Claim · model-written summary
The hssB3.0 gene partially interrupted canker development.
Not reportedTaxonMaterialCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleTreatmentComparatorSettingValueQualifier
Verbatim
e0“hssB3.0 induces a defense response on the host but partially interrupts canker development elicited by the pathogenicity gene in this bacterium.”
Title
Hiroshi Shiotani; Takashi Fujikawa; Hiromichi Ishihara; et al. Journal of Bacteriology 2007. doi:10.1128/jb.01790-06
Other claims from this paper (9)
- Observation Bacterial strains differed in aggressiveness on Citrus grandis but not Citrus sinensis.
- Observation Mutant KC21T46 regained normal aggressiveness on a C. grandis cultivar.
- Mechanism Inactivated hssB3.0 was responsible for suppressed virulence on C. grandis.
- Observation Sequence analysis identified hssB3.0 as a new pthA homolog distinguished by tandem repeat number.
- Observation hssB3.0 appears to be a chimera of pB3.1 and pB3.7.
- Mechanism hssB3.0 may have arisen through recombination between pB3.1 and pB3.7.
- Association hssB3.0 occurred in every tested weakly aggressive isolate and no normally aggressive isolate.
- Mechanism The hssB3.0 gene induced a defense response in the host.
- Observation Disruption of pthA-KC21 yielded virulence-deficient mutant KC21T14.