULTS
To determine if patterns of gene duplication differed between pathogens and non-pathogens, we identified gene families across nine euascomycete and two basidiomycete species. Gene family size distributions were fit to power laws to compare gene duplication trends in pathogens versus non-pathogens. Fungal phytopathogens showed globally altered patterns of gene duplication, as indicated by differences in gene family size distribution. We also identified sixteen examples of gene family expansion and five instances of gene family contraction in pathogenic lineages. Expanded gene families included those predicted to be important in melanin biosynthesis, host cell wall degradation and transport functions. Contracted families included those encoding genes involved in toxin production, genes with oxidoreductase activity, as well as subunits of the vacuolar ATPase complex. Surveys of the functional distribution of gene duplicates indicated that pathogens show enrichment for gene duplicates associated with receptor and hydrolase activities, while euascomycete pathogens appeared to have not only these differences, but also significantly more duplicates associated with regulatory and carbohydrate binding functions.


CONCLUSIONS
Differences in the overall levels of gene duplication in phytopathogenic species versus non-pathogenic relatives implicate gene inventory flux as an important virulence-associated process in fungi. We hypothesize that the observed patterns of gene duplicate enrichment, gene family expansion and contraction reflect adaptation within pathogenic life histories. These adaptations were likely shaped by ancient, as well as contemporary, intimate associations with monocot hosts.
Powell
Amy J
AJ
Department of Computational Systems Biology, Sandia National Laboratories, Albuquerque, NM, USA. ajpowel@sandia.gov
Conant
Gavin C
GC
Brown
Douglas E
DE
Carbone
Ignazio
I
Dean
Ralph A
RA
D019295:Computational Biology; D019143:Evolution, Molecular; D005658:Fungi / Q000235:genetics* / Q000472:pathogenicity*; D020440:Gene Duplication; D023281:Genomics; D005810:Multigene Family / Q000235:genetics*; D017385:Sequence Homology