The Northern Corn Leaf Blight Resistance Gene, Ht1, Encodes an NLR Immune Receptor
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ABSTRACT:
PROVIDER: PRJNA852956 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19854500_1.fastq.gz | Fastqsanger.gz | |||
| SRR19854500_2.fastq.gz | Fastqsanger.gz | |||
| SRR19854501.fastq.gz | Fastqsanger.gz | |||
| SRR19854502.fastq.gz | Fastqsanger.gz | |||
| SRR19854503.fastq.gz | Fastqsanger.gz |
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Project description:Northern corn leaf blight (NLB), caused by the fungal pathogen Exserohilum turcicum, results significant yield reductions in infected corn. The first major locus conferring resistance to E. turcicum race 0, Ht1, was identified over 50 years ago, but despite widespread deployment the underlying gene has remained unknown. We employed map-based cloning to identify the Ht1 causal gene, which was found to be a coiled-coil nucleotide-binding, leucine-rich repeat (NLR) gene, termed PH4GP-Ht1. Transgenic testing confirmed that addition of the native PH4GP-Ht1 sequence to the susceptible maize variety PH184C resulted in resistance to E. turcicum race 0. A survey of the maize NAM genomes revealed that susceptible Ht1 alleles had very low to no expression, but overexpression of the susceptible B73 allele did not result in resistant plants, indicating that relatively minor protein sequence variations may underlie the resistance phenotype. Modeling of the PH4GP-Ht1 protein indicated that it has structural homology to the Arabidopsis NLR resistance gene ZAR1, and likely forms a similar homo-pentamer structure following activation. RNA-seq data from an infection time course revealed that one week after inoculation there was a threefold reduction in fungal biomass and a dramatic increase in DEGs when comparing mock to inoculated PH4GP-Ht1 transgenic plants and null plants. These results demonstrate that the NLR PH4GP-Ht1 is the causal gene underlying the NLB resistance phenotype of Ht1.
2022-10-03 | GSE206951 | GEO
Project description:Northern corn leaf blight, caused by the fungal pathogen Exserohilum turcicum, is a major disease of maize. The first major locus conferring resistance to E. turcicum race 0, Ht1, was identified over 50 years ago, but the underlying gene has remained unknown. We employed a map-based cloning strategy to identify the Ht1 causal gene, which was found to be a coiled-coil nucleotide-binding, leucine-rich repeat (NLR) gene, which we named PH4GP-Ht1. Transgenic testing confirmed that introducing the native PH4GP-Ht1 sequence to a susceptible maize variety resulted in resistance to E. turcicum race 0. A survey of the maize nested association mapping genomes revealed that susceptible Ht1 alleles had very low to no expression of the gene. Overexpression of the susceptible B73 allele, however, did not result in resistant plants, indicating that sequence variations may underlie the difference between resistant and susceptible phenotypes. Modelling of the PH4GP-Ht1 protein indicated that it has structural homology to the Arabidopsis NLR resistance gene ZAR1, and probably forms a similar homopentamer structure following activation. RNA sequencing data from an infection time course revealed that 1 week after inoculation there was a threefold reduction in fungal biomass in the PH4GP-Ht1 transgenic plants compared to wild-type plants. Furthermore, PH4GP-Ht1 transgenics had significantly more inoculation-responsive differentially expressed genes than wild-type plants, with enrichment seen in genes associated with both defence and photosynthesis. These results demonstrate that the NLR PH4GP-Ht1 is the causal gene underlying Ht1, which represents a different mode of action compared to the previously reported wall-associated kinase northern corn leaf blight resistance gene Htn1/Ht2/Ht3.
