Characterization of Oryza rufipogon–Derived Resistance to Tungro Disease in Rice

Abstract

Rice tungro disease (RTD) is caused by the interaction between Rice tungro spherical virus (RTSV) and Rice tungro bacilliform virus (RTBV), both of which are transmitted by green leafhoppers (GLH). In order to define the resistance against RTD in rice cv. Matatag 9 which was developed by interspecific hybridization between RTD-susceptible cv. IR64 and Oryza rufipogon, the reactions of Matatag 9 to the viruses and GLH were evaluated in comparison with RTD-susceptible and -resistant rice cultivars. The incidences of infection with RTSV and RTBV in Matatag 9 were significantly lower than those in the susceptible parent cv. IR64; however, no substantial differences in virus accumulation were observed between IR64 and Matatag 9 once infected with the viruses. Symptoms in Matatag 9 infected with RTBV and RTSV were milder than those observed in IR64. A higher level of antixenosis to GLH was observed in Matatag 9 compared with IR64. The levels of antibiosis against GLH in Matatag 9 were comparable with those in another GLH-resistant cultivar, and significantly higher than those in RTD-susceptible cultivars. Collectively, these results suggest that tolerance to tungro viruses and resistance to GLH both contribute to the apparent resistance to RTD in Matatag 9, although possible involvement of other resistance mechanisms cannot be excluded.

Novel alleles of rice eIF4G generated by CRISPR/Cas9‐targeted mutagenesis confer resistance to Rice tungro spherical virus

“…The in-frame mutations found in the T 2 plants from the 1146 events and those from the 1148 events occurred further upstream or immediately downstream of the YVV (and SVLFPNLAGKS) residues. The inconclusive reactions could be a consequence of (i) minor effects on the reactions to RTSV by the mutations, (ii) moderate GLH resistance of IR64 that might prevent successful transmission of RTSV (Shibata et al, 2007;Zenna et al, 2008) or (iii) combination of both. In any case, the amino acids mutated in a nearly full-length [1918][1919][1920][1921][1922][1923][1924][1925][1926][1927] eIF4G of the T 2 plants from 1146 and 1148 events are most likely not to have a significant effect on the reactions to RTSV.…”

NbEXPA1, an α‐expansin, is plasmodesmata‐specific and a novel host factor for potyviral infection

“…In Cucumber mosaic virus (CMV)-infected N. tabacum plants, the expression levels of genes encoding expansins in LGTs are lower than those in DGIs (Chen et al, 2017). Infections by Rice dwarf virus (RDV), Rice stripe virus (RSV) and Rice tungro spherical virus (RTSV) also suppress various cell wall-related genes such as cellulose synthase, extensin and expansin, leading to the stunting phenotype (Shibata et al, 2007;Satoh et al, 2010Satoh et al, , 2011Budot et al, 2014). In rice seedlings infected by Rice grassy stunt virus (RGSV), GH3 genes are upregulated, which inhibits plant growth by suppressing expansins and auxin content (Ding et al, 2008;Domingo et al, 2009).…”

Genetic engineering of rice to resist rice tungro disease

“…The nature of breakdown of resistance to GLH causes the characteristic boom-and-bust cycles of RTD epidemics and threatens sustainable rice production (Azzam and Chancellor 2002;Mew et al 2004). In cultivars such as Matatag 9, the titer of tungro viruses can reach levels similar to that in a susceptible cultivar (Shibata et al 2007) and can serve as sources of inoculum if GLH resistance breaks down. Introduction of PDR will aid in resolving issues related to vector resistance breakdown.…”

“…IR64 and O. rufipogon, resists GLH feeding and reduces the incidence of infection with RTSV and RTBV (Shibata et al 2007). Although no substantial differences in virus accumulation were observed between susceptible cultivar IR64 and Matatag 9 following infection, RTD symptoms in Matatag 9 infected by RTBV and RTSV were significantly milder than those observed in IR64 (Shibata et al 2007). Tolerance to tungro viruses in Matatag 9 suggests that there are important specific interactions between the host and the viruses.…”