Beet mild yellowing virus (BMYV, genus Polerovirus, family Solemoviridae) is one among the complex of viruses causing virus yellows (VY) disease in sugar beet.
More...Beet mild yellowing virus (BMYV, genus Polerovirus, family Solemoviridae) is one among the complex of viruses causing virus yellows (VY) disease in sugar beet. It is transmitted mainly by the green peach aphid (Myzus persicae), and neonicotinoids have been used for preventing VY through aphid management. However, because of the recent ban on neonicotinoids in Europe, the risks for outbreaks of VY have increased dramatically. In the development of resistant/tolerant varieties, knowledge on host responses to the virus at the transcriptomic level would be highly useful. To study the sugar beet responses to BMYV infection and identify the differentially expressed genes (DEGs), we conducted an RNAseq experiment using a wild resistant and a susceptible genotype. The experiment contained three treatments: exposure to aphids with virus, aphids without virus and only insecticide spray. Ten aphids were placed on each plant at the stage of the first true leaf pair. Leaves (old and young) were collected for ELISA and RNA extraction at 0, 1, 4, 14, 21 and 28 days post-inoculation (DPI). Resistant plants did not show any chlorosis even at 28 DPI, whereas susceptible plants displayed typical virus symptoms. Using ELISA and RT-qPCR, BMYV could be detected already at 1 DPI in both genotypes. At 14, 21 and 28 DPI, the virus titre in young and old leaves of the susceptible genotype was higher than in those of the resistant genotype. A significant difference in viral load between genotypes was observed only at 21 DPI in young leaves. Using RNAseq, more DEGs were identified for the susceptible genotype compared to the resistant one. In the resistant genotype, DEGs were more abundant at later time points, while in the susceptible genotype, there were more DEGs at early time points. This shows that the plant responses to virus infection appear earlier in the susceptible compared to the resistant genotype. Preliminary analyses show that some genes significantly upregulated in the resistant genotype encode proteins involved in protein processing in the ER. This could be one mechanism contributing to the absence of symptoms in this genotype. This study in sugar beet offers new insights into the transcriptomic events and genetic pathways regulating the defence response to BMYV in a partially resistant genotype. We present a set of candidate genes contributing towards partial resistance to BMYV and one of the possible mechanisms contributing to the reduced virus levels and absence of symptoms. The findings from this research could be beneficial for understanding the resistance and susceptibility to viruses in plants in general. Additionally, it will be helpful for future functional studies and breeding for resistance to one of the poleroviruses causing virus yellows disease in sugar beet.
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