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Dynamics of Small RNA Profiles of Virus and Host Origin in Wheat Cultivars Synergistically Infected by Wheat Streak Mosaic Virus and Triticum Mosaic Virus: Virus Infection Caused a Drastic Shift in the Endogenous Small RNA Profile

机译:小麦条纹花叶病毒和小麦花叶病毒协同感染的小麦品种中病毒和宿主起源小RNA谱的动力学:病毒感染导致内源性小RNA谱急剧变化

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摘要

Co-infection of wheat (Triticum aestivum L.) by Wheat streak mosaic virus (WSMV, a Tritimovirus) and Triticum mosaic virus (TriMV, a Poacevirus) of the family Potyviridae causes synergistic interaction. In this study, the effects of the synergistic interaction between WSMV and TriMV on endogenous and virus-derived small interfering RNAs (vsiRNAs) were examined in susceptible (‘Arapahoe’) and temperature-sensitive resistant (‘Mace’) wheat cultivars at 18°C and 27°C. Single and double infections in wheat caused a shift in the profile of endogenous small RNAs from 24 nt being the most predominant in healthy plants to 21 nt in infected wheat. Massive amounts of 21 and 22 nt vsiRNAs accumulated in singly and doubly infected Arapahoe at both temperatures and in Mace at 27°C but not 18°C. The plus- and minus-sense vsiRNAs were distributed throughout the genomic RNAs in Arapahoe at both temperature regimens and in Mace at 27°C, although some regions served as hot-spots, spawning an excessive number of vsiRNAs. The vsiRNA peaks were conserved among cultivars, suggesting that the Dicer-like enzymes in susceptible and resistant cultivars similarly accessed the genomic RNAs of WSMV or TriMV. Accumulation of large amounts of vsiRNAs in doubly infected plants suggests that the silencing suppressor proteins encoded by TriMV and WSMV do not prevent the formation of vsiRNAs; thus, the synergistic effect observed is independent from RNA-silencing mediated vsiRNA biogenesis. The high-resolution map of endogenous and vsiRNAs from WSMV- and/or TriMV-infected wheat cultivars may form a foundation for understanding the virus-host interactions, the effect of synergistic interactions on host defense, and virus resistance mechanisms in wheat.
机译:小麦条纹病毒(WSMV,Tritimovirus)和小麦嵌合病毒(Potyviridae)的小麦花叶病毒(TriMV,Poacevirus)共同感染小麦(Triticum aestivum L.)会引起协同相互作用。在这项研究中,研究了易感性('Arapahoe')和温度敏感性('Mace')小麦品种在18°C下WSMV和TriMV协同相互作用对内源和病毒衍生的小干扰RNA(vsiRNA)的影响。 C和27°C。小麦的单次和两次感染导致内源性小RNA的分布从健康植物中最主要的24 nt转移到受感染小麦中的21 nt。在27°C而非18°C的温度下和梅斯州,在单个和双重感染的Arapahoe中累积了大量的21和22 nt vsiRNA。正反义vsiRNA分布在整个温度方案下的Arapahoe和27°C的梅斯地区的整个基因组RNA中,尽管某些区域是热点,产生了过多的vsiRNA。 vsiRNA峰在不同品种之间是保守的,这表明易感和抗性品种中的Dicer样酶类似地进入WSMV或TriMV的基因组RNA。在双重感染的植物中大量vsiRNA的积累表明,TriMV和WSMV编码的沉默抑制蛋白不能阻止vsiRNA的形成。因此,观察到的协同作用独立于RNA沉默介导的vsiRNA生物发生。来自WSMV和/或TriMV感染小麦品种的内源和vsiRNA的高分辨率图谱可为理解病毒与宿主之间的相互作用,协同相互作用对宿主防御的影响以及小麦的抗病毒机制奠定基础。

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