Summary: Catalase controls cellular H₂O₂ and plays important roles in the adaptation of plants to various stresses, but little is known about the signaling events that lead to the expression of CAT1 and the production of H₂O₂. Here we report the dependence of CAT1 expression and H₂O₂ production on a mitogen‐activated protein kinase (MAPK) cascade. CAT1 transcript was induced in an ABA‐dependent way and the induction was abolished in the T‐DNA insertion mutant mkk1 (SALK_015914), while AtMKK1 overexpression significantly enhanced the ABA‐induced CAT1 expression and H₂O₂ production. AtMPK6, another component in the MAPK cascade, was also involved: mpk6 mutant blocked and overexpressing AtMPK6 enhanced the ABA‐dependent expression of CAT1 and H₂O₂ production. The activity of AtMPK6 was increased by ABA in an AtMKK1‐dependent manner. These data clearly suggest an ABA‐dependent signaling pathway connecting CAT1 expression through a phosphorelay including AtMKK1 and AtMPK6. In further support of this view, mkk1 mutant reduced both the sensitivity to ABA during germination and the drought tolerance of seedlings, whereas the AtMKK1 overexpression line showed the opposite responses when compared with the wild type. The data suggest AtMKK1–AtMPK6 to be a key module in an ABA‐dependent signaling cascade causing H₂O₂ production and stress responses.

Catalase and hydrogen peroxide (H₂O₂) have been extensively studied for their roles in various stress responses. However, little is known about the triggering mechanisms for stress-induced catalase gene expression or about H₂O₂ production as a stress signal. It is reported here that ABA-, drought-, and salt stress-induced gene expression of CAT1 catalase is mediated by AtMEK1, an Arabidopsis MAPK kinase, by triggering H₂O₂ signal production. Both CAT1 expression and AtMEK1 activity were activated by ABA, drought, and salt stresses. The mek1 mutant totally blocked stress-induced CAT1 expression and, interestingly, stress-induced H₂O₂ production was also blocked. Over-expression of AtMEK1 significantly promoted stress-induced CAT1 expression, and also promoted H₂O₂ production. These results conclusively indicate that stress-induced CAT1 expression is mediated by AtMEK1 and, furthermore, that the triggering of H₂O₂ production might be involved in this process, as further proved by the observation that CAT1 expression was induced by applied H₂O_2. Surprisingly, the signalling mechanisms for stress-induced gene expression of CAT2 and CAT3 were very different from that of CAT1. Except for drought stress, expression of CAT2 or CAT3 was also activated by salt stress or ABA treatment, and AtMEK1 was not proved to be involved in the drought-induced expression of CAT2 or CAT3. Further studies showed that stomatal movement was much less sensitive to ABA in AtMEK1 mutant (mek1), and over-expression of AtMEK1 in Arabidopsis increased plant resistance to drought or salt stress, which further demonstrated that AtMEK1 is a crucial mediator in plant stress signal transduction.

The plant hormone abscisic acid (ABA) accumulates in plant tissues which experience water deficit (stress ABA). This study analysed its accumulation as a function of both synthesis and catabolism in maize tissues. By following the disappearance of the stress ABA when ABA synthesis was blocked by nordihydroguaiaretic acid (NDGA), the rate of the catabolism of stress ABA was determined. When compared with the catabolic rate of baseline (non-stress) ABA, stress ABA showed a catabolic rate >11 times higher. With such an elevated catabolic rate, it is proposed that the xanthophyll precursor pool may not be able to sustain the ABA accumulation, and such a proposition has been substantiated by further experiments where fluridone is used to limit the availability of upstream ABA precursors. When fluridone was used, stress ABA accumulation could only be sustained for a few hours, i.e. ∼5 h for leaf and 1 h for root tissues. In detached roots, stress ABA accumulation could not be sustained even if fluridone was not used, suggesting that stress ABA accumulation in root systems requires the continuous import of ABA precursors from the shoots. Such an assumption was substantiated by the observation that defoliation or shading significantly reduced ABA accumulation in intact roots. The present study suggests that ABA catabolism is rapid enough to play an important role in the regulation of ABA accumulation.

Whereas the regulatory mechanisms that direct fruit ripening have been studied extensively, little is known about the signaling mechanisms underlying this process, especially for nonclimacteric fruits. In this study, we demonstrated that a SUCROSE NONFERMENTING1-RELATED PROTEIN KINASE2, designated as FaSnRK2.6, is a negative regulator of fruit development and ripening in the nonclimacteric fruit strawberry (Fragaria × ananassa) and can also mediate temperature-modulated strawberry fruit ripening. FaSnRK2.6 was identified as an ortholog of OPEN STOMATA1. Levels of FaSnRK2.6 transcript rapidly decreased during strawberry fruit development and ripening. FaSnRK2.6 was found to be capable of physically interacting with strawberry ABSCISIC ACID INSENSITIVE1, a negative regulator in strawberry fruit ripening. RNA interference-induced silencing of FaSnRK2.6 significantly promoted fruit ripening. By contrast, overexpression of FaSnRK2.6 arrested fruit ripening. Strawberry fruit ripening is highly sensitive to temperature, with high temperatures promoting ripening and low temperatures delaying it. As the temperature increased, the level of FaSnRK2.6 expression declined. Furthermore, manipulating the level of FaSnRK2.6 expression altered the expression of a variety of temperature-responsive genes. Taken together, this study demonstrates that FaSnRK2.6 is a negative regulator of strawberry fruit development and ripening and, furthermore, that FaSnRK2.6 mediates temperature-modulated strawberry fruit ripening.

As the nerve-mediated signaling in animals, long-distance signaling in plants is a prerequisite for plants to be able to perceive environmental stimuli and initiate adaptive responses. While intrac...

The regulatory mechanisms that link WRKY gene expression to fruit ripening are largely unknown. Using transgenic approaches, we showed that a WRKY gene from wild strawberry (Fragaria vesca), FvWRKY48, may be involved in fruit softening and ripening. We showed that FvWRKY48 is localized to the nucleus and that degradation of the pectin cell wall polymer homogalacturonan, which is present in the middle lamella and tricellular junction zones of the fruit, was greater in FvWRKY48-OE (overexpressing) fruits than in empty vector (EV)-transformed fruits and less substantial in FvWRKY48-RNAi (RNA interference) fruits. Transcriptomic analysis indicated that the expression of pectate lyase A (FvPLA) was significantly downregulated in the FvWRKY48-RNAi receptacle. We determined that FvWRKY48 bound to the FvPLA promoter via a W-box element through yeast one-hybrid, electrophoretic mobility shift, and chromatin immunoprecipitation quantitative polymerase chain reaction experiments, and β-glucosidase activity assays suggested that this binding promotes pectate lyase activity. In addition, softening and pectin degradation were more intense in FvPLA-OE fruit than in EV fruit, and the middle lamella and tricellular junction zones were denser in FvPLA-RNAi fruit than in EV fruit. We speculated that FvWRKY48 maybe increase the expression of FvPLA, resulting in pectin degradation and fruit softening.