BackgroundAvocado (Persea americana Mill.) is a commercially important fruit crop worldwide. A major limitation to production is the oomycete Phytophthora cinnamomi, which causes root rot leading to branch-dieback and tree death. The decline of orchards infected with P. cinnamomi occurs much faster when exposed to flooding, even if flooding is only transient. Flooding is a multifactorial stress compromised of several individual stresses, making breeding and selection for tolerant varieties challenging. With more plantations occurring in marginal areas, with imperfect irrigation and drainage, understanding the response of avocado to these stresses will be important for the industry.ResultsMaintenance of energy production was found to be central in the response to flooding, as seen by up-regulation of transcripts related to glycolysis and induction of transcripts related to ethanolic fermentation. Energy-intensive processes were generally down-regulated, as evidenced by repression of transcripts related to processes such as secondary cell-wall biosynthesis as well as defence-related transcripts. Aquaporins were found to be down-regulated in avocado roots exposed to flooding, indicating reduced water-uptake under these conditions.ConclusionsThe transcriptomic response of avocado to flooding and P. cinnamomi was investigated utilizing microarray analysis. Differences in the transcriptome caused by the presence of the pathogen were minor compared to transcriptomic perturbations caused by flooding. The transcriptomic response of avocado to flooding reveals a response to flooding that is conserved in several species. This data could provide key information that could be used to improve selection of stress tolerant rootstocks in the avocado industry.Electronic supplementary materialThe online version of this article (doi:10.1186/s12870-016-0893-2) contains supplementary material, which is available to authorized users.

Phytophthora cinnamomi Rands (Pc) is a hemibiotrophic oomycete and the causal agent of Phytophthora root rot (PRR) of the commercially important fruit crop avocado (Persea americana Mill.). Plant defense against pathogens is modulated by phytohormone signaling pathways such as salicylic acid (SA), jasmonic acid (JA), ethylene (ET), auxin and abscisic acid. The role of specific signaling pathways induced and regulated during hemibiotroph-plant interactions has been widely debated. Some studies report SA mediated defense while others hypothesize that JA responses restrict the spread of pathogens. This study aimed to identify the role of SA- and JA- associated genes in the defense strategy of a resistant avocado rootstock, Dusa in response to Pc infection. Transcripts associated with SA-mediated defense pathways and lignin biosynthesis were upregulated at 6 hours post-inoculation (hpi). Results suggest that auxin, reactive oxygen species (ROS) and Ca2+ signaling was also important during this early time point, while JA signaling was absent. Both SA and JA defense responses were shown to play a role during defense at 18 hpi. Induction of genes associated with ROS detoxification and cell wall digestion (β-1-3-glucanase) was also observed. Most genes induced at 24 hpi were linked to JA responses. Other processes at play in avocado at 24 hpi include cell wall strengthening, the formation of phenolics and induction of arabinogalactan, a gene linked to Pc zoospore immobility. This study represents the first transcriptome wide analysis of a resistant avocado rootstock treated with SA and JA compared to Pc infection. The results provide evidence of a biphasic defense response against the hemibiotroph, which initially involves SA-mediated gene expression followed by the enrichment of JA-mediated defense from 18 to 24 hpi. Genes and molecular pathways linked to Pc resistance are highlighted and may serve as future targets for manipulation in the development of PRR resistant avocado rootstocks.

The genomes of Cercospora zeina, Fusarium pininemorale, Hawksworthiomyces lignivorus, Huntiella decipiens, and Ophiostoma ips are presented in this genome announcement. Three of these genomes are from plant pathogens and otherwise economically important fungal species. Fusarium pininemorale and H. decipiens are not known to cause significant disease but are closely related to species of economic importance. The genome sizes range from 25.99 Mb in the case of O. ips to 4.82 Mb for H. lignivorus. These genomes include the first reports of a genome from the genus Hawksworthiomyces. The availability of these genome data will allow the resolution of longstanding questions regarding the taxonomy of these species. In addition these genome sequences through comparative studies with closely related organisms will increase our understanding of how these species or close relatives cause disease.

