A New branch of endoplasmic reticulum stress signaling and the osmotic signal converge on Plant-specific Asparagine-rich proteins to promote cell death

• Autor(a) principal: Costa, Maximiller D. L.
• Data de Publicação: 2008
• Outros Autores: Reis, Pedro A. B., Valente, Maria Anete S., Irsigler, André S. T., Carvalho, Claudine M., Loureiro, Marcelo E., Aragão, Francisco J. L., Boston, Rebecca S., Fietto, Luciano G., Fontes, Elizabeth P. B.
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: LOCUS Repositório Institucional da UFV
• Texto Completo: https://doi.org/10.1074/jbc.M802654200; http://www.locus.ufv.br/handle/123456789/19047
• topic: Endoplasmic reticulum; Asparagine-rich

NRPs (N-rich proteins) were identified as targets of a novel adaptive pathway that integrates endoplasmic reticulum (ER) and osmotic stress signals based on coordinate regulation and synergistic up-regulation by tunicamycin and polyethylene gly- col treatments. This integrated pathway diverges from the molecular chaperone-inducing branch of the unfolded protein response (UPR) in several ways. While UPR-specific targets were inversely regulated by ER and osmotic stresses, NRPs required both signals for full activation. Furthermore, BiP (binding protein) overexpression in soybean prevented activa- tion of the UPR by ER stress inducers, but did not affect activa- tion of NRPs. We also found that this integrated pathway trans- duces a PCD signal generated by ER and osmotic stresses that result in the appearance of markers associated with leaf senes- cence. Overexpression of NRPs in soybean protoplasts induced caspase-3-like activity and promoted extensive DNA fragmen- tation. Furthermore, transient expression of NRPs in planta caused leaf yellowing, chlorophyll loss, malondialdehyde pro- duction, ethylene evolution, and induction of the senescence marker gene CP1. This phenotype was alleviated by the cytoki- nin zeatin, a potent senescence inhibitor. Collectively, these results indicate that ER stress induces leaf senescence through activation of plant-specific NRPs via a novel branch of the ER stress response.