SummaryThe mechanisms by which the maize antioxidant Cat1 gene responds to abscisic acid (ABA) and osmotic stress have been investigated. Results show that during late embryogenesis, Cat1 expression in vivo is independent of endogenous ABA levels. However, exogenously applied ABA signi®cantly enhances Cat1 expression. Transient assays using particle bombardment show that the proximal ABRE2 element on the Cat1 promoter is responsible for the induction of Cat1 expression by ABA. We further show that ABA induces the expression of Cat1 via the interaction between ABRE2 and one of its binding proteins, CBF1 (Cat1 binding factor 1). Using ABA-de®cient mutant embryos, we show that osmotic stress induces Cat1 expression through two alternate signal transduction pathways: an ABA signaling pathway leading to the interaction between the ABRE2 motif and CBF1, and a pathway via the interaction of ABRE2 and CBF2 (Cat1 binding factor 2) that is independent of ABA. The data presented clearly suggest that hydrogen peroxide (H 2 O 2 ) plays an important intermediary role in the ABA signal transduction pathway leading to the induction of the Cat1 gene.

The response of the maize catalase genes

The effects of abscisic acid (ABA) and high osmoticum on catalase (Cat) gene expression in maize have been examined. Each Cat gene responds differently to ABA and osmotic stress at different developmental stages and in different tissues. Cat1 transcript accumulates to high levels in developing and germinating embryos, and in leaves. In embryos, Cat2 and Cat3 transcripts are up‐regulated only at very high ABA concentrations during late embryogenesis and in response to various concentrations of ABA in germinating embryos. Cat3 transcript is down‐regulated by ABA and osmotic stress in leaves. Accumulation of Cat1 transcript in response to osmotic stress is a consequence of increased endogenous ABA levels. Our data suggest that two separate pathways might be involved in the ABA‐mediated induction of Cat1. The Vp1 trans‐acting factor is required for maximum induction of Cat1 transcript in wild‐type (Vp1/—) and in W64A developing embryos; however, Vp1 is not required for inducing the Cat1 transcript in vp1 mutant developing embryos, nor in W64A germinating embryos or in leaves. Given the fact that the Cat genes have a known function, we hypothesize that the increase in Cat gene products in response to ABA is due, in part, to ABA‐mediated metabolic changes leading to changes in oxygen free radical levels, which in turn, lead to the induction of the antioxidant defense system.

The maize (Zea mays) superoxide dismutase genes Sod4 and Sod4A are highly similar in structure but each responds differentially to environmental signals. We examined the effects of the hormone abscisic acid (ABA) on the developmental response of Sod4 and Sod4A. Although both Sod4 and Sod4A transcripts accumulate during late embryogenesis, only Sod4 is up-regulated by ABA and osmotic stress. Accumulation of Sod4 transcript in response to osmotic stress is a consequence of increased endogenous ABA levels in developing embryos. Sod4 mRNA is up-regulated by ABA in viviparous-1 mutant embryos. Sod4 transcript increases within 4 h with ABA not only in developing embryos but also in mature embryos and in young leaves. Sod4A transcript is upregulated by ABA only in young leaves, but neither Sod4 nor Sod4A transcripts changed in response to osmotic stress. Our data suggest that in leaves Sod4 and Sod4A may respond to ABA and osmotic stress via alternate pathways. Since the Sod genes have a known function, we hypothesize that the increase in Sod mRNA in response to ABA is due in part to ABA-mediated metabolic changes leading to changes in oxygen free radical levels, which in turn lead to the induction of the antioxidant defense system.

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