Rosellinia necatrix is the causal agent of avocado white root rot (WRR). Control of this soil-borne disease is difficult, and the use of tolerant rootstocks may present an effective method to lessen its impact. To date, no studies on the molecular mechanisms regulating the avocado plant response towards this pathogen have been undertaken. To shed light on the mechanisms underpinning disease susceptibility and tolerance, molecular analysis of the gene’s response in two avocado rootstocks with a contrasting disease reaction was assessed. Gene expression profiles against R . necatrix were carried out in the susceptible ‘Dusa’ and the tolerant selection BG83 avocado genotypes by micro-array analysis. In ‘Dusa’, the early response was mainly related to redox processes and cell-wall degradation activities, all becoming enhanced after disease progression affected photosynthetic capacity, whereas tolerance to R . necatrix in BG83 relied on the induction of protease inhibitors and their negative regulators, as well as genes related to tolerance to salt and osmotic stress such as aspartic peptidase domain-containing proteins and gdsl esterase lipase proteins. In addition, three protease inhibitors were identified, glu protease, trypsin and endopeptidase inhibitors, which were highly overexpressed in the tolerant genotype when compared to susceptible ‘Dusa’, after infection with R . necatrix , reaching fold change values of 52, 19 and 38, respectively. The contrasting results between ‘Dusa’ and BG83 provide new insights into the different mechanisms involved in avocado tolerance to Phytophthora cinnamomi and R . necatrix , which are consistent with their biotrophic and necrotrophic lifestyles, respectively. The differential induction of genes involved in salt and osmotic stress in BG83 could indicate that R . necatrix penetration into the roots is associated with osmotic effects, suggesting that BG83’s tolerance to R . necatrix is related to the ability to withstand osmotic imbalance. In addition, the high expression of protease inhibitors in tolerant BG83 compared to susceptible ‘Dusa’ after infection with the pathogen suggests the important role that these proteins may play in the defence of avocado rootstocks against R . necatrix .

Gray leaf spot (GLS), caused by the sibling species Cercospora zeina orCercospora zeae-maydis, is cited as one of the most important diseases threatening global maize production. C. zeina fails to produce cercosporin in vitro, and in most cases causes large coalescing lesions during maize infection; a symptom generally absent from cercosporin-deficient mutants in other Cercospora spp. Here we describe the C. zeina cercosporin toxin biosynthetic gene cluster. The oxidoreductase gene CTB7 contained several insertions and deletions as compared to the C. zeae-maydis ortholog. We set out to determine whether complementing the defective CTB7 gene with the full-length gene from C. zeae-maydis could confer in vitro cercosporin production. C. zeina transformants containing C. zeae-maydis CTB7 were generated by Gray leaf spot continues to be a devastating maize foliar disease of global importance that has resulted in extensive yield losses over the past few decades (Ward et al. 1999; Crous and Braun 2003). Previously classified as Cercospora zeae-maydis Group I and Group II, the causative agents of GLS, C. zeae-maydis and Cercospora zeina are differentiated by both genetic distance and phenotypic characteristics, such as their ability to produce the phytotoxin cercosporin (Goodwin et al. 2001;. Cercospora zeina predominates throughout Africa, while C. zeae-maydis is most prevalent in the majority of the USA and Mexico (Wang et al. 1998;Dunkle and Levy 2000; Goodwin et al. 2001;).The genus Cercospora is part of the class Dothideomycetes and consists of more than 600 recognized species of plant pathogens (Crous and Braun 2003). Although Cercospora species generally exhibit relatively narrow host ranges, many produce cercosporin, a photosensitizing perylenequinone that functions as a non-specific toxin that has been identified as a major pathogenicity factor (Daub and Ehrenshaft 2000;Weiland et al. 2010).Cercosporin production has been demonstrated for several Cercospora species, with isolates of Cercospora kikuchii, Cercospora beticola, C. zeae-maydis, Cercospora asparagi and Cercospora nicotianae all shown to accumulate cercosporin in vitro (Jenns et al. 1989).Isolates of C. zeina however demonstrate a lack of cercosporin production in vitro (Dunkle and Levy 2000; Goodwin et al. 2001; Koshikumo et al. 2014). These species all cause leaf spot diseases that are characterised by severe blighting of leaves (Daub and Ehrenshaft 2000). In contrast to this, isolates of the peanut pathogen Cercospora arachidicola, fail to produce cercosporin and induce only small chlorotic lesions (Fore et al. 1988). Isolates of C.arachidicola have however been shown to produce other toxins which may aid in virulence (Fore et al. 1988). Cercosporin biosynthesis mainly involves a cluster of eight cercosporin toxin biosynthetic (CTB) genes, all of which are transcriptionally induced upon exposure to light in the tobacco pathogen C. nicotianae (Chen et al. 2007b). Targeted disruption of any CTB gene blocked cercosporin production and reduced viru...