Claim · model-written summary
Sequence analysis identified hssB3.0 as a new pthA homolog distinguished by tandem repeat number.
Not reportedTaxonMaterialCompoundOrgan / stageInteractorInteractor roleSecond interactorSecond interactor roleTreatmentComparatorSettingDirectionValue
Verbatim
e0“Sequence analysis revealed it to be a new member of the pthA homologs, which was almost identical in sequence to the other homologs except for the number of tandem repeats in the central region of the gene.”
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 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.
- Mechanism The hssB3.0 gene partially interrupted canker development.
- Observation Disruption of pthA-KC21 yielded virulence-deficient mutant KC21T14.