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A helitron-induced RabGDIα variant causes quantitative recessive resistance to maize rough dwarf disease.
Nature Communications ( IF 14.7 ) Pub Date : 2020-01-24 , DOI: 10.1038/s41467-020-14372-3
Qingcai Liu 1 , Suining Deng 1 , Baoshen Liu 2 , Yongfu Tao 1 , Haiyue Ai 1 , Jianju Liu 1 , Yongzhong Zhang 2 , Yan Zhao 2 , Mingliang Xu 1
Affiliation  

Maize rough dwarf disease (MRDD), caused by various species of the genus Fijivirus, threatens maize production worldwide. We previously identified a quantitative locus qMrdd1 conferring recessive resistance to one causal species, rice black-streaked dwarf virus (RBSDV). Here, we show that Rab GDP dissociation inhibitor alpha (RabGDIα) is the host susceptibility factor for RBSDV. The viral P7-1 protein binds tightly to the exon-10 and C-terminal regions of RabGDIα to recruit it for viral infection. Insertion of a helitron transposon into RabGDIα intron 10 creates alternative splicing to replace the wild-type exon 10 with a helitron-derived exon 10. The resultant splicing variant RabGDIα-hel has difficulty being recruited by P7-1, thus leading to quantitative recessive resistance to MRDD. All naturally occurring resistance alleles may have arisen from a recent single helitron insertion event. These resistance alleles are valuable to improve maize resistance to MRDD and potentially to engineer RBSDV resistance in other crops.

中文翻译:

Helitron诱导的RabGDIα变体导致对玉米粗矮病的定量隐性抗性。

由各种斐济病毒属引起的玉米粗矮病(MRDD)威胁着全世界的玉米生产。我们先前确定了定量位点qMrdd1,它赋予一种因果物种水稻黑条矮化病毒(RBSDV)隐性抗性。在这里,我们显示了Rab GDP离解抑制剂α(RabGDIα)是RBSDV的宿主敏感性因子。病毒P7-1蛋白与RabGDIα的外显子10和C末端区域紧密结合,从而募集其用于病毒感染。将Helitron转座子插入RabGDIα内含子10产生替代剪接,以用Helitron衍生的外显子10替代野生型外显子10。所得的剪接变体RabGDIα-hel很难被P7-1募集,从而导致定量的隐性抗性到MRDD。所有自然产生的抗性等位基因可能是由于最近的单个高电子插入事件引起的。这些抗性等位基因对于提高玉米对MRDD的抗性以及对其他作物的RBSDV抗性具有潜在价值。
更新日期:2020-01-24
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