Claim · model-written summary
Arabidopsis plants expressing Hg30C02-complementary dsRNA strongly resisted H. schachtii infection.
- Taxon
- Arabidopsis
Arabidopsise0 - Treatment
- expressed dsRNA and its processed small interfering RNA complementary to the Hg30C02 sequencee0
- Interactor
- H. schachtiiHeterodera schachtiie0pathogen
- Outcome
- resistance to infectione0
- Direction
- stronge0
- Comparator
- non-transformed plantse0
Not reportedMaterialGeneCompoundOrgan / stageSecond interactorSecond interactor roleSettingValueQualifier
Organisms pictured · Representative pictures of the matched species, not figures from the paper.
Verbatim
e0“Arabidopsis plants that expressed dsRNA and its processed small interfering RNA complementary to the Hg30C02 sequence were not phenotypically different from non-transformed plants, but they exhibited a strong RNA interference-mediated resistance to infection by H. schachtii”
Title
Noureddine Hamamouch; Chunying Li; Tarek Hewezi; et al. Journal of Experimental Botany 2012. doi:10.1093/jxb/ers058
Other claims from this paper (9)
- Intervention effect Hg30C02 expression did not affect Arabidopsis growth and development.
- Intervention effect Hg30C02 expression increased Arabidopsis susceptibility to H. schachtii infection.
- Observation The 30C02 protein interacted with host AT4G16260 β-1,3-endoglucanase in yeast and plant cells.
- Observation Peak nematode 30C02 and plant-root At4g16260 expression coincided around 3–5 days after infection.
- Observation Relative At4g16260 expression declined significantly after the coincident peak.
- Observation An Arabidopsis At4g16260 T-DNA mutant had increased susceptibility to cyst nematode infection.
- Observation At4g16260-overexpressing plants had reduced nematode susceptibility.
- Intervention effect Arabidopsis plants expressing Hg30C02-complementary dsRNA showed no phenotype difference from non-transformed plants.
- Mechanism The authors infer that nematode suppression of host defense supports parasitism and offers a target to disrupt it.