The dependence of leaf senescence on the balance between 1-aminocyclopropane-1-carboxylate acid synthase 1 (ACS1)-catalysed ACC generation and nitric oxide-associated 1 (NOS1)-dependent NO accumulation in Arabidopsis.

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.

The antidepressant roles of Wnt2 and Wnt3 in stress-induced depression-like behaviors.

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.

Correlation of trauma and cause of death to accident reconstruction: a case of a flight accident report.

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.