LOCAL NECROTIC SYMPTOMS ON TNVA-INOCULATED TOBACCO LEAF DOES NOT SUPPRESS SYSTEMIC SPREAD OF VIRUS INFECTION

GARCÍA LUCILA; MARANO MARIA ROSA; MARTIN ANA PAULA; MARTINEZ MARI FLORENCIA

Virtual

Congreso; LVI SAIB MEETING; 2020

SAIB SAMIGE

A successful virus infection (compatible plant?virus interaction) depends on the ability of the virus to take advantage of hostfactors and to cope 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 of biotrophic pathogen,the virus should not cause the death of the infected tissue in a susceptible host. Nevertheless, extreme symptoms of a viralinfection may lead to a rapid death of the whole plant or may infect the plant without producing any evident symptom,according if the susceptible host is sensitive or tolerant, respectively. Between those ends, pathogen develops high adaptationlevels forced by plant defense strategies that result in a wide symptoms variety. Necrotic lesions are often associated withdisease symptoms development after adapted pathogen infection, leading serious crop yield losses. Systemic necrosis incompatible 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-associatedsymptom in compatible systems are largely unknown. Tobacco necrosis virus A (TNVA) belongs to the genus Alphanecrovirusof Tombusviridae family. The viral genome consists of a single positive-sense (+) RNA of approximately 3.8 kb and containsfive open reading frames (ORFs), the 5? end of the RNA is not capped and the 3? end does not have a poly (A) tail. Symptomsof TNVA-induced disease are characterized by of necrotic lesions on inoculated leaves in a wide host range, includingAmaranthaceae, Curcubitaceaes, Brassicaceae, Fabaceae among others. Rarely, TNVA inoculation results in systemicdisease, except in Glycine max, Nicotiana benthamiana and Valerianella locusta were systemic necrotic diseases wasobserved. 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 localviral-derived siRNA, cell wall reinforcement, generation of ROS and induction of SA signaling pathway. Although TNVAnecrotic lesions resemble an HR resistance response, infectious viral particles can spread to non-inoculated leaves to stablisha systemic infection without systemic necrosis development and susceptible to a second infection. Our results suggest that alocal PTI is responsible for the necrotic cell-death and could also imply the presence of a viral protein to suppress systemicRNAi signaling or modulate the symptom remission to successfully infect the plant. Moreover, N. tobacco-TNVA interactionis an interesting system to reveal new viral mechanism to counteract plant defense responses.