Light on perenniality: Para‐dormancy is based on ABA‐GA antagonism and endo‐dormancy on the shutdown of GA biosynthesis

Abstract

AbstractPerennial para‐ and endo‐dormancy are seasonally separate phenomena. Whereas para‐dormancy is the suppression of axillary buds (AXBs) by a growing shoot, endo‐dormancy is the short‐day elicited arrest of terminal and AXBs. In hybrid aspen (Populus tremula x P. tremuloides) compromising the apex releases para‐dormancy, whereas endo‐dormancy requires chilling. ABA and GA are implicated in both phenomena. To untangle their roles, we blocked ABA biosynthesis with fluridone (FD), which significantly reduced ABA levels, downregulated GA‐deactivation genes, upregulated the major GA3ox‐biosynthetic genes, and initiated branching. Comprehensive GA‐metabolite analyses suggested that FD treatment shifted GA production to the non‐13‐hydroxylation pathway, enhancing GA4 function. Applied ABA counteracted FD effects on GA metabolism and downregulated several GA3/4‐inducible α‐ and γ‐clade 1,3‐β‐glucanases that hydrolyze callose at plasmodesmata (PD), thereby enhancing PD‐callose accumulation. Remarkably, ABA‐deficient plants repressed GA4 biosynthesis and established endo‐dormancy like controls but showed increased stress sensitivity. Repression of GA4 biosynthesis involved short‐day induced DNA methylation events within the GA3ox2 promoter. In conclusion, the results cast new light on the roles of ABA and GA in dormancy cycling. In para‐dormancy, PD‐callose turnover is antagonized by ABA, whereas in short‐day conditions, lack of GA4 biosynthesis promotes callose deposition that is structurally persistent throughout endo‐dormancy.