Gene expression in wheat heads treated with Fusarium graminearum mutants that produce a priming-induced resistance to fusarium head blight
Ontology highlight
ABSTRACT:
ORGANISM(S): Triticum aestivum
PROVIDER: GSE69509 | GEO | 2015/06/03
SECONDARY ACCESSION(S): PRJNA285754
REPOSITORIES: GEO
Similar Datasets
Project description:Two mutants (tri6Δ and noxABΔ) of the fungal pathogen Fusarium graminearum were assessed for their ability to prime immune responses in wheat (cv. Roblin) against challenge with pathogenic F. graminearum. Priming treatments generated Fusarium head blight (FHB)-resistant wheat phenotypes and reduced the accumulation of fungal mycotoxins in infected tissues. Microarray analysis identified 260 transcripts that were differentially expressed during the priming period. Expression changes were observed in genes associated with immune surveillance systems, signalling cascades, antimicrobial compound production, oxidative burst, secondary metabolism, and detoxification and transport. Specifically, genes related to jasmonate, gibberellin and ethylene biosynthesis exhibited differential expression during priming. In addition, the induction of the phenylpropanoid pathways that lead to flavonoid, coumarin and hydroxycinnamic acid amide accumulation was also observed. This study highlights the utility of nonpathogenic mutants to both elicit and delineate stages of defence responses in wheat.
| S-EPMC6638912 | biostudies-literature
Project description:Fusarium head blight (FHB) of wheat, caused by Fusarium graminearum (Schwabe), is a destructive disease worldwide, reducing wheat yield and quality. To accelerate the improvement of scab tolerance in wheat, we assessed the International Triticeae Mapping Initiative mapping population (ITMI/MP) for Type I and II resistance against a wide population of Argentinean isolates of F. graminearum. We discovered a total of 27 additive QTLs on ten different (2A, 2D, 3B, 3D, 4B, 4D, 5A, 5B, 5D and 6D) wheat chromosomes for Type I and Type II resistances explaining a maximum of 15.99% variation. Another four and two QTLs for thousand kernel weight in control and for Type II resistance, respectively, involved five different chromosomes (1B, 2D, 6A, 6D and 7D). Furthermore, three, three and five QTLs for kernel weight per spike in control, for Type I resistance and for Type II resistance, correspondingly, involved ten chromosomes (2A, 2D, 3B, 4A, 5A, 5B, 6B, 7A, 7B, 7D). We were also able to detect five and two epistasis pairs of QTLs for Type I and Type II resistance, respectively, in addition to additive QTLs that evidenced that FHB resistance in wheat is controlled by a complex network of additive and epistasis QTLs.
| S-EPMC8707622 | biostudies-literature
Project description:Fusarium head blight (FHB) is a major disease of cereal crops caused by the fungus Fusarium graminearum (Fg). FHB affects the flowering heads (or spikes) and developing seeds. This study compares the gene expression profile of heads from the susceptible cultivar Roblin after inoculation with either water (dH2O) or the disarmed Fg strain noxABΔ (NoxAB). noxABΔ is a double deletion mutant of NoxA and NoxB, which function are component of the NADPH oxidase enzyme complex converting molecular oxygen in a stepwise reduction to superoxides leading to the production of H2O2. Deletion mutants of Nos A and B have been described in more details in Li Wang, Christopher Mogg, Sean Walkowiak, Manisha Joshi & Rajagopal Subramaniam (2014). Characterization of NADPH oxidase genes NoxA and NoxB in Fusarium graminearum. Can. J. Plant Pathol. 36: 12-21, DOI: 10.1080/07060661.2013.868370. This manuscript characterizes the role of the catalytic subunit (gp91phox) of Nox, NoxA and NoxB in F. graminearum. Targeted deletion of NoxA and NoxB show that these genes differentially regulate the production of superoxides during mycelia development. The nitro blue tetrazolium staining revealed that both the single noxA mutant and the double noxA/B mutant strains are restricted in the production of superoxides. This limitation, however, did not affect their ability to synthesize 15-ADON in culture. Deletion analyses also revealed that NoxA, but not NoxB is involved in perithecia development and ascospore production. An in-vitro based cellophane breach assay indicated that both NoxA and NoxB contribute to virulence. The pathogenicity tests performed on a susceptible variety of wheat, ‘Roblin’ confirmed that these two genes act synergistically to promote virulence. Cumulatively, we provide evidence that the Nox homologues have non-redundant functions in F. graminearum.
