The low temperature response pathways for cold acclimation and vernalization are independent

Vernalization is the promotion of flowering in response to the prolonged cold of winter. To survive sub‐zero winter temperatures, plants must first acclimate to low, non‐freezing temperatures (cold acclimation). Induction of VERNALIZATION INSENSITIVE 3 (VIN3), the first gene in the vernalization pathway, is initiated within the same time frame as the induction of genes in the cold acclimation pathway raising the question of whether there are common elements in the signal transduction pathways that activate these two responses to cold. We show that none of the signalling components required for cold acclimation, including the ‘master regulator’INDUCTION OF CBF EXPRESSION1 (ICE1) or HIGH EXPRESSION OF OSMOTICALLY RESPONSIVE GENE1 (HOS1), which has been described as a link between cold acclimation and vernalization, play a role in VIN3 induction. We also show that the hormone abscisic acid (ABA) does not modulate VIN3 induction, consistent with earlier reports that ABA signalling plays no role in the vernalization response. The cold acclimation pathway is activated at 12 °C, at which temperature there is no induction of VIN3 expression. Taken together, our data demonstrate that the responses to low temperatures leading to cold acclimation and vernalization are controlled by distinct signalling pathways.     

The Vitis vinifera C-repeat binding protein 4 (VvCBF4) transcriptional factor enhances freezing tolerance in wine grape

Chilling and freezing can reduce significantly vine survival and fruit set in Vitis vinifera wine grape. To overcome such production losses, a recently identified grapevine C‐repeat binding factor (CBF) gene, VvCBF4, was overexpressed in grape vine cv. ‘Freedom’ and found to improve freezing survival and reduced freezing‐induced electrolyte leakage by up to 2 °C in non‐cold‐acclimated vines. In addition, overexpression of this transgene caused a reduced growth phenotype similar to that observed for CBF overexpression in Arabidopsis and other species. Both freezing tolerance and reduced growth phenotypes were manifested in a transgene dose‐dependent manner. To understand the mechanistic basis of VvCBF4 transgene action, one transgenic line (9–12) was genotyped using microarray‐based mRNA expression profiling. Forty‐seven and 12 genes were identified in unstressed transgenic shoots with either a >1.5‐fold increase or decrease in mRNA abundance, respectively. Comparison of mRNA changes with characterized CBF regulons in woody and herbaceous species revealed partial overlaps, suggesting that CBF‐mediated cold acclimation responses are widely conserved. Putative VvCBF4‐regulon targets included genes with functions in cell wall structure, lipid metabolism, epicuticular wax formation and stress‐responses suggesting that the observed cold tolerance and dwarf phenotypes are the result of a complex network of diverse functional determinants.     

OST1‐mediated BTF3L phosphorylation positively regulates CBFs during plant cold responses

Cold stress is a major environmental factor that negatively affects plant growth and survival. OST1 has been identified as a key protein kinase in plant response to cold stress; however, little is known about the underlying molecular mechanism. In this study, we identified BTF3 and BTF3L (BTF3‐like), β‐subunits of a nascent polypeptide‐associated complex (NAC), as OST1 substrates that positively regulate freezing tolerance. OST1 phosphorylates BTF3 and BTF3L in vitro and in vivo, and facilitates their interaction with C‐repeat‐binding factors (CBFs) to promote CBF stability under cold stress. The phosphorylation of BTF3L at the Ser50 residue by OST1 is required for its function in regulating freezing tolerance. In addition, BTF3 and BTF3L proteins positively regulate the expression of CBF genes. These findings unravel a molecular mechanism by which OST1‐BTF3‐CBF module regulates plant response to cold stress.