Abstract
BackgroundLasiodiplodia theobromae is a fungus of the Botryosphaeriaceae that causes grapevine vascular disease, especially in regions with hot climates. Fungi in this group often remain latent within their host and become virulent under abiotic stress. Transcriptional regulation analysis of L. theobromae exposed to heat stress (HS) was first carried out in vitro in the presence of grapevine wood (GW) to identify potential pathogenicity genes that were later evaluated for in planta expression.ResultsA total of 19,860 de novo assembled transcripts were obtained, forty-nine per cent of which showed homology to the Botryosphaeriaceae fungi, Neofusicoccum parvum or Macrophomina phaseolina. Three hundred ninety-nine have homology with genes involved in pathogenic processes and several belonged to expanded gene families in others fungal grapevine vascular pathogens. Gene expression analysis showed changes in fungal metabolism of phenolic compounds; where genes encoding for enzymes, with the ability to degrade salicylic acid (SA) and plant phenylpropanoid precursors, were up-regulated during in vitro HS response, in the presence of GW. These results suggest that the fungal L-tyrosine catabolism pathway could help the fungus to remove phenylpropanoid precursors thereby evading the host defense response. The in planta up-regulation of salicylate hydroxylase, intradiol ring cleavage dioxygenase and fumarylacetoacetase encoding genes, further supported this hypothesis. Those genes were even more up-regulated in HS-stressed plants, suggesting that fungus takes advantage of the increased phenylpropanoid precursors produced under stress. Pectate lyase was up-regulated while a putative amylase was down-regulated in planta, this could be associated with an intercellular growth strategy during the first stages of colonization.ConclusionsL. theobromae transcriptome was established and validated. Its usefulness was demonstrated through the identification of genes expressed during the infection process. Our results support the hypothesis that heat stress facilitates fungal colonization, because of the fungus ability to use the phenylpropanoid precursors and SA, both compounds known to control host defense.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-016-2952-3) contains supplementary material, which is available to authorized users.
Highlights
Lasiodiplodia theobromae is a fungus of the Botryosphaeriaceae that causes grapevine vascular disease, especially in regions with hot climates
We propose that a general mechanism for becoming pathogenic under heat stress (HS) conditions is conserved among several fungal taxa, whereby melanin metabolism could play a role in pathogenicity in plants, to fungal mammalian pathogens
Genes involved in melanin production were co-regulated with key transcription factors that control carbon and nitrogen usage, suggesting that strong metabolic and morphological changes occurs during fungal heat stress adaptation, in a similar manner to those documented for some fungal mammal’s pathogens
Summary
Lasiodiplodia theobromae is a fungus of the Botryosphaeriaceae that causes grapevine vascular disease, especially in regions with hot climates. Fungi in this group often remain latent within their host and become virulent under abiotic stress. Two independent studies have analyzed, at the molecular level, the interaction of trees susceptible to fungal pathogens Both studies highlighted the adaptation capability of the fungus to metabolize terpenoids and stilbene, the main defensive compounds produced by the host in response to infection, and use them as carbon sources for wood colonization [7, 8]. Both compounds are produced in response to biotic and abiotic stress in plants [9, 10], suggesting that the fungal colonization is favored when plants are under abiotic stress
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