2015-06-02 | GSE69490 | GEO
Project description:Fusarium head blight (FHB) is a major disease of cereal crops caused by the fungus Fusarium graminearum (Fg). FHB affects the flowering heads (or spikes) and developing seeds. This study compares the gene expression profile of heads from the susceptible cultivar Roblin after inoculation with either water (W) or the disarmed Fg strain tri6Δ (T6). Tri6 is a global transcription regulator affecting the trichothecene biosynthesis pathway.
2015-06-02 | GSE69437 | GEO
Project description:Fusarium head blight (FHB) is a major disease of cereal crops caused by the fungus Fusarium graminearum (Fg). FHB affects the flowering heads (or spikes) and developing seeds. This study compare the gene expression profile in wheat spikelets (spk 2) inoculated with either water (mock treatment) or a pathogenic strain of Fusarium graminearum (WT); spikelets 2 were inoculated 24 hrs after a neighbour spikelet (spk 0) was treated with either water or F. graminerum mutant strain Tri6Δ or NoxABΔ. Spikelets 2 were sampled 8 and 24 hrs after the second treatment.
2015-05-28 | GSE55653 | GEO
Project description:Fusarium head blight (FHB) is a devastating disease of wheat. Molecular mapping led to the identification of two major FHB resistance QTL, Fhb1 and Qfhs.ifa-5A. The actual function of these resistance genes is still unknown. The resistant line CM82036, the susceptible line Remus and two sister lines from the cross CM82036/Remus were analysed for gene expression. The sister lines show contrasting levels of FHB resistance due to the presence or absence of resistance alleles at Fhb1 and Qfhs.ifa-5A. At anthesis plants were challenged by Fusarium graminearum or water under controlled conditions. At six-time points after inoculation (0-72 h) gene expression of specific wheat floral tissue was analysed by cDNA-AFLPs in two biological replications. Altered expression patterns after F. graminearum inoculation were observed for 164 transcript-derived fragments (TDFs), corresponding to 3.4% of the analysed fragments. Fourteen TDFs, 0.28% of the total analysed fragments, displayed differential expression after fungal attack depending on the genotype; five of these TDFs were differentially expressed between the sister lines and are possibly associated with the possession of Fhb1 and Qfhs-ifa-5A and the FHB resistance level of the genotypes. Sequencing and annotation of these gene tags revealed homologies to a UDP-glucosyltransferase, phenylalanine ammonia-lyase, Dna-J like protein, pathogenesis-related family protein and to one gene with unknown function providing initial clues for guiding further functional studies on the resistance reaction of wheat against FHB. This work is the first report on differential gene expression between related, resistant and susceptible, wheat lines after F. graminearum attack.
| S-EPMC3194064 | biostudies-literature
Project description:Breeding for Fusarium head blight (FHB) resistance in durum wheat is complicated by the quantitative trait expression and narrow genetic diversity of available resources. High-density mapping of the FHB resistance quantitative trait loci (QTL), evaluation of their co-localization with plant height and maturity QTL and the interaction among the identified QTL are the objectives of this study. Two doubled haploid (DH) populations, one developed from crosses between Triticum turgidum ssp. durum lines DT707 and DT696 and the other between T. turgidum ssp. durum cv. Strongfield and T. turgidum ssp. carthlicum cv. Blackbird were genotyped using the 90K Infinium iSelect chip and evaluated phenotypically at multiple field FHB nurseries over years. A moderate broad-sense heritability indicated a genotype-by-environment interaction for the expression of FHB resistance in both populations. Resistance QTL were identified for the DT707 × DT696 population on chromosomes 1B, 2B, 5A (two loci) and 7A and for the Strongfield × Blackbird population on chromosomes 1A, 2A, 2B, 3A, 6A, 6B and 7B with the QTL on chromosome 1A and those on chromosome 5A being more consistently expressed over environments. FHB resistance co-located with plant height and maturity QTL on chromosome 5A and with a maturity QTL on chromosome 7A for the DT707 × DT696 population. Resistance also co-located with plant height QTL on chromosomes 2A and 3A and with maturity QTL on chromosomes 1A and 7B for the Strongfield × Blackbird population. Additive × additive interactions were identified, for example between the two FHB resistance QTL on chromosome 5A for the DT707 × DT696 population and the FHB resistance QTL on chromosomes 1A and 7B for the Strongfield × Blackbird population. Application of the Single Nucleotide Polymorphic (SNP) markers associated with FHB resistance QTL identified in this study will accelerate combining genes from the two populations.
