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

GARCIA, LUCILA; ANA PAULA MARTIN; MARTINEZ, MA. FLORENCIA; MARANO, MA. ROSA

Congreso; LVI SAIB Meeting ? XV SAMIGE 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 virusshould not cause the death of the infected tissue in a susceptible host. Nevertheless, extreme symptoms of a viral infection maylead to a rapid death of the whole plant or may infect the plant without producing any evident symptom, according if thesusceptible host is sensitive or tolerant, respectively. Between those ends, pathogen develops high adaptation levels forced byplant defense strategies that result in a wide symptoms variety. Necrotic lesions are often associated with disease symptomsdevelopment after adapted pathogen infection, leading serious crop yield losses. Systemic necrosis in compatible interactionsexhibits both features and signaling pathways associated with a hypersensitive response (HR) induction, resembling an effectortrigger immune (ETI) response. Molecular processes underlying local necrosis-associated symptom in compatible systems arelargely unknown. Tobacco necrosis virus A (TNVA) belongs to the genus Alphanecrovirus of Tombusviridae family. The viralgenome consists of a single positive-sense (+) RNA of approximately 3.8 kb and contains five open reading frames (ORFs), the5? end of the RNA is not capped and the 3? end does not have a poly (A) tail. Symptoms of TNVA-induced disease arecharacterized by of necrotic lesions on inoculated leaves in a wide host range, including Amaranthaceae, Curcubitaceaes,Brassicaceae, Fabaceae among others. Rarely, TNVA inoculation results in systemic disease, except in Glycine max, Nicotianabenthamiana and Valerianella locusta were systemic necrotic diseases was observed. In this work, we have characterized themechanisms underlying TNVA-induced local necrosis symptoms in N. tabacum. We show that the necrotic local lesion involvesa plant defense response associated with the accumulation of local viral-derived siRNA, cell wall reinforcement, generation ofROS and induction of SA signaling pathway. Although TNVA-necrotic lesions resemble an HR resistance response, infectiousviral particles can spread to non-inoculated leaves to stablish a systemic infection without systemic necrosis development andsusceptible to a second infection. Our results suggest that a local PTI is responsible for the necrotic cell-death and could alsoimply the presence of a viral protein to suppress systemic RNAi signaling or modulate the symptom remission to successfullyinfect the plant. Moreover, N. tobacco-TNVA interaction is an interesting system to reveal new viral mechanism to counteractplant defense responses.