| S-EPMC10257041 | biostudies-literature
Project description:Northern corn leaf blight (NCLB) caused by the hemibiotrophic fungus Exserohilum turcicum is an important foliar disease of maize that is mainly controlled by growing resistant maize cultivars. The Htn1 locus confers quantitative and partial NCLB resistance by delaying the onset of lesion formation. Htn1 represents an important source of genetic resistance that was originally introduced from a Mexican landrace into modern maize breeding lines in the 1970s. Using a high-resolution map-based cloning approach, we delimited Htn1 to a 131.7-kb physical interval on chromosome 8 that contained three candidate genes encoding two wall-associated receptor-like kinases (ZmWAK-RLK1 and ZmWAK-RLK2) and one wall-associated receptor-like protein (ZmWAK-RLP1). TILLING (targeting induced local lesions in genomes) mutants in ZmWAK-RLK1 were more susceptible to NCLB than wild-type plants, both in greenhouse experiments and in the field. ZmWAK-RLK1 contains a nonarginine-aspartate (non-RD) kinase domain, typically found in plant innate immune receptors. Sequence comparison showed that the extracellular domain of ZmWAK-RLK1 is highly diverse between different maize genotypes. Furthermore, an alternative splice variant resulting in a truncated protein was present at higher frequency in the susceptible parents of the mapping populations compared with in the resistant parents. Hence, the quantitative Htn1 disease resistance in maize is encoded by an unusual innate immune receptor with an extracellular wall-associated kinase domain. These results further highlight the importance of this protein family in resistance to adapted pathogens.
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Project description:Plants growing in soil are challenged by multiple biotic (e.g. pathogens) and abiotic (e.g. heavy metals) stressors. Stress resistance is a key determinant for plants to thrive in the environment. Resistance to pathogens requires innate immunity 1, whereas tolerance to metal ions is accomplished by mechanisms such as complexation and compartmentation2,3. Some transition metals can enhance plant’s defense against pathogens4,5, but the mechanism remains unclear. Here, we show that an Arabidopsis head-to-head gene pair of intracellular nucleotide-binding leucine-rich repeat (NLR) receptors antagonistically control transition metal-triggered immunity. One NLR, STM2 directly perceives transition metal ions, such as Cd2+, Cu2+ and Zn2+, as a ligand to activate its NAD+ hydrolytic activity and immune responses, triggering enhanced resistance to the soil-borne bacterial wilt pathogen Ralstonia solanacearum. The other NLR, STM1 suppresses STM2 to protect plants from transition metal-triggered immunity and growth inhibition in the presence of excess metals. STM1 also dampens resistance to the pathogen. Our study defines an NLR activated by transition metals and reveals a trade-off between resistance to pathogens and tolerance to transition metals that are pervasive in soil.
2025-03-10 | GSE291114 | GEO
Project description:Plants growing in soil are challenged by multiple biotic (e.g. pathogens) and abiotic (e.g. heavy metals) stressors. Stress resistance is a key determinant for plants to thrive in the environment. Resistance to pathogens requires innate immunity , whereas tolerance to metal ions is accomplished by mechanisms such as complexation and compartmentation. Some transition metals can enhance plant’s defense against pathogens4,5, but the mechanism remains unclear. Here, we show that an Arabidopsis head-to-head gene pair of intracellular nucleotide-binding leucine-rich repeat (NLR) receptors antagonistically control transition metal-triggered immunity. One NLR, STM2 directly perceives transition metal ions, such as Cd2+, Cu2+ and Zn2+, as a ligand to activate its NAD+ hydrolytic activity and immune responses, triggering enhanced resistance to the soil-borne bacterial wilt pathogen Ralstonia solanacearum. The other NLR, STM1 suppresses STM2 to protect plants from transition metal-triggered immunity and growth inhibition in the presence of excess metals. STM1 also dampens resistance to the pathogen. Our study defines an NLR activated by transition metals and reveals a trade-off between resistance to pathogens and tolerance to transition metals that are pervasive in soil.
