Signals and Signal Conduits Co-ordinately Regulate Dormancy Cycling at the Perennial Shoot Apical Meristem

The shoot apical meristem (SAM) is a unit of self-organization that reiterates its dynamic organization while peripherally releasing cells for determination. In perennials of temperate climates the functioning of the SAM over multiple years is challenged by declining daylength and temperatures at the end of the growth season. However, species like Populus have evolved mechanisms that monitor environmental change and set in train molecular and physiological processes that ensure survival through winter. Characteristically, early during dormancy induction the symplasmic organisation of the SAM is disrupted by formation of callosic sphincters at plasmodesmata (PD). This prevents primary morphogenesis, but permits acclimation of the disconnected cells. Release of the disconnected dormant state into a re-connected quiescent state is promoted by low temperatures (chilling), which simultaneously increase freezing-tolerance. We identified 10 dormancy cycling regulators that belong to the 1,3-beta-glucanase family (GH17 proteins), which can degrade PD-callose. Their expression is modulated by daylength, temperature, and the gibberellins GA₃ and GA₄. Both gibberellins are crucial in the cycle, but at different phases. The selected GA₃-regulated GH17 proteins reside on lipid bodies that are crucial for dormancy release, while GA₄-regulated GH17 proteins, equipped with a GPI-anchor and/or a callose-binding domain, mainly function in growth activation and morphogenetic patterning. In addition, the increasing and decreasing temperatures during the change of seasons differentially regulate the expression of the genes FLOWERING LOCUS T and CENTRORADIALIS-LIKE1. We conjecture that collectively these factors regulate signal production and the long-and short-distance signalling conduits to drive dormancy cycling in synchrony with the seasons. Supported by the Norwegian Research Council, FRIBIO grants 171970 and 192013