Evaluation of the role of rice transcription factors RF2A and RF2B in the development of rice tungro disease

Tungro disease remains a very important disease in rice. Specific regions in the tungro virus genome interact with host proteins resulting in the development of disease symptoms. It is possible that endogenous transcription factors RF2a and RF2b become sequestered by the viruses during infection and their limiting status disrupts plant development and causes disease symptoms. To test this hypothesis, four Taipei 309- derived transgenic rice lines over-expressing RF2a and RF2b together with wild type, resistant and susceptible controls were infected with viruliferous green leafhopper 25 days after sowing. Symptom development and ELISA index for the two viruses were monitored at 0,1,2,3,4,5,6,7 and 30 days after inoculation. No remarkable differences among all the test entries in terms of RTBV titer were evident until four days after inoculation (DAI). Wild type TP309, however, showed increased RTBV titer starting at 6 DAI that eventually went down to a level similar to the other entries at 30 DAI. For RTSV, a more divergent pattern was observed among the entries and even among the over-expression lines. TP309 showed a trend similar to most of the over-expression lines until 4 DAI but this was followed by a distinct elevated RTSV titer starting at 6 up to 30 DAI. Most of the transgenic plants recovered from tungro damage at 30 DAI. With a rating of moderately resistant, all the transgenic lines had relatively better reaction to the disease compared to wild type Taipei 309. Some individual transgenic plants had better reaction to the disease. It was evident that among the four entries tested, line RbMT6 had the highest number of plants that did not show tungro symptoms at 34.6% uninfected plants as opposed to 26.1% in Matatag 6, the resistant check. Based on these results the improved resistance of transgenic lines suggests that over-expressing Rf2a and Rf2b transcription factors in the plant may minimize the development of the disease symptoms.