Abstract

Perennial 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.

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