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OsHRZ1 negatively regulates rice resistant to Magnaporthe oryzae infection by targeting OsVOZ2
Rice blast disease caused by Magnaporthe oryzae significantly reduces yield production. Blast resistance is closely associated with iron (Fe) status, but the mechanistic basis linking iron status to immune function in rice remains largely unknown. Here, iron-binding haemerythrin RING ubiquitin ligas...
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Published in: | Transgenic research 2024-10, Vol.33 (5), p.489-501 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites |
Online Access: | Get full text |
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Summary: | Rice blast disease caused by
Magnaporthe oryzae
significantly reduces yield production. Blast resistance is closely associated with iron (Fe) status, but the mechanistic basis linking iron status to immune function in rice remains largely unknown. Here, iron-binding haemerythrin RING ubiquitin ligases OsHRZ1 was confirmed to play key roles in iron-mediated rice blast resistance. The expression of
OsHRZ1
was suppressed by
M. oryzae
inoculation and high iron treatment. Both mutants of
OsHRZ1
enhanced rice resistance to
M. oryzae
.
OsPR1a
was up-regulated in
OsHRZ1
mutants. Yeast two-hybrid, bimolecular fluorescence complementation, and Co-IP assay results indicated that OsHRZ1 interacts with Vascular Plant One Zinc Finger 2 (OsVOZ2) in the nucleus. Additionally, the vitro ubiquitination assay indicated that OsHRZ1 can ubiquitinate OsVOZ2 and mediate the degradation of OsVOZ2. The mutants of OsVOZ2 showed reduced resistance to
M. oryzae
and down-regulated the expression of
OsPR1a
. Yeast one-hybrid, EMSA, and dual-luciferase reporter assay results indicated that OsVOZ2 directly binds to the promoter of
OsPR1a
, activating its expression. In summary, OsHRZ1 plays an important role in rice disease resistance by mediated degradation of OsVOZ2 thus shaping PR gene expression dynamics in rice cells. This highlights an important link between iron signaling and rice pathogen defenses. |
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ISSN: | 0962-8819 1573-9368 1573-9368 |
DOI: | 10.1007/s11248-024-00415-8 |