Pangenomic analysis reveals pathogen-specific regions and novel effector candidates in<i>Fusarium oxysporum</i>f. sp.<i>cepae</i>

Armitage, Andrew D.; Taylor, Andrew; Sobczyk, Maria K.; Baxter, Laura; Greenfield, Bethany P. J.; Bates, Helen; Wilson, Frank J.; Jackson, Alison C.; Ott, Sascha; Harrison, Richard J.; Clarkson, John P.

doi:10.1101/182238

Cited by 3 publications

(2 citation statements)

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“…Analysis of 60 F. graminearum isolates form North America identified an accessory genome close to 1700 genes that seems to concentrate in AT‐rich regions, probably centromeres or telomeres (Kelly & Ward, ). Similar results have been obtained for F. fujikuroi (Chiara et al ., ; Niehaus et al ., ), and F. oxysporum (Armitage et al ., ). Together, these studies have focused either on geographically delimited isolates or have compared a handful of isolates.…”

Section: Metabolic Complexitymentioning

confidence: 97%

Fungal evolution: cellular, genomic and metabolic complexity

Naranjo‐Ortiz

Gabaldón

2020

Biological Reviews

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The question of how phenotypic and genomic complexity are inter‐related and how they are shaped through evolution is a central question in biology that historically has been approached from the perspective of animals and plants. In recent years, however, fungi have emerged as a promising alternative system to address such questions. Key to their ecological success, fungi present a broad and diverse range of phenotypic traits. Fungal cells can adopt many different shapes, often within a single species, providing them with great adaptive potential. Fungal cellular organizations span from unicellular forms to complex, macroscopic multicellularity, with multiple transitions to higher or lower levels of cellular complexity occurring throughout the evolutionary history of fungi. Similarly, fungal genomes are very diverse in their architecture. Deep changes in genome organization can occur very quickly, and these phenomena are known to mediate rapid adaptations to environmental changes. Finally, the biochemical complexity of fungi is huge, particularly with regard to their secondary metabolites, chemical products that mediate many aspects of fungal biology, including ecological interactions. Herein, we explore how the interplay of these cellular, genomic and metabolic traits mediates the emergence of complex phenotypes, and how this complexity is shaped throughout the evolutionary history of Fungi.

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Section: Metabolic Complexitymentioning

confidence: 97%

Fungal evolution: cellular, genomic and metabolic complexity

Naranjo‐Ortiz

Gabaldón

2020

Biological Reviews

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“…The emergence of new effector genes in individual pathogen lineages played an important role in the evolution of pathogenicity and changes in host range (Liao et al, 2016). This is supported by comparative genomics studies that showed that most effector genes are taxonomically restricted (or orphans) to a set of closely related species or even to a subset of individuals within a species (Stukenbrock et al, 2012;Grandaubert et al, 2015;Plissonneau et al, 2016;Armitage et al, 2017). The gain and loss of individual fungal effectors are associated with major gains in pathogenicity (Huang et al, 2014;Yoshida et al, 2016;.…”

Section: Introductionmentioning

confidence: 95%

The emergence of the multi‐species NIP1 effector in Rhynchosporium was accompanied by high rates of gene duplications and losses

Mohd‐Assaad

McDonald

Croll

2019

Environmental Microbiology

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Summary Plant pathogens secrete effector proteins to manipulate the host and facilitate infection. Cognate hosts trigger strong defence responses upon detection of these effectors. Consequently, pathogens and hosts undergo rapid coevolutionary arms races driven by adaptive evolution of effectors and receptors. Because of their high rate of turnover, most effectors are thought to be species‐specific and the evolutionary trajectories are poorly understood. Here, we investigate the necrosis‐inducing protein 1 (NIP1) effector in the multihost pathogen genus Rhynchosporium. We retraced the evolutionary history of the NIP1 locus using whole‐genome assemblies of 146 strains covering four closely related species. NIP1 orthologues were present in all species but the locus consistently segregated presence–absence polymorphisms suggesting long‐term balancing selection. We also identified previously unknown paralogues of NIP1 that were shared among multiple species and showed substantial copy‐number variation within R. commune. The NIP1A paralogue was under significant positive selection suggesting that NIP1A is the dominant effector variant coevolving with host immune receptors. Consistent with this prediction, we found that copy number variation at NIP1A had a stronger effect on virulence than NIP1B. Our analyses unravelled the origins and diversification mechanisms of a pathogen effector family shedding light on how pathogens gain adaptive genetic variation.

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