| S-EPMC6181299 | biostudies-other
Project description:Fusarium head blight (FHB), caused by Fusarium graminearum, is a very important disease of wheat globally. Damage caused by F. graminearum includes reduced grain yield, reduced grain functional quality, and results in the presence of the trichothecene mycotoxin deoxynivalenol in Fusarium-damaged kernels. The development of FHB resistant wheat cultivars is an important component of integrated management. The objective of this study was to identify QTL for FHB resistance in a recombinant inbred line (RIL) population of the spring wheat cross Kenyon/86ISMN 2137. Kenyon is a Canadian spring wheat, while 86ISMN 2137 is an unrelated spring wheat. The RIL population was evaluated for FHB resistance in six FHB nurseries. Nine additive effect QTL for FHB resistance were identified, six from Kenyon and three from 86ISMN 2137. Rht8 and Ppd-D1a co-located with two FHB resistance QTL on chromosome arm 2DS. A major QTL for FHB resistance from Kenyon (QFhb.crc-7D) was identified on chromosome 7D. The QTL QFhb.crc-2D.4 from Kenyon mapped to the same region as a FHB resistance QTL from Wuhan-1 on chromosome arm 2DL. This result was unexpected since Kenyon does not share common ancestry with Wuhan-1. Other FHB resistance QTL on chromosomes 4A, 4D, and 5B also mapped to known locations of FHB resistance. Four digenic epistatic interactions were detected for FHB resistance, which involved eight QTL. None of these QTL were significant based upon additive effect QTL analysis. This study provides insight into the genetic basis of native FHB resistance in Canadian spring wheat.
| S-EPMC5061752 | biostudies-other
Project description:Fusarium head blight (FHB) is a devastating fungal disease responsible for significant yield losses in wheat and other cereal crops across the globe. FHB infection of wheat spikes results in grain contamination with mycotoxins, reducing both grain quality and yield. Breeding strategies have resulted in the production of FHB-resistant cultivars, however, the underlying molecular mechanisms of resistance in the majority of these cultivars are still poorly understood. To improve our understanding of FHB-resistance, we performed a transcriptomic analysis of FHB-resistant AC Emerson, FHB-moderately resistant AC Morley, and FHB-susceptible CDC Falcon in response to Fusarium graminearum. Wheat spikelets located directly below the point of inoculation were collected at 7-days post inoculation (dpi), where dual RNA-sequencing was performed to explore differential expression patterns between wheat cultivars in addition to the challenging pathogen. Differential expression analysis revealed distinct defense responses within FHB-resistant cultivars including the enrichment of physical defense through the lignin biosynthesis pathway, and DON detoxification through the activity of UDP-glycosyltransferases. Nucleotide sequence variants were also identified broadly between these cultivars with several variants being identified within differentially expressed putative defense genes. Further, F. graminearum demonstrated differential expression of mycotoxin biosynthesis pathways during infection, leading to the identification of putative pathogenicity factors.
| S-EPMC10794533 | biostudies-literature
Project description:Fusarium head blight (FHB) caused by Fusarium pathogens are devastating diseases worldwide. Host-induced gene silencing (HIGS) which involves host expression of double-stranded RNA (dsRNA)-generating constructs directed against genes in the pathogen has been a potential strategy for the ecological sound control of FHB. In this study, we constructed transgenic Brachypodium distachyon lines carrying RNA interference (RNAi) cassettes to target two essential protein kinase genes Fg00677 and Fg08731, and cytochrome P450 lanosterol C14-?-demethylase (CYP51) encoding genes (CYP51A, CYP51B, and CYP51C) of Fusarium graminearum, respectively. Northern blotting confirmed the presence of short interfering RNAs (siRNA) derived from Fg00677, Fg08731, and CYP51 in transgenic B. distachyon plants, and the transcript levels of the corresponding genes were down-regulated in the F. graminearum colonizing B. distachyon spikes. All the corresponding independent, Fg00677-RNAi, Fg08731-RNAi, and CYP51-RNAi transgenic T2 lines exhibited strong resistance to F. graminearum, suggesting that silencing molecules produced by transgenic plants inhibited the corresponding gene function by down-regulating its expression, thereby reducing pathogenicity. Our results indicate that Fg00677 and Fg08731 are effective targets for HIGS and can be applied to construct transgenic HIGS materials to enhance FHB resistance in wheat and other cereal crops.
| S-EPMC6831556 | biostudies-literature