Nuclease I enzymes are responsible for the degradation of RNA and single-stranded DNA during several plant growth and developmental processes, including senescence. However, in the case of senescence the corresponding genes have not been reported. We describe the identification and characterization of BFN1 of Arabidopsis, and demonstrate that it is a senescence-associated nuclease I gene. BFN1 nuclease shows high similarity to the sequence of a barley nuclease induced during germination and a zinnia (Zinnia elegans) nuclease induced during xylogenesis. In transgenic plants overexpressing the BFN1 cDNA, a nuclease activity of about 38 kD was detected on both RNase and DNase activity gels. Levels of BFN1 mRNA were extremely low or undetectable in roots, leaves, and stems. In contrast, relatively high BFN1 mRNA levels were detected in flowers and during leaf and stem senescence. BFN1 nuclease activity was also induced during leaf and stem senescence. The strong response of the BFN1 gene to senescence indicated that it would be an excellent tool with which to study the mechanisms of senescence induction, as well as the role of the BFN1 enzyme in senescence using reverse genetic approaches in Arabidopsis.

SummaryInduction of defense-related genes is one way in which plants respond to mechanical injury. We investigated whether RNases are involved in the wound response in Arabidopsis thaliana. As in other plant systems, several activities are induced with various timings in damaged leaves, stems and seedlings in Arabidopsis, including at least three bifunctional nucleases, capable of degrading both RNA and DNA, as well as RNS1, a member of the ubiquitous RNase T 2 family of RNases. The strong induction of RNS1 is particularly interesting because it occurs both locally and systemically following wounding. The systemic induction of this RNase indicates that members of this family may be involved in defense mechanisms in addition to their previously hypothesized functions in nutrient recycling and remobilization. Additionally, the systemic induction appears to be controlled independently of jasmonic acid, and the local induction of RNS1 and the nuclease activities are independent of both JA and oligosaccharide elicitors. Consequently, a novel systemic pathway, likely involving a third signal, appears to exist in Arabidopsis.

Injured plants induce a wide range of genes whose products are thought to help to repair the plant or to defend against opportunistic pathogens that might infect the wounded plant. In Arabidopsis thaliana L., oligogalacturonides (OGAs) and jasmonic acid (JA) are the main regulators of the signaling pathways that control the local and systemic wound response, respectively. RNS1, a secreted ribonuclease, is induced by wounding in Arabidopsis independent of these two signals, thus indicating that another wound-response signal exists. Here we show that abscisic acid (ABA), which induces wound-responsive genes in other systems, also induces RNS1. In the absence of ABA signaling, wounding induces only approximately 45% of the endogenous levels of RNS1 mRNA. However, significant levels of RNS1 still accumulate in the absence of ABA signaling. Our results suggest that wound-responsive increases in ABA production may amplify induction of RNS1 by a novel ABA-independent pathway. To elucidate this novel pathway, we show here that the wound induction of RNS1 is due in part to transcriptional regulation by wounding and ABA. We also show evidence of post-transcriptional regulation which may contribute to the high levels of RNS1 transcript accumulation in response to wounding.

Yeast apoptosis debate continues east, as a unicellular organism, would seem to benefit most from self-preservation. But yeast altruism, in the form of apoptosis, is a new-found, if controversial, field of study. Many doubt the validity of experiments supporting programmed cell death in yeast and call for better controls. In this issue, the debate continues with two new articles that suggest that yeast cells do organize their own deaths-for the sake of their brethren. Biologists often address how a phenomenon occurs, but seldom why. For the yeast apoptosis field, however, why is a painfully obvious question. On page 1055, Fabrizio et al. suggest a method to the madness. They show that yeast populations survive better in the long run when they initiate an early death program through superoxide. Superoxides are produced by the everyday activities of life, but their mutational and death-inducing activities can be curtailed by superoxide dismutases (Sods). The authors find that Sods are normally downregulated in older yeast cultures, which are surviving in nutrient-poor medium, leading to cell death. Mutants that circumvented this programmed death mechanism by maintaining high Sod activity had extended life spans. These long-lived populations, however, were unable to repopulate their culture once most of the cells died, a phenomenon known as adaptive regrowth. As a result, in competition experiments, strains that initiated early death eventually outgrew the wild type. Early death probably allows the bestadapted cells in a population to reproduce before they are too old by using nutrients left behind by the dead yeasts. Superoxides are mutation inducers. The higher mutation