Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: November 10, 2010
Publication Date: March 1, 2011
Citation: Manfre, A.J., Glenn, D.M., Nunez, A., Moreau, R.A., Dardick, C.D. 2011. Light quantity and photosystem function mediate host susceptibility to turnip mosaic virus via a salicylic acid-independent mechanism. Molecular Plant-Microbe Interactions. 24(3):315-327. Interpretive Summary: We used modern imaging technologies to study the ability of tobacco plants to become infected by a common virus. We found that in the absence of light and when photosynthesis is blocked, the tobacco plants become sicker with the virus. Several photography studies suggested that under these conditions, the plants showed more sites of viral infection and that the infection sites developed faster. The rate of virus movement through the plant was also faster, although the rate of cell-to-cell movement appeared the same. This work also showed that certain plant defense responses are not blocked and therefore, not likely to cause these changes in the ability of the virus to infect tobacco. This work is important because it expands the current understanding of which plant defense responses are active when plants are infected by viruses, and how photosynthesis and the chloroplast are required for defense.
Technical Abstract: Evidence going as far back as the early part of the 20th century suggests that both light and chloroplast function may play key roles in host susceptibility to viruses. Despite the long history of such work, confirmation of these phenomena and a determination of the underlying mechanisms remain elusive. Here, we revisited these questions using modern imaging technologies to study the susceptibility of Nicotiana benthamiana to Turnip mosaic potyvirus (TuMV). We found that both light deficiency and photosystem impairment increased the susceptibility of N. benthamiana to TuMV infection. Time-lapse photography studies indicated that under these conditions, rub inoculated plants exhibited greater numbers of infection foci and more rapid foci development. The rate of systemic movement was also accelerated, though cell-to-cell movement appeared unchanged. Inhibition of Salicylic Acid (SA) mediated defense responses is not likely responsible for changes in susceptibility, as SA and Pr gene induction were not affected by light deficiency or chloroplast impairment, and treatment of plants with SA had no impact on TuMV infection. Taken together, these data suggest that both light and optimal chloroplast function may be important for either the establishment of TuMV replication complexes or alternatively, the activation of SA-independent defenses.