Local necrotic symptoms on TNVA-inoculated tobacco leaf does not suppress systemic spread of virus infection.

GARCIA L.; MARTIN A.P.; MARTINEZ M.F.,; MARANO M.R.

Virtual

Congreso; LVI Reunion Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular (SAIB)- Asociacion Civil de Microbiología General (SAMIGE).; 2020

SAIB-SAMIGE

A successful virus infection (compatible plant?virus interaction) depends on the ability of the virus to take advantage of host factors and to cope with the antiviral plant defense responses (host susceptibility), either inhibiting the small interfering RNAs (siRNA) biogenesis or suppressing plant trigger immunity (PTI). Consequently, due to its condition as a biotrophic pathogen, the virus should not cause the death of the infected tissue in a susceptible host. Nevertheless, extreme symptoms of a viral infection may lead to rapid death of the whole plant or may infect the plant without producing any evident symptom, according to if the susceptible host is sensitive or tolerant, respectively. Between those ends, the pathogen develops high adaptation levels forced by plant defense strategies that result in a wide symptoms variety. Necrotic lesions are often associated with disease symptoms development after adapted pathogen infection, leading to serious crop yield losses. Systemic necrosis, in compatible interactions, exhibits both features and signaling pathways associated with a hypersensitive response (HR) induction, resembling an effector trigger immune (ETI) response. Molecular processes underlying local necrosis-associated symptoms in compatible systems are largely unknown. Tobacco necrosis virus A (TNVA) belongs to the genus Alphanecrovirus of Tombusviridae family. The viral genome consists of a single positive-sense (+) RNA of approximately 3.8 kb and contains five open reading frames (ORFs), the 5? end of the RNA is not capped, and the 3? end does not have a poly (A) tail. Symptoms of TNVA-induced disease are characterized by necrotic lesions on inoculated leaves in a wide host range, including Amaranthaceae, Curcubitaceae, Brassicaceae, Fabaceae, among others. Rarely, TNVA inoculation results in systemic disease, except in Glycine max, Nicotiana benthamiana, and Valerianella locusta where systemic necrotic diseases were observed. In this work, we have characterized the mechanisms underlying TNVA-induced local necrosis symptoms in N. tabacum. We show that the necrotic local lesion involves a plant defense response associated with the accumulation of local viral-derived siRNA, cell wall reinforcement, generation of ROS, and induction of the SA signaling pathway. Although TNVA-necrotic lesions resemble an HR resistance response, infectious viral particles can spread to non-inoculated leaves to establish a systemic infection without systemic necrosis development and susceptible to a second infection. Our results suggest that a local PTI is responsible for the necrotic cell death and could also imply the presence of a viral protein to suppress systemic RNAi signaling or modulate the symptom remission to successfully infect the plant. Moreover, N. tabacum-TNVA interaction is an interesting system to reveal new viral mechanisms to counteract plant defense responses.