Project description:The hemibiotrophic fungal pathogen Colletotrichum graminicola is the causal agent of anthracnose disease on maize stalks and leaves. After the formation of appressoria the host cell wall is penetrated by the conversion of appressorial turgor pressure into forceful ejection of a penetration peg. Subsequently, C. graminicola establishes biotrophic hyphae in the penetrated epidermis cell at around 36 hours post inoculation (hpi) until a switch of hyphal morphology and lifestyle takes place during the colonization of neighboring host cells at around 72 hpi. During the ensuing necrotrophic growth, dark necrotic lesions are formed that are visible as anthracnose symptoms. We used microarrays to detail the global programme of gene expression during the infection process of Colletotrichum graminicola in its host plant to get insight into the defense response of this compatible interaction and into the metabolic reprogramming needed to supply the fungus with nutrients. In three independent experiments, maize plants were infected with conidia of the Colletotrichum graminicola strain CgM2 by spray inoculation of leaves. Samples from infected leaves were taken at 36 and 96 hours post infection, corresponding to initial biotrophic and necrotrophic phase, respectively. Samples from uninfected control plants were taken at the same time points.
Project description:Species from the genus Colletotrichum are the causal agents of anthracnose which contribute to significant losses to the production of commercially grown crops. The genomes of Colletotrichum orbiculare, which infects cucurbits and Nicotiana benthamiana, as well as Colletotrichum gloeosporioides, which infects a wide range of fruits and vegetables, were sequenced. A custom microarray was designed for Colletotrichum orbiculare and used to assess gene expression during infection of Nicotiana benthamiana. Gene expression of Colletotrichum orbiculare growing on its host Nicotiana benthamiana was assessed at 24 hours post inoculation, 3 days post inoculation and 7 days post inoculation. Mycelia growing in vitro and ungerminated conidia were used as controls. Three replicates were performed for each time point.
Project description:The hemibiotrophic fungal pathogen Colletotrichum graminicola is the causal agent of anthracnose disease on maize stalks and leaves. After the formation of appressoria the host cell wall is penetrated by the conversion of appressorial turgor pressure into forceful ejection of a penetration peg. Subsequently, C. graminicola establishes biotrophic hyphae in the penetrated epidermis cell at around 36 hours post inoculation (hpi) until a switch of hyphal morphology and lifestyle takes place during the colonization of neighboring host cells at around 72 hpi. During the ensuing necrotrophic growth, dark necrotic lesions are formed that are visible as anthracnose symptoms. We used microarrays to detail the global programme of gene expression during the infection process of Colletotrichum graminicola in its host plant to get insight into the defense response of this compatible interaction and into the metabolic reprogramming needed to supply the fungus with nutrients.
Project description:To further confirm whether the expression of NRT genes were influenced by pathogen infection, maize leaves were sampled at 0h, 24h, 40h, 60h and 96h post inoculation with wild-type strain Colletotrichum graminicola, the causing agent of maize anthracnose disease.
Project description:Anthracnose caused by the ascomycete Colletotrichum graminicola is one of the most severe fungal diseases of Zea maize. Cultivars with different levels of resistance have been described. However, which genes contribute to cultivar-specific constitutive and/or induced defense in this economically important pathosystem is still elusive. Transcriptome analyses of infected maize leaves of varieties Golden Jubilee (GJ) and B73 by RNA-Seq was performed for the penetration, biotrophic and necrotrophic phases.
Project description:Metabolomics has emerged as a powerful approach to comprehensively interrogate cellular biochemistry. As such, we applied an untargeted liquid chromatography-mass spectrometry metabolomic strategy to elucidate metabolome changes in the anthracnose-causing hemibiotrophic sorghum pathogen, Colletotrichum sublineolum. An in vitro batch culture study model with different carbon sources, glucose, arabinose and rhamnose, were used to support fungal growth over a period of twelve days. Metabolites representing the intracellular and extracellular (secreted) metabolomes were extracted with methanol and subjected to LC-MS analyses. Chemometric modelling revealed a metabolic variation trajectory, comprising three distinct stages that metabolically describe the adaptation of the fungus to diminishing nutrients. Selected marker gene expression indicated stage one (0-3 d.p.i) as corresponding to the early logarithmic phase. Stage two can be interpreted as an intermediate transitionary stage with stage three corresponding to the stationary phase (9-12 d.p.i). Stage one was characterised by up-regulation of endo-metabolites such as ferricrocin, fatty acids and flavone-conjugates, while stage three was characterised by the secretion of phytotoxins, including colletotrichin and colletotric acid. Ultimately, results from our in vitro model reveal previously unknown insights into the dynamic aspects of metabolome reprogramming in the growth phases of Colletotrichum spp as determined by nutrients obtainable from plant cell walls.
Project description:Walnut anthracnose caused by Colletotrichum gloeosporioides (Penz.) Penz. and Sacc. is a major disease affecting walnut production in China. Although the long non-coding RNAs (lncRNAs) are important for plant disease resistance , the molecular mechanisms underlying resistance to C. gloeosporioides in walnut remain poorly understood.The anthracnose-resistant F26 fruits from the B26 clone and the anthracnose susceptible F423 fruits from the 4-23 clone of walnut were used as the test materials. Specifically, we performed a comparative transcriptome analysis of F26 fruit bracts and F423 to identify differentially expressed LncRNAs (DELs) at five time-points (tissues at 0 hpi, pathological tissues at 24 hpi, 48 hpi, 72 hpi, and distal uninoculated tissues at 120 hpi). Compared with F423, a total of 14525 DELs were identified, including 10645 upregulated lncRNAs and 3846 downregulated lncRNAs in F26. The number of upregulated lncRNAs in F26 compared to in F423 was significantly higher at the early stages of C. gloeosporioides infection. A total of 5 modules related to disease resistance were screened by WGCNA and the target genes of lncRNAs were obtained. Bioinformatic analysis showed that the target genes of upregulated lncRNAs were enriched in immune-related processes during the infection of C. gloeosporioides , such as activation of innate immune response, defense response to bacterium, incompatible interaction and immune system process, and enriched in plant hormone signal transduction, phenylpropanoid biosynthesis and other pathways. And 124 known target genes for 96 hub lncRNAs were predicted, including 10 known resistance genes. The expression of 5 lncRNAs and 5 target genes was confirmed by qPCR, which was consistent with the RNA-seq data.The results of this study provide the basis for future functional characterizations of lncRNAs regarding the C. gloeosporioides resistance of walnut fruit bracts.
Project description:Colletotrichum is a large genus of fungal phytopathogens that cause major economic losses on a wide range of crop plants throughout the world. These pathogenes vary widely in their host specificity and may have either broad or narrow host ranges. Here, we report the first complete genome of the alfalfa (Medicago sativa) pathogen, Colletotrichum destructivum, which will facilitate the genomic analysis of host adaptation and comparison with other members of the Destructivum clade. We identified a specific 1.2Mb region within chromosome 1 displaying all the hallmarks of fungal accessory chromosomes, which may have arisen through the integration of a mini-chromosome into a core chromosome and possibly linked with the pathogenicity of this fungus. We show this region is also a focus for chromosomal rearrangements, which may contribute to generating genetic diversity for adaptive evolution. Finally, we report infection by this fungus of the model legume, Medicago truncatula, providing a novel pathosystem for studying fungal-plant interactions.