Liebe Sebastian, Maiss Edgar, Varrelmann Mark
Department of Phytopathology, Institute of Sugar Beet Research, Göttingen, Germany.
Department of Phytomedicine, Plant Virology, Institute of Horticultural Production Systems, Leibniz University, Hannover, Germany.
Front Plant Sci. 2023 Mar 31;14:1098786. doi: 10.3389/fpls.2023.1098786. eCollection 2023.
Beet necrotic yellow vein virus (BNYVV) causes rhizomania disease in sugar beet (), which is controlled since more than two decades by cultivars harboring the resistance gene. The development of resistance-breaking strains has been favored by a high selection pressure on the soil-borne virus population. Resistance-breaking is associated with mutations at amino acid positions 67-70 (tetrad) in the RNA3 encoded pathogenicity factor P25 and the presence of an additional RNA component (RNA5). However, natural BNYVV populations are highly diverse making investigations on the resistance-breaking mechanism rather difficult. Therefore, we applied a reverse genetic system for BNYVV (A type) to study resistance-breaking by direct agroinoculation of sugar beet seedlings. The bioassay allowed a clear discrimination between susceptible and resistant plants already four weeks after infection, and resistance-breaking was independent of the sugar beet genotype. A comprehensive screen of natural tetrads for resistance-breaking revealed several new mutations allowing BNYVV to overcome . The supplementation of an additional RNA5 encoding the pathogenicity factor P26 allowed virus accumulation in the genotype independent of the P25 tetrad. This suggests the presence of two distinct resistance-breaking mechanisms allowing BNYVV to overcome . Finally, we showed that the resistance-breaking effect of the tetrad and the RNA5 is specific to and has no effect on the stability of the second resistance gene . Consequently, double resistant cultivars (+) should provide effective control of resistance-breaking strains. Our study highlights the flexibility of the viral genome allowing BNYVV to overcome host resistance, which underlines the need for a continuous search for alternative resistance genes.
甜菜坏死黄脉病毒（BNYVV）会引发甜菜的根腐病，二十多年来一直通过携带抗性基因的品种来控制该病。土壤传播的病毒群体面临的高选择压力促进了抗性突破株系的发展。抗性突破与RNA3编码的致病因子P25中氨基酸位置67 - 70（四联体）的突变以及额外RNA组分（RNA5）的存在有关。然而，天然的BNYVV群体高度多样化，使得对抗性突破机制的研究相当困难。因此，我们应用了针对BNYVV（A型）的反向遗传系统，通过直接农杆菌接种甜菜幼苗来研究抗性突破。生物测定在感染后四周就能清晰区分易感和抗性植株，且抗性突破与甜菜基因型无关。对天然四联体进行全面的抗性突破筛选，发现了几个新的突变，使BNYVV能够克服抗性。补充编码致病因子P26的额外RNA5能使病毒在基因型中积累，而与P25四联体无关。这表明存在两种不同的抗性突破机制，使BNYVV能够克服抗性。最后，我们表明四联体和RNA5的抗性突破效应具有特异性，对第二个抗性基因的稳定性没有影响。因此，双抗性品种（+）应能有效控制抗性突破株系。我们的研究突出了病毒基因组的灵活性，使BNYVV能够克服宿主抗性，这强调了持续寻找替代抗性基因的必要性。
