ArticleNature communications2024
ZmGDIα-hel counters the RBSDV-induced reduction of active gibberellins to alleviate maize rough dwarf virus disease.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Blue Light Receptor PHR2-Mediated Spectrum Antiviral Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ZmNPSN13 Potentiates Maize Rough Dwarf Disease Upon Recruitment by the RBSDV P7-1 Effector.Molecular plant pathology · 2026Article
- Yeast-Secreted Protein PgSCP and Citrus Transcription Factor CsMIKC Synergize to Activate Green Mould Resistance in Fruit.Molecular plant pathology · 2025Article
- Gibberellin-mediated internode elongation in grasses with a focus on bamboo: molecular pathways and regulatory networks.Frontiers in plant science · 2025Review
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Authors and funding
10 authors.
Funding
Abstract
Maize rough dwarf disease (MRDD) threatens maize production globally. The P7-1 effector of the rice black-streaked dwarf virus (RBSDV) targets maize Rab GDP dissociation inhibitor alpha (ZmGDIα) to cause MRDD. However, P7-1 has difficulty recruiting a ZmGDIα variant with an alternative helitron-derived exon 10 (ZmGDIα-hel), resulting in recessive resistance. Here, we demonstrate that P7-1 can recruit another maize protein, gibberellin 2-oxidase 13 (ZmGA2ox7.3), which also exhibits tighter binding affinity for ZmGDIα than ZmGDIα-hel. The oligomerization of ZmGA2ox7.3 is vital for its function in converting bioactive gibberellins into inactive forms. Moreover, the enzymatic activity of ZmGA2ox7.3 oligomers increases when forming hetero-oligomers with P7-1/ZmGDIα, but decreases when ZmGDIα-hel replaces ZmGDIα. Viral infection significantly promotes ZmGA2ox7.3 expression and oligomerization in ZmGDIα-containing susceptible maize, resulting in reduced bioactive GA
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