Hydrogen Peroxide Activates Cell Death and Defense Gene Expression in Birch

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Abstract
The function of hydrogen peroxide (H2O2) as a signal molecule regulating gene expression and cell death induced by external stresses was studied in birch (Betula pendula). Ozone (O3),Pseudomonas syringae pv syringae(Pss), and wounding all induced cell death of various extents in birch leaves. This was temporally preceded and closely accompanied by H2O2 accumulation at, and especially surrounding, the lesion sites. O3 andPss, along with an artificial H2O2 producing system glucose (Glc)/Glc oxidase, elicited elevated mRNA levels corresponding to genes encoding reactive oxygen species detoxifying enzymes, Pal,Ypr10, and mitochondrial phosphate translocator 1. In addition to the regulation of gene expression, Glc/Glc oxidase also induced endogenous H2O2 production in birch leaves, accompanied by cell death that resembled O3 andPss damage. Wound-induced gene expression differed from that induced by O3 and Pss. Thus, it appears that at least two separate defense pathways can be activated in birch leaves by stress factors, even though the early H2O2 accumulation response is common among them all.