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      Evolution and genome architecture in fungal plant pathogens

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      Journal: Nature Reviews Microbiology
      Publisher: Springer Nature

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          Abstract

          The fungal kingdom contains many important plant pathogens, and some species show remarkable variation in genome size and architecture. In this Review, Möller and Stukenbrock summarize key examples from fungal plant pathogen genomics and discuss evolutionary processes in pathogenic fungi in the context of molecular evolution, population genetics and agriculture.

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          The origins of genome complexity.

          Michael Lynch, John Conery (2003)
          Complete genomic sequences from diverse phylogenetic lineages reveal notable increases in genome complexity from prokaryotes to multicellular eukaryotes. The changes include gradual increases in gene number, resulting from the retention of duplicate genes, and more abrupt increases in the abundance of spliceosomal introns and mobile genetic elements. We argue that many of these modifications emerged passively in response to the long-term population-size reductions that accompanied increases in organism size. According to this model, much of the restructuring of eukaryotic genomes was initiated by nonadaptive processes, and this in turn provided novel substrates for the secondary evolution of phenotypic complexity by natural selection. The enormous long-term effective population sizes of prokaryotes may impose a substantial barrier to the evolution of complex genomes and morphologies.
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            Pathogen population genetics, evolutionary potential, and durable resistance.

            Bruce McDonald, Celeste Linde (2002)
            We hypothesize that the evolutionary potential of a pathogen population is reflected in its population genetic structure. Pathogen populations with a high evolutionary potential are more likely to overcome genetic resistance than pathogen populations with a low evolutionary potential. We propose a flexible framework to predict the evolutionary potential of pathogen populations based on analysis of their genetic structure. According to this framework, pathogens that pose the greatest risk of breaking down resistance genes have a mixed reproduction system, a high potential for genotype flow, large effective population sizes, and high mutation rates. The lowest risk pathogens are those with strict asexual reproduction, low potential for gene flow, small effective population sizes, and low mutation rates. We present examples of high-risk and low-risk pathogens. We propose general guidelines for a rational approach to breed durable resistance according to the evolutionary potential of the pathogen.
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              Fungal small RNAs suppress plant immunity by hijacking host RNA interference pathways.

              Arne Weiberg, Ming Wang, Feng-Mao Lin … (2013)
              Botrytis cinerea, the causative agent of gray mold disease, is an aggressive fungal pathogen that infects more than 200 plant species. Here, we show that some B. cinerea small RNAs (Bc-sRNAs) can silence Arabidopsis and tomato genes involved in immunity. These Bc-sRNAs hijack the host RNA interference (RNAi) machinery by binding to Arabidopsis Argonaute 1 (AGO1) and selectively silencing host immunity genes. The Arabidopsis ago1 mutant exhibits reduced susceptibility to B. cinerea, and the B. cinerea dcl1 dcl2 double mutant that can no longer produce these Bc-sRNAs displays reduced pathogenicity on Arabidopsis and tomato. Thus, this fungal pathogen transfers "virulent" sRNA effectors into host plant cells to suppress host immunity and achieve infection, which demonstrates a naturally occurring cross-kingdom RNAi as an advanced virulence mechanism.
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                Author and article information

                Journal
                Title: Nature Reviews Microbiology
                Abbreviated Title: Nat Rev Micro
                Publisher: Springer Nature
                ISSN (Print): 1740-1526
                ISSN (Electronic): 1740-1534
                Publication date Created: August 7 2017
                Publication date (Print): August 7 2017
                Volume:
                Issue:
                Article
                DOI: 10.1038/nrmicro.2017.76
                PubMed ID: 28781365
                SO-VID: 8d72a4a0-b881-41e3-8e93-9311a19a77b5
                Copyright © © 2017
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