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URI permanente para esta coleçãohttps://locus.ufv.br/handle/123456789/11847

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    N-rich protein (NRP)-mediated cell death signaling: a new branch of the ER stress response with implications for plant biotechnology
    (Plant Signaling & Behavior, 2012-06-01) Reis, Pedro A.B.; Fontes, Elizabeth P.B.
    Upon disruption of ER homeostasis, plant cells activate at least two branches of the unfolded protein response (UPR) through IRE1-like and ATAF6-like transducers, resulting in the upregulation of ER-resident molecular chaperones and the activation of the ER-associated degradation protein system. Here, we discuss a new ER stress response pathway in plants that is associated with an osmotic stress response in transducing a cell death signal. Both ER and osmotic stress induce the expression of the novel transcription factor GmERD15, which binds and activates N-rich protein (NRP) promoters to induce NRP expression and cause the upregulation of GmNAC6, an effector of the cell death response. In contrast to this activation mechanism, the ER-resident molecular chaperone binding protein (BiP) attenuates the propagation of the cell death signal by modulating the expression and activity of components of the ER and osmotic stress-induced NRP-mediated cell death signaling. This interaction attenuates dehydration-induced cell death and promotes a better adaptation of BiP-overexpressing transgenic lines to drought.
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    Sustained NIK-mediated antiviral signalling confers broad-spectrum tolerance to begomoviruses in cultivated plants
    (Plant Biotechnology Journal, 2015-01-06) Brustolini, Otávio J.B.; Machado, Joao Paulo B.; Condori-Apfata, Jorge A.; Coco, Daniela; Deguchi, Michihito; Loriato, Virgílio A.P.; Pereira, Welison A.; Alfenas-Zerbini, Poliane; Zerbini, Francisco M.; Inoue-Nagata, Alice K.; Santos, Anesia A.; Chory, Joanne; Silva, Fabyano F.; Fontes, Elizabeth P.B.
    Begomovirus-associated epidemics currently threaten tomato production worldwide due to the emergence of highly pathogenic virus species and the proliferation of a whitefly B biotype vector that is adapted to tomato. To generate an efficient defence against begomovirus, we modulated the activity of the immune defence receptor nuclear shuttle protein (NSP)-interacting kinase (NIK) in tomato plants; NIK is a virulence target of the begomovirus NSP during infection. Mutation of T474 within the kinase activation loop promoted the constitutive activation of NIK-mediated defences, resulting in the down-regulation of translation-related genes and the suppression of global translation. Consistent with these findings, transgenic lines harbouring an activating mutation (T474D) were tolerant to the tomato-infecting begomoviruses ToYSV and ToSRV. This phenotype was associated with reduced loading of coat protein viral mRNA in actively translating polysomes, lower infection efficiency and reduced accumulation of viral DNA in systemic leaves. Our results also add some relevant insights into the mechanism underlying the NIK-mediated defence. We observed that the mock-inoculated T474D-overexpressing lines showed a constitutively infected wild-type transcriptome, indicating that the activation of the NIK- mediated signalling pathway triggers a typical response to begomovirus infection. In addition, the gain-of-function mutant T474D could sustain an activated NIK-mediated antiviral response in the absence of the virus, further confirming that phosphorylation of Thr-474 is the crucial event that leads to the activation of the kinase.
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    N-rich protein (NRP)-mediated cell death signaling
    (Plant Signaling & Behavior, 2012-03-22) Reis, Pedro A.B.; Fontes, Elizabeth P.B.
    Upon disruption of ER homeostasis, plant cells activate at least two branches of the unfolded protein response (UPR) through IRE1-like and ATAF6-like transducers, resulting in the upregulation of ER-resident molecular chaperones and the activation of the ER-associated degradation protein system. Here, we discuss a new ER stress response pathway in plants that is associated with an osmotic stress response in transducing a cell death signal. Both ER and osmotic stress induce the expression of the novel transcription factor GmERD15, which binds and activates N-rich protein (NRP) promoters to induce NRP expression and cause the upregulation of GmNAC6, an effector of the cell death response. In contrast to this activation mechanism, the ER-resident molecular chaperone binding protein (BiP) attenuates the propagation of the cell death signal by modulating the expression and activity of components of the ER and osmotic stress-induced NRP-mediated cell death signaling. This interaction attenuates dehydration-induced cell death and promotes a better adaptation of BiP-overexpressing transgenic lines to drought.
