The dependence of leaf senescence on the balance between 1-aminocyclopropane-1-carboxylate acid synthase 1 (ACS1) -catalyzed 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 (ACSs), and NO production is controlled by NO-associated 1 (NOA1). However, the integration mechanisms of ACSs and NOA1 activity still needs to be explored during leaf senescence. Here using some experimental techniques, such as physiological and molecular detection, liquid chromatograph-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, and 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 these were compared with wild type (WT). But the leaf senescence promoted by the NO-deficiency noa1 mutant was not involved in the ACS1 expression. There was a similar sharp reduction of the ACS1 and NOA1 expression with the increase of WT leaf age, and this inflection point appeared in mature leaves, and coincided with the onset of leaf senescence. These findings suggested that NOA1-dependent NO accumulation blocked the ACS1-induced onset of leaf senescence, and that ACS1 activity corresponded to the onset of leaf senescence in Arabidopsis. This article is protected by copyright. All rights reserved.