Regulatory roles of benzyl adenine and sucrose during wound response of the ribosomal protein gene, rpL34
We previously reported that a large subunit ribosomal protein gene, rpL34, was wound-inducible in tobacco leaves, and that benzyl adenine (BA) enhanced the wound-inducible expression of the gene. Here we report that the wound-inducible expression of the rpL34 gene is enhanced by sucrose. The regulatory roles of BA and sucrose in wound-signalling pathways were investigated using transgenic plants expressing a fusion molecule between the rpL34 promoter and the chloramphenicol acetyltransferase (cat) gene. Wounding caused a progressive increase in CAT activity; BA and sucrose enhanced the response. This indicates that regulation occurs at the transcriptional level. Diethyldithiocarbamic acid (DIECA) and other potent inhibitors of the octadecanoid pathway inhibited the rpL34 promoter, and also reduced BA inducibility of that wound response. However, inhibitors of the octadecanoid pathway did not affect the sucrose response. Protein kinase inhibitors increased BA enhancement while decreasing the sucrose effect, suggesting that protein kinases differentially regulate BA- and sucrose-signalling in the promoter's wound response. Taken together, BA and sucrose enhanced the wound response of the rpL34 promoter via different signalling pathways, although they exerted overlapping effects on wound-induction of the promoter.