Abstract
BackgroundSoil-borne fungi of the Fusarium oxysporum species complex cause devastating wilt disease on many crops including legumes that supply human dietary protein needs across many parts of the globe. We present and compare draft genome assemblies for three legume-infecting formae speciales (ff. spp.): F. oxysporum f. sp. ciceris (Foc-38-1) and f. sp. pisi (Fop-37622), significant pathogens of chickpea and pea respectively, the world’s second and third most important grain legumes, and lastly f. sp. medicaginis (Fom-5190a) for which we developed a model legume pathosystem utilising Medicago truncatula.ResultsFocusing on the identification of pathogenicity gene content, we leveraged the reference genomes of Fusarium pathogens F. oxysporum f. sp. lycopersici (tomato-infecting) and F. solani (pea-infecting) and their well-characterised core and dispensable chromosomes to predict genomic organisation in the newly sequenced legume-infecting isolates. Dispensable chromosomes are not essential for growth and in Fusarium species are known to be enriched in host-specificity and pathogenicity-associated genes. Comparative genomics of the publicly available Fusarium species revealed differential patterns of sequence conservation across F. oxysporum formae speciales, with legume-pathogenic formae speciales not exhibiting greater sequence conservation between them relative to non-legume-infecting formae speciales, possibly indicating the lack of a common ancestral source for legume pathogenicity. Combining predicted dispensable gene content with in planta expression in the model legume-infecting isolate, we identified small conserved regions and candidate effectors, four of which shared greatest similarity to proteins from another legume-infecting ff. spp.ConclusionsWe demonstrate that distinction of core and potential dispensable genomic regions of novel F. oxysporum genomes is an effective tool to facilitate effector discovery and the identification of gene content possibly linked to host specificity. While the legume-infecting isolates didn’t share large genomic regions of pathogenicity-related content, smaller regions and candidate effector proteins were highly conserved, suggesting that they may play specific roles in inducing disease on legume hosts.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2486-8) contains supplementary material, which is available to authorized users.
Highlights
Soil-borne fungi of the Fusarium oxysporum species complex cause devastating wilt disease on many crops including legumes that supply human dietary protein needs across many parts of the globe
We demonstrate that distinction of core and potential dispensable genomic regions of novel F. oxysporum genomes is an effective tool to facilitate effector discovery and the identification of gene content possibly linked to host specificity
The addition of the genomic sequences of the legumeinfecting F. oxysporum ff. spp. presented here adds to the accumulated bioinformatics resources for Fusarium oxysporum formae speciales and helps provide a powerful knowledge-base for predicting lineage-specific genes involved in host-specific pathogenicity
Summary
Soil-borne fungi of the Fusarium oxysporum species complex cause devastating wilt disease on many crops including legumes that supply human dietary protein needs across many parts of the globe. While some F. oxysporum isolates are non-pathogenic saprophytes and may even have symbiotic or bio-control properties [4] this species notably contains more than 150 host-specific plant-pathogenic sub-species [5], known as formae speciales Dispensable genomic regions encoding genes that play a role in pathogenicity and host-specificity, including effector genes, have been identified in Fusarium isolates infecting a range of plant hosts [9,10,11,12,13]. Sp lycopersici (Fol), the genes residing on CDCs define its host range and these chromosomes when transferred to non-pathogenic species can confer pathogenicity on a new host. Genes that do not confer pathogenicity on the new host would be more susceptible to shuffling and subsequent loss, as has been observed for Fol and F. solani CDCs relative to core chromosomes [11]
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