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1.
Plant Biol (Stuttg) ; 21(4): 595-603, 2019 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-30734982

RESUMEN

Ethylene and nitric oxide (NO) act as endogenous regulators during leaf senescence. Levels of ethylene or its precursor 1-aminocyclopropane-1-carboxylate acid (ACC) depend on the activity of ACC synthases (ACS), and NO production is controlled by NO-associated 1 (NOA1). However, the integration mechanisms of ACS and NOA1 activity still need to be explored during leaf senescence. Here, using experimental techniques, such as physiological and molecular detection, liquid chromatography-tandem mass spectrometry and fluorescence measurement, we investigated the relevant mechanisms. Our observations showed that the loss-of-function acs1-1 mutant ameliorated age- or dark-induced leaf senescence syndrome, such as yellowing and loss of chlorophyll, that acs1-1 reduced ACC accumulation mainly in mature leaves and that acs1-1-promoted NOA1 expression and NO accumulation mainly in juvenile leaves, when compared with the wild type (WT). But the leaf senescence promoted by the NO-deficient noa1 mutant was not involved in ACS1 expression. There was a similar sharp reduction of ACS1 and NOA1 expression with the increase in WT leaf age, and this inflection point appeared in mature leaves and coincided with the onset of leaf senescence. These findings suggest that NOA1-dependent NO accumulation blocked the ACS1-induced onset of leaf senescence, and that ACS1 activity corresponds to the onset of leaf senescence in Arabidopsis.


Asunto(s)
Aminoácidos Cíclicos/metabolismo , Proteínas de Arabidopsis/fisiología , Arabidopsis/crecimiento & desarrollo , Liasas/metabolismo , Óxido Nítrico Sintasa/metabolismo , Óxido Nítrico/metabolismo , Hojas de la Planta/crecimiento & desarrollo , Arabidopsis/enzimología , Arabidopsis/metabolismo , Proteínas de Arabidopsis/metabolismo , Clorofila/metabolismo , Glucuronidasa/metabolismo , Liasas/fisiología , Óxido Nítrico Sintasa/fisiología , Hojas de la Planta/enzimología , Hojas de la Planta/metabolismo , Transcriptoma
2.
Transl Psychiatry ; 6(9): e892, 2016 09 13.
Artículo en Inglés | MEDLINE | ID: mdl-27622936

RESUMEN

Wnts-related signaling pathways have been reported to play roles in the pathogenesis of stress-induced depression-like behaviors. However, there is relatively few direct evidence to indicate the effect of Wnt ligands on this process. Here, we investigated the role of Wnts in mediating chronic restraint stress (CRS)-induced depression-like behaviors. We found that CRS induced a significant decrease in the expression of Wnt2 and Wnt3 in the ventral hippocampus (VH) but not in the dorsal hippocampus. Knocking down Wnt2 or Wnt3 in the VH led to impaired Wnt/ß-catenin signaling, neurogenesis deficits and depression-like behaviors. In contrast, overexpression of Wnt2 or Wnt3 reversed CRS-induced depression-like behaviors. Moreover, Wnt2 and Wnt3 activated cAMP response element-binding protein (CREB) and there was CREB-dependent positive feedback between Wnt2 and Wnt3. Finally, fluoxetine treatment increased Wnt2 and Wnt3 levels in the VH and knocking down Wnt2 or Wnt3 abolished the antidepressant effect of fluoxetine. Taken together, our study indicates essential roles for Wnt2 and Wnt3 in CRS-induced depression-like behaviors and antidepressant.


Asunto(s)
Conducta Animal , Depresión/genética , Hipocampo/metabolismo , Estrés Psicológico/genética , Proteína wnt2/genética , Proteína Wnt3/genética , Animales , Antidepresivos de Segunda Generación/farmacología , Proteína de Unión a Elemento de Respuesta al AMP Cíclico/metabolismo , Depresión/metabolismo , Fluoxetina/farmacología , Técnicas de Silenciamiento del Gen , Hipocampo/efectos de los fármacos , Masculino , Ratones , Neurogénesis/genética , Restricción Física , Estrés Psicológico/metabolismo , Vía de Señalización Wnt , Proteína wnt2/efectos de los fármacos , Proteína wnt2/metabolismo , Proteína Wnt3/efectos de los fármacos , Proteína Wnt3/metabolismo
3.
J Forensic Sci ; 37(2): 585-9, 1992 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-1500900

RESUMEN

This paper reports on the disaster that occurred after a flight was hijacked at Baiyuen International Airport in Guangzhou, China, on Tuesday, 2 Oct. 1990. The authors show the results of analyses for the causes of death and trauma and compare the disaster with several previous flight accidents that have occurred in China. The authors show, with the analysis on this accident, the possibility and reliability of reconstructing a disaster by medicolegal investigation.


Asunto(s)
Accidentes de Aviación , Causas de Muerte , Medicina Legal/métodos , Heridas y Lesiones/etiología , Adolescente , Adulto , Anciano , Niño , China , Femenino , Humanos , Masculino , Persona de Mediana Edad
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