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1.
Plant Cell Rep ; 41(8): 1733-1750, 2022 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-35751667

RESUMO

KEY MESSAGE: Fumonisin B1 induces rapid programmed cell death in Arabidopsis cells, oxidative and nitrosative bursts, and differentially modulates cell death responsive genes. Glutathione is the main antioxidant involved in the stress response. Fumonisin B1 (FB1) is a fungal toxin produced by Fusarium spp. able to exert pleiotropic toxicity in plants. FB1 is known to be a strong inducer of the programmed cell death (PCD); however, the exact mechanism underling the plant-toxin interactions and the molecular events that lead to PCD are still unclear. Therefore, in this work, we provided a comprehensive investigation of the response of the model organism Arabidopsis thaliana at the nuclear, transcriptional, and biochemical level after the treatment with FB1 at two different concentrations, namely 1 and 5 µM during a time-course of 96 h. FB1 induced oxidative and nitrosative bursts and a rapid cell death in Arabidopsis cell cultures, which resembled a HR-like PCD event. Different genes involved in the regulation of PCD, antioxidant metabolism, photosynthesis, pathogenesis, and sugar transport were upregulated, especially during the late treatment time and with higher FB1 concentration. Among the antioxidant enzymes and compounds studied, only glutathione appeared to be highly induced in both treatments, suggesting that it might be an important stress molecule induced during FB1 exposure. Collectively, these findings highlight the complexity of the signaling network of A. thaliana and provide information for the understanding of the physiological, molecular, and biochemical responses to counteract FB1-induced toxicity.


Assuntos
Arabidopsis , Fumonisinas , Micotoxinas , Antioxidantes/metabolismo , Arabidopsis/metabolismo , Técnicas de Cultura de Células , Morte Celular , Fumonisinas/metabolismo , Fumonisinas/toxicidade , Glutationa/metabolismo , Micotoxinas/metabolismo , Micotoxinas/toxicidade , Estresse Oxidativo
2.
Biomolecules ; 9(11)2019 10 24.
Artigo em Inglês | MEDLINE | ID: mdl-31653042

RESUMO

Heavy metal pollution is an increasing global concern. Among heavy metals, mercury (Hg) is especially dangerous because of its massive release into the environment and high toxicity, especially for aquatic organisms. The molecular response mechanisms of algae to Hg exposure are mostly unknown. Here, we combine physiological, biochemical, and transcriptomic analysis to provide, for the first time, a comprehensive view on the pathways activated in Chromera velia in response to toxic levels of Hg. Production of hydrogen peroxide and superoxide anion, two reactive oxygen species (ROS), showed opposite patterns in response to Hg2+ while reactive nitrogen species (RNS) levels did not change. A deep RNA sequencing analysis generated a total of 307,738,790 high-quality reads assembled in 122,874 transcripts, representing 89,853 unigenes successfully annotated in databases. Detailed analysis of the differently expressed genes corroborates the biochemical results observed in ROS production and suggests novel putative molecular mechanisms in the algal response to Hg2+. Moreover, we indicated that important transcription factor (TF) families associated with stress responses differentially expressed in C. velia cultures under Hg stress. Our study presents the first in-depth transcriptomic analysis of C. velia, focusing on the expression of genes involved in different detoxification defense systems in response to heavy metal stress.


Assuntos
Alveolados/efeitos dos fármacos , Mercúrio/toxicidade , Transcriptoma/efeitos dos fármacos , Poluentes Químicos da Água/toxicidade , Alveolados/genética , Alveolados/crescimento & desenvolvimento , Alveolados/metabolismo , Clorofila/metabolismo , Peróxido de Hidrogênio/metabolismo , Espécies Reativas de Nitrogênio/metabolismo , Espécies Reativas de Oxigênio/metabolismo
3.
Plant Physiol Biochem ; 135: 359-371, 2019 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-30612058

RESUMO

Hydrogen sulfide (H2S) has been recently found as an important signaling molecule especially in root system architecture of plants. The regulation of root formation through H2S has been reported in previous works; while the profiling of metabolites in response to H2S is not clearly discussed. To this end, different concentrations of sodium hydrosulfide (an H2S donor) were applied to the culture of Linum album hairy roots. Subsequently, the amino acid profiles, soluble carbohydrates, and central intermediates of phenylpropanoid pathway with two branches of lignans and flavonoids were assessed by spectroscopy and high performance liquid chromatography techniques. An analysis of the signaling molecules (nitric oxide, hydrogen peroxide, and salicylic acid) was also conducted as they proposed to act in conjunction with H2S. The H2S activated antioxidant systems and caused a shift from flavonoid to lignan production (podophyllotoxin and 6-methoxypodophyllotoxin); although, some of the flavonoids increased in a dose-dependent manner. The H2S decreased the contents of phenylalanine and tyrosine as substrates of the phenylpropanoid pathway, but increased proline and histidine as an osmolyte and antioxidant, respectively. These findings propose that H2S modulates other signaling molecules, regulates free amino acids, and mediates biosynthesis of lignans and flavonoids in the phenylpropanoids biosynthesis pathway.


Assuntos
Linho/metabolismo , Sulfeto de Hidrogênio/farmacologia , Lignanas/biossíntese , Raízes de Plantas/metabolismo , Aminoácidos/análise , Aminoácidos/metabolismo , Metabolismo dos Carboidratos/efeitos dos fármacos , Carboidratos/análise , Cromatografia Líquida de Alta Pressão , Relação Dose-Resposta a Droga , Flavonoides/análise , Flavonoides/metabolismo , Linho/química , Linho/efeitos dos fármacos , Peróxido de Hidrogênio/análise , Peróxido de Hidrogênio/metabolismo , Nitritos/análise , Nitritos/metabolismo , Raízes de Plantas/química , Raízes de Plantas/efeitos dos fármacos , Prolina/análise , Prolina/metabolismo , Análise Espectral
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