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Research article2019Peer reviewedOpen access

A Tree Ortholog of SHORT VEGETATIVE PHASE Floral Repressor Mediates Photoperiodic Control of Bud Dormancy

Singh, Rajesh Kumar; Miskolczi, Pal; Maurya, Jay P.; Bhalerao, Rishikesh P.

Abstract

Perennials in boreal and temperate ecosystems display seasonally synchronized growth. In many tree species, prior to the advent of winter, exposure to photoperiods shorter than a critical threshold for growth (short days; SDs) induces growth cessation, culminating in the formation of an apical bud that encloses the shoot apical meristem and arrested leaf primordia [1-4]. Following growth cessation, subsequent exposure to SDs induces transition to dormancy in the shoot apex [5]. Establishment of dormancy is crucial for winter survival and is characterized by the inability of the shoot meristem to respond to growth-promotive signals [6]. Recently, SDs were shown to induce bud dormancy by activating the abscisic acid (ABA) pathway. ABA upregulates expression of CALLOSE SYNTHASE 1 (CALS1) and suppresses glucanases that break down callose to induce the blockage of intracellular conduits (plasmodesmata; PDs) with callosic plugs called "dormancy sphincters" that by restricting access to growth-promotive signals promote dormancy [7]. However, components downstream of ABA in dormancy regulation remain largely unknown, and thus there are significant gaps in our understanding of photoperiodic control of bud dormancy. Here we demonstrate that SVL, orthologous to Arabidopsis floral repressor SHORT VEGETATIVE PHASE (SVP), is a mediator of photoperiodic control of dormancy downstream of the ABA pathway in hybrid aspen. SVL downregulation impairs dormancy, whereas SVL overexpression suppresses dormancy defects resulting from ABA insensitivity. Downstream, SVL induces callose synthase expression and negatively regulates the gibberellic acid (GA) pathway to promote dormancy, thus revealing the regulatory module mediating photoperiodic control of dormancy by ABA.

Published in

Current Biology
2019, Volume: 29, number: 1, pages: 128-+
Publisher: CELL PRESS