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    The binding protein BiP attenuates stress-induced cell death in soybean via modulation of the N-Rich protein-mediated signaling pathway
    (Plant Physiology, 2011-12) Reis, Pedro A.A.; Rosado, Gustavo L.; Silva, Lucas A.C.; Oliveira, Luciana C.; Oliveira, Lucas B.; Costa, Maximiller D.L.; Alvim, Fátima C.; Fontes, Elizabeth P.B.
    The molecular chaperone binding protein (BiP) participates in the constitutive function of the endoplasmic reticulum (ER) and protects the cell against stresses. In this study, we investigated the underlying mechanism by which BiP protects plant cells from stress-induced cell death. We found that enhanced expression of BiP in soybean (Glycine max) attenuated ER stress- and osmotic stress-mediated cell death. Ectopic expression of BiP in transgenic lines attenuated the leaf necrotic lesions that are caused by the ER stress inducer tunicamycin and also maintained shoot turgidity upon polyethylene glycol-induced dehydration. BiP-mediated attenuation of stress-induced cell death was confirmed by the decreased percentage of dead cell, the reduced induction of the senescence-associated marker gene GmCystP, and reduced DNA fragmentation in BiP-overexpressing lines. These phenotypes were accompanied by a delay in the induction of the cell death marker genes N-RICH PROTEIN-A (NRP-A), NRP-B, and GmNAC6, which are involved in transducing a cell death signal generated by ER stress and osmotic stress through the NRP-mediated signaling pathway. The prosurvival effect of BiP was associated with modulation of the ER stress- and osmotic stress-induced NRP-mediated cell death signaling, as determined in transgenic tobacco (Nicotiana tabacum) lines with enhanced (sense) and suppressed (antisense) BiP levels. Enhanced expression of BiP prevented NRP- and NAC6-mediated chlorosis and the appearance of senescence-associated markers, whereas silencing of endogenous BiP accelerated the onset of leaf senescence mediated by NRPs and GmNAC6. Collectively, these results implicate BiP as a negative regulator of the stress-induced NRP-mediated cell death response.
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    Translational control in plant antiviral immunity
    (Genetics and Molecular Biology, 2016-09-27) Machado, João Paulo B.; Iara P., Calil; Santos, Anésia A.; Fontes, Elizabeth P.B.
    Due to the limited coding capacity of viral genomes, plant viruses depend extensively on the host cell machinery to support the viral life cycle and, thereby, interact with a large number of host proteins during infection. Within this context, as plant viruses do not harbor translation-required components, they have developed several strategies to subvert the host protein synthesis machinery to produce rapidly and efficiently the viral proteins. As a countermeasure against infection, plants have evolved defense mechanisms that impair viral infections. Among them, the host-mediated translational suppression has been characterized as an efficient mean to restrict infection. To specifically suppress translation of viral mRNAs, plants can deploy susceptible recessive resistance genes, which encode translation initiation factors from the eIF4E and eIF4G family and are required for viral mRNA translation and multiplication. Additionally, recent evidence has demonstrated that, alternatively to the cleavage of viral RNA targets, host cells can suppress viral protein translation to silence viral RNA. Finally, a novel strategy of plant antiviral defense based on suppression of host global translation, which is mediated by the transmembrane immune receptor NIK1 (nuclear shuttle protein (NSP)-Interacting Kinase1), is discussed in this review.
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    Early responsive to DEHYDRATION 15, a new transcription factor that integrates stress signaling pathways
    (Plant Signaling & Behavior, 2011-12-01) Alves, Murilo S.; Fontes, Elizabeth P.B.; Fietto, Luciano G.
    The Early Responsive to Dehydration (ERD) genes are defined as those genes that are rapidly activated during drought stress. The encoded proteins show a great structural and functional diversity, with a particular class of proteins acting as connectors of stress response pathways. Recent studies have shown that ERD15 proteins from different species of plants operate in cross-talk among different response pathways. In this mini-review, we show the recent progress on the functional role of this diverse family of proteins and demonstrate that a soybean ERD15 homolog can act as a connector in stress response pathways that trigger a programmed cell death signal.