Duplications and losses in gene families of rust pathogens highlight putative effectors.

Front Plant Sci 2014 26;5:299. Epub 2014 Jun 26.

Plant Molecular and Cellular Biology Program, University of Florida Gainesville, FL, USA ; Genetics Institute, University of Florida Gainesville, FL, USA ; School of Forest Resources and Conservation, University of Florida Gainesville, FL, USA.

Rust fungi are a group of fungal pathogens that cause some of the world's most destructive diseases of trees and crops. A shared characteristic among rust fungi is obligate biotrophy, the inability to complete a lifecycle without a host. This dependence on a host species likely affects patterns of gene expansion, contraction, and innovation within rust pathogen genomes. The establishment of disease by biotrophic pathogens is reliant upon effector proteins that are encoded in the fungal genome and secreted from the pathogen into the host's cell apoplast or within the cells. This study uses a comparative genomic approach to elucidate putative effectors and determine their evolutionary histories. We used OrthoMCL to identify nearly 20,000 gene families in proteomes of 16 diverse fungal species, which include 15 basidiomycetes and one ascomycete. We inferred patterns of duplication and loss for each gene family and identified families with distinctive patterns of expansion/contraction associated with the evolution of rust fungal genomes. To recognize potential contributors for the unique features of rust pathogens, we identified families harboring secreted proteins that: (i) arose or expanded in rust pathogens relative to other fungi, or (ii) contracted or were lost in rust fungal genomes. While the origin of rust fungi appears to be associated with considerable gene loss, there are many gene duplications associated with each sampled rust fungal genome. We also highlight two putative effector gene families that have expanded in Cqf that we hypothesize have roles in pathogenicity.

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Source
http://dx.doi.org/10.3389/fpls.2014.00299DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4071342PMC
July 2014
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