2025-03-11 | GSE291226 | GEO
Project description:Northern corn leaf blight (NCLB), a corn disease infected by Exserohilum turcicum, can cause loss of harvest and economy. Identification or evaluation of NCLB-resistant quantitative trait loci (QTL) and genes could improve maize breeds. This study aimed to identify novel QTLs for NCLB-resistance.Two maize strains (BB and BC) were utilized to generate B73 × B97 and B73 × CML322 and constructed the genetic linkage using high-throughput single nucleotide polymorphism (SNP) linkage map analysis of 170 (BB) and 163(BC) recombinant inbred line (RIL) genomic DNA samples. NCLB-resistant QTL was associated with phenotypic data from the field trial of 170 BB and 163 BC strains over two years using these 1100 SNPs to identify high-density NCLB-resistant QTLs.In BB, QTL of the NCLB resistance was on chromosome 1 and 3 (LOD scores between 2.74 and 5.44); in BC, QTL of NCLB resistance was on chromosome 1, 2, 4, 8, and 9 (LOD scores between 2.52 and 8.53). A number of genes or genetic information related to NCLB resistance in both BB and BC were identified with the maximum number of genes/NCLB resistance-related QTL on chromosome 3 for BB and on chromosome 1 for BC.This study successfully mapped and identified NCLB-resistant QTL and genes for these 2 different maize strains, which provides insightful information for future study of NCLB-resistance and selection of NCLB-resistant maize variants.
| S-EPMC7402768 | biostudies-literature
Project description:Transcriptional profiling of sweet corn response to plant density (crowding stress). Determine the extent to which hybrid and environment influences crowding stress response and identify crowding stress transcriptional response in sweet corn
2021-06-01 | GSE72434 | GEO
Project description:Northern corn leaf blight (NCLB), caused by the fungal pathogen Exserohilum turcicum, poses a grave threat to maize production worldwide. The resistance gene in A619Ht3, discovered decades ago, is an important genetic resource for NCLB control. By using a pair of near-isogenic lines (NILs) A619Ht3 and A619, together with the resistant and susceptible bulks derived from the cross of A619Ht3 and L3162 lines, we initially detected a Ht3-like (Ht3L) locus in bin 8.06 that was closely associated with NCLB resistance. We then performed five rounds of fine-mapping, which ultimately delimited the Ht3L locus to a 577-kb interval flanked by SNP markers KA002081 and KA002084. Plants homozygous for the Ht3L/Ht3L genotype exhibited an average reduction in diseased leaf area (DLA) by 16.5% compared to plants lacking Ht3L locus. The Ht3L locus showed extensive variation in genomic architecture among different maize lines and did not appear to contain any genes encoding canonical cell wall-associated kinases against NCLB. Moreover, the Ht3L locus was located ∼2.7 Mb away from the known Htn1 locus. We speculate that the Ht3L locus may contain a bona fide Ht3 gene or a novel NCLB resistance gene closely linked to Ht3. In practice, the Ht3L locus is a valuable resource for improving maize resistance to NCLB.
| S-EPMC9506542 | biostudies-literature
Project description:Plants utilize cell surface-localized pattern recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeat (NLR) receptors to detect non-self and elicit robust immune responses. During plant development and especially during aging, fine-tuning the homeostasis of these receptors is critical to prevent their hyperactivation. Here, we show that Arabidopsis plants lacking metacaspase 1 (AtMC1) display autoimmunity dependent on immune signalling components downstream of NLR and PRR activation. Overexpression of catalytically inactive AtMC1 in an atmc1 background triggers severe autoimmunity partially dependent on the same immune signalling components. Although individual mutations in NLRs, PRRs or other immune-related components that interact with catalytically inactive AtMC1 do not rescue the autoimmune phenotype, overexpression of SNIPER1, a master regulator of NLR homeostasis, fully attenuates the phenotype, inferring that a broad defect in NLR turnover may underlie the severe autoimmunity observed. As opposed to Wt AtMC1 which exhibits a nucleocytoplasmic localization, catalytically inactive AtMC1 localizes to puncta structures that are degraded through autophagy. We infer that the phenotypes observed in plants overexpressing catalytically inactive AtMC1 may represent an additive phenotype to the relatively milder autoimmunity observed in atmc1 mutants. Altogether and considering previous evidence on the proteostatic functions of AtMC1, we speculate that Wt AtMC1 may either directly or indirectly control NLR protein levels as plants approach adulthood, thus preventing autoimmunity.
2025-03-21 | PXD048924 | Pride