Apoplastic H2 O2 plays a critical role in axillary bud outgrowth by altering auxin and cytokinin homeostasis in tomato plants.

ABSTRACT

Although phytohormones such as indole-3-acetic acid (IAA), cytokinin (CK) and strigolactone are important modulators of plant architecture, it remains unclear whether reactive oxygen species are involved in the regulation of phytohormone-dependent axillary bud outgrowth in plants. We used diverse techniques, including transcriptional suppression, HPLC-MS, biochemical methodologies and gene transcript analysis to investigate the signaling pathway for apoplastic hydrogen peroxide (H2 O2 )-induced axillary bud outgrowth. Silencing of tomato RESPIRATORY BURST OXIDASE HOMOLOG 1 (RBOH1) and WHITEFLY INDUCED 1 (WFI1), two important genes involved in H2 O2 production in the apoplast, enhanced bud outgrowth, decreased transcript of FZY - a rate-limiting gene in IAA biosynthesis and IAA accumulation in the apex - and increased the transcript of IPT2 involved in CK biosynthesis and CK accumulation in the stem node. These effects were fully abolished by the application of exogenous H2 O2 . Both decapitation and the silencing of FZY promoted bud outgrowth, and downregulated and upregulated the transcripts for IAA3 and IAA15, and IPT2, respectively. However, these effects were not blocked by treatment with exogenous H2 O2 but by napthaleneacetic acid (NAA) treatment. These results suggest that RBOHs-dependent apoplastic H2 O2 promotes IAA biosynthesis in the apex, which, in turn, inhibits CK biosynthesis and subsequent bud outgrowth in tomato plants.