Consistently, transgenic plants overexpressing apple MdoDAMb and MdoSVPa genes show delayed bud break 8. Moreover, PmDAM6 gene from Japanese apricot induces early growth cessation and terminal bud set when overexpressed in transgenic poplar 7 and apple 9. The ectopic expression of DAM1 gene from leafy spurge ( Euphorbia esula) delays flowering and decreases the expression of the flowering gene FLOWERING LOCUS T ( FT) in Arabidopsis thaliana 13.
In addition, RNA silencing of the MdDAM1 gene results in an evg-like phenotype in apple 12. A deletion of four out of six tandemly repeated DAM genes has been proposed to cause the non-dormant phenotype of the evergrowing ( evg) mutant of peach ( Prunus persica) 10, 11. In Rosaceae tree species and other perennial plants, DORMANCY-ASSOCIATED MADS-BOX ( DAM) genes, phylogenetically related to the Arabidopsis thaliana flowering factor SHORT VEGETATIVE PHASE ( SVP), act as key regulators of bud dormancy maintenance and release 7, 8, 9. This state is widely known as ecodormancy. After dormancy release, buds become competent for growing, requiring a period of mild temperatures for initiating bud break. This chilling requirement for dormancy release is quantitative and specific for different genotypes. Paradoxically, bud dormancy completion is also favored by prolonged chilling 6. Prior to bud dormancy induction, cessation of meristem growth and bud set are induced by photoperiod changes (short daylength) and/or low temperature conditions in apical vegetative meristems 3, 4, whereas the growth of axillary vegetative meristems and differentiated flowers is stopped by correlative bud inhibition 5. Among them, dormancy facilitates survival of growing tissues under the low and freezing temperatures of autumn and winter by interrupting cell division and growth, and activating general and specific defense mechanisms 1, 2. Throughout evolution, perennial plants have developed different strategies to adapt to seasonal changing environmental conditions. The expression of many of these genes is also modified in flower buds of peach concomitantly with PpeDAM6 downregulation, which suggests a role of hormone homeostasis mechanisms in PpeDAM6-dependent maintenance of floral bud dormancy and growth repression. These alterations in vegetative growth of transgenic lines associate with impaired hormone homeostasis due to the modulation of genes involved in jasmonic acid, cytokinin, abscisic acid, and gibberellin pathways, and the downregulation of shoot meristem factors, specifically in transgenic leaf and apical tissues. On the other hand, the heterologous overexpression of PpeDAM6 in European plum ( Prunus domestica) alters plant vegetative growth, resulting in dwarf plants tending toward shoot meristem collapse. Moreover, PpeBPC1 represses PpeDAM6 promoter activity by transient expression experiments. We have identified three peach BASIC PENTACYSTEINE PROTEINs (PpeBPCs) interacting with two GA-repeat motifs present in this H3K27me3-enriched region. PpeDAM6 expression is downregulated concomitantly with the perception of a given genotype-dependent accumulation of winter chilling time, and the coincident enrichment in H3K27me3 chromatin modification at a specific genomic region. Particularly, PpeDAM6 has been proposed to act as a major repressor of bud dormancy release and bud break in peach ( Prunus persica). DORMANCY-ASSOCIATED MADS-BOX ( DAM) genes have recently emerged as key potential regulators of the dormancy cycle and climate adaptation in perennial species.
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