Claim · model-written summary
The effector protein SyCD1 from Saccharothrix yanglingensis Hhs.015 enters apple leaf cells.
- Taxon
- Apple
Malus domesticat0 - Organ / stage
- leaf cellse0
- Interactor
- Saccharothrix yanglingensis Hhs.015Saccharothrix longispora subsp. yanglingensise0biocontrol_agent
- Gene
- SyCD1e0
- Outcome
- enters apple ( Malus domestica ) leaf cellse0
Verbatim
t0“Apple”
e0“the effector protein SyCD1 from Saccharothrix yanglingensis Hhs.015 enters apple ( Malus domestica ) leaf cells and reduces Cu 2+ levels”
Title
Hongjia Yu; Zhouzheng Yang; Hanqi Zhou; et al. Molecular Plant Pathology 2026. doi:10.1111/mpp.70297
Other claims from this paper (10)
- Intervention effect SyCD1 reduces Cu2+ levels in apple leaf cells.
- Mechanism By reducing Cu2+, SyCD1 relieves the Cu2+-associated repression of the transcription factor MdbZIP11.
- Mechanism The Cu2+ reduction promotes the accumulation and transcriptional activation of MdbZIP11.
- Mechanism The Cu2+ reduction enables downstream activation of abscisic acid (ABA) biosynthesis-mediated immune responses.
- Observation MdbZIP11 physically interacts with the ABA-related protein kinase MdSnRK2A.
- Association The MdbZIP11-MdSnRK2A interaction is associated with phosphorylation of MdbZIP11 and increased transcriptional activity.
- Observation MdbZIP11 directly binds to the promoter of the HD-ZIP transcription factor gene MdHAT5.
- Mechanism MdbZIP11 transcriptionally activates the expression of MdHAT5 by binding its promoter.
- Mechanism MdHAT5 functions as a positive regulator of ABA accumulation and disease resistance.
- Mechanism Genetic epistasis analysis confirms that MdHAT5 is indispensable for MdbZIP11-mediated ABA accumulation and disease resistance.