03555nam a2200253 a 450000100080000000500110000800800410001910000170006024501390007726001550021630000110037152027090038265000140309165000260310565000280313165000210315965000140318065000110319465000110320570000240321670000190324070000220325970000200328121584842023-11-17       2023    bl uuuu     u00u1 u    #d1 aARENA, G. D.  aLeprose Dos CitrosbUm Estudo Dos Fatores Da Planta E Do Vírus Envolvidos Na Interação Patógeno-Hospedeiro.h[electronic resource]  aIn: SIMPÓSIO BRASILEIRO DE GENÉTICA MOLECULAR DE PLANTAS, 8. 2023, Florianópolis, SC. Anais... Florianópolis: SBG, 30 de maio a 2 jun. 2023.c2023  ap. 106  aAbstract: Citrus leprosis virus C (CiLV-C, genus Cilevirus, fam. Kitaviridae) causes citrus leprosis, a disease endemic in the Americas. Economically, citrus leprosis is the most important viral disease affecting citrus orchards in Brazil, costing millions of dollars per year for the chemical control of the viral vector, the mite Brevipalpus yothersi. Scientifically, the virus draws attention due to its atypical inability to spread systemically in any of its known plant hosts, remaining restricted to local lesions around the feeding sites of the vector. We have dissected molecular mechanisms involved in plant/CiLV-C interplay using transcriptomic and histochemical analyses. The host response to the viral infection is spearheaded by the activation of the plant immune system involving RNA silencing and salicylic acid (SA)-mediated pathways, reactive oxygen species (ROS) burst, and cell death, including the upregulation of genes involved in the hypersensitive response (HR). Moreover, the ectopic expression of CiLV-C proteins unveiled that P61, a putative glycoprotein of cileviruses, produces an HR-like and mimics the primary responses observed during plant/CiLV-C interaction, placing P61 in the epicenter of the processes leading to the HR-like symptoms associated with the virus infection. Studies on the subcellular localization of CiLV-C proteins showed that P61 accumulates in the ER lumen, likely causing its disruption. Disturbance of the ER by P61 raised the hypothesis that P61 induces an unmitigated ER stress which, in turn, triggers the HR-like. Upon ER stress, plant cells induce unfolded protein response (UPR) to restore the ER homeostasis; instead, the inability to revert the ER stress may lead to plant cell death, a process interconnected with the SA pathway. In this study, we have confirmed the occurrence of ER stress and the upregulation of UPR marker genes after the transient expression of P61. Accordingly, expression of a truncated version of P61, lacking its signal peptide, drastically reduced both the cell death phenotype and transcript levels of HR and ER marker genes, suggesting that P61 entry into the ER is essential for triggering the HR-like response. Conversely, the expression of P61 in nahG transgenic plants caused an enhanced cell death phenotype and stronger induction of HR and UPR marker genes. The spliced form of the bZIP60 mRNA,which characterizes the activation of the UPR pathway during plant virus infection, was also detected in P61- expressing plants. Altogether, our findings support the involvement of ER stress in the development of the HR-like in presence of P61 and, hypothetically, in the symptoms caused by the CiLV-C infection.  aCilevirus  aEndoplasmic reticulum  aHypersensitive response  aLeprose Cítrica  aPatógeno  aPlanta  aVírus1 aGONZÁLEZ, P. L. R.1 aMARTINELLI, G.1 aREZENDE, J. A. M.1 aASTUA, J. de F.