ZmGDIα-hel counters the RBSDV-induced reduction of active gibberellins to alleviate maize rough dwarf virus disease

Suining Deng, Siqi Jiang, Baoshen Liu, Tao Zhong, Qingcai Liu, Jianju Liu, Yuanliang Liu, Can Yin, Chen Sun and Mingliang Xu ()
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Suining Deng: China Agricultural University
Siqi Jiang: China Agricultural University
Baoshen Liu: Shandong Agricultural University
Tao Zhong: China Agricultural University
Qingcai Liu: China Agricultural University
Jianju Liu: China Agricultural University
Yuanliang Liu: China Agricultural University
Can Yin: China Agricultural University
Chen Sun: China Agricultural University
Mingliang Xu: China Agricultural University

Nature Communications, 2024, vol. 15, issue 1, 1-18

Abstract: 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 GA1/GA4 levels. This causes an auxin/cytokinin imbalance and ultimately manifests as MRDD syndrome. Conversely, in resistant maize, ZmGDIα-hel counters these virus-induced changes, thereby mitigating MRDD severity.

Date: 2024
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DOI: 10.1038/s41467-024-51726-7

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