Abstract
Abstract Polyploidization is a major driver of plant evolution and stress adaptation, yet its role in modulating biotic stress resistance through epigenetic mechanisms remains poorly understood. This study demonstrates that autotetraploidization in Chrysanthemum lavandulifolium significantly enhances resistance to Alternaria alternata, the cause of black spot disease. Whole-genome methylome and transcriptome analyses reveal that polyploidization induces locus-specific CHH hypomethylation in the promoters of a subset of WRKY transcription factors, leading to their transcriptional activation upon fungal infection. Functional characterization of CIWRKY103, a key hypomethylated WRKY gene, confirms its critical role in conferring disease resistance. Chemical inhibition of DNA methylation (5-azacytidine treatment) in diploid plants mimics the tetraploid phenotype by activating WRKY103 expression and enhancing resistance. This epigenetic regulatory mechanism is conserved across diverse chrysanthemum species, highlighting the potential of targeting DNA methylation to modulate fungal disease resistance in polyploid crops. Our findings unveil a novel link between polyploidy, epigenetic reprogramming, and pathogen defense, offering strategic insights for sustainable crop protection.
Abstract from the paper’s OpenAlex record; open copy licensed cc-by. Read at the source ↗
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Claims 7
Claim · model-written summary
Autotetraploidization increased Alternaria resistance.
- Taxon
- Chrysanthemum lavandulifolium
Chrysanthemum lavandulifoliume0 - Treatment
- autotetraploidizatione0
- Interactor
- Alternaria alternata
.jpg?width=60)
Alternaria alternatae0pathogen - Outcome
- resistance to Alternaria alternatae0
- Direction
- enhancese0
Not reportedComparator
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
.jpg?width=500)
Verbatim
e0“autotetraploidization in Chrysanthemum lavandulifolium significantly enhances resistance to Alternaria alternata”
Claim · model-written summary
Polyploidization caused promoter CHH hypomethylation in WRKY factors.
- Taxon
- Chrysanthemum lavandulifoliumChrysanthemum lavandulifoliumt0
- Gene
- WRKY transcription factorse0
- Outcome
- CHH hypomethylatione0
Not reportedDirection
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“polyploidization induces locus-specific CHH hypomethylation in the promoters of a subset of WRKY transcription factors”
t0“in Chrysanthemum lavandulifolium”
Claim · model-written summary
WRKY transcription was activated upon fungal infection.
- Taxon
- Chrysanthemum lavandulifoliumChrysanthemum lavandulifoliume1
- Gene
- WRKYst0
- Outcome
- transcriptional activatione0
- Qualifier
- upon fungal infectione0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“leading to their transcriptional activation upon fungal infection”
t0“WRKYs”
e1“autotetraploidization in Chrysanthemum lavandulifolium significantly enhances resistance to Alternaria alternata”
Claim · model-written summary
CIWRKY103 was important for disease resistance.
- Taxon
- Chrysanthemum lavandulifoliumChrysanthemum lavandulifoliumt0
- Gene
- CIWRKY103e0
- Outcome
- disease resistancee0
- Qualifier
- critical rolee0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“Functional characterization of CIWRKY103, a key hypomethylated WRKY gene, confirms its critical role in conferring disease resistance.”
t0“in Chrysanthemum lavandulifolium”
Claim · model-written summary
5-azacytidine activated WRKY103 expression in diploids.
- Taxon
- Chrysanthemum lavandulifoliumChrysanthemum lavandulifoliumt0
- Treatment
- 5-azacytidine treatmente0
- Gene
- WRKY103e0
- Outcome
- WRKY103 expressione0
- Direction
- activatinge0
- Comparator
- tetraploid phenotypee0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“Chemical inhibition of DNA methylation (5-azacytidine treatment) in diploid plants mimics the tetraploid phenotype by activating WRKY103 expression and enhancing resistance.”
t0“in Chrysanthemum lavandulifolium”
Claim · model-written summary
5-azacytidine increased resistance in diploids.
- Taxon
- Chrysanthemum lavandulifoliumChrysanthemum lavandulifoliumt0
- Treatment
- 5-azacytidine treatmente0
- Outcome
- resistancee0
- Direction
- enhancinge0
- Comparator
- tetraploid phenotypee0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“Chemical inhibition of DNA methylation (5-azacytidine treatment) in diploid plants mimics the tetraploid phenotype by activating WRKY103 expression and enhancing resistance.”
t0“in Chrysanthemum lavandulifolium”
Claim · model-written summary
The epigenetic mechanism was conserved across chrysanthemum species.
- Taxon
- chrysanthemum species
.jpeg?width=60)
Chrysanthemume0 - Outcome
- epigenetic regulatory mechanisme0
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
.jpeg?width=500)
Verbatim
e0“This epigenetic regulatory mechanism is conserved across diverse chrysanthemum species”