| Bud dormancy,which can protect buds from cold temperatures in winter and early spring,is an important adaptive mechanism of deciduous fruit trees to cope with seasonal environmental changes and temperate climates.With increasing global warming,the temperature rises quickly in spring,and fruit trees bud and bloom so early that they are vulnerable to the damage of late spring coldness,which reduces the yield of fruit trees and affects economic income.Therefore,it is of great significance for controlling bud break and preventing the damage of late spring coldness to understand the regulatory mechanism of bud break in fruit trees.MYB,the largest transcription factor(TF)family in plants,is widely involved in the response to abiotic stress and the biosynthesis of secondary metabolites.Recent studies have found that it also plays an important role in regulating seed dormancy and germination.However,the molecular mechanism underlying the involvement of MYB TFs during the bud break of peach is still unclear.In this study,the PpMYB52(Prupe.5G2400000.1)gene was isolated and identified from peach bud of ’Zhongyou 4’(Prunus persica var.nectarina cv.Zhongyou 4).It was found to play a negative regulatory role in the process of bud break.In addition,RING-type E3 ligase PpMIEL1 was screened as an interaction protein of PpMYB52,and it was found that the PpMIEL1 gene played a positive regulatory role in bud break.The main findings are as follows:1.The expression of PpMYB52 was maintained at a high level in the endodormancy stage,continued to decrease in the process of bud break,and decreased to the lowest level before bud break,which was negatively correlated with bud break.Tissue-specific analysis showed that the PpMYB52 gene was highly expressed in peach buds during endodormancy but was expressed at low levels in the flower buds before bud break,and in the flowers,petals,leaves and phloem.ABA could promote the expression of PpMYB52,while GA could inhibit its expression.Subcellular localization revealed that the PpMYB52 was localized in the nucleus.2.Overexpression of PpMYB52 inhibited seed germination of transgenic tomato and Arabidopsis thaliana.In addition,overexpression of PpMYB52 resulted in the decrease of plant height and Rosette diameter.3.PpMYB52 has autoactivation,and the 1-100 aa region containing the functional domain of Myb＿DNA-bind＿6 has no autoactivation.Through yeast two-hybrid screening library,PpMYB52(1-100 aa)may interact with PpMIEL1.The interaction between PpMYB52 and PpMIEL1 was further verified by Bi FC assay.4.The expression of PpMIEL1 was maintained at a low level in the endodormancy stage,increased in the process of bud break,and increased to the highest level before bud break,which was positively correlated with bud break.Tissue-specific analysis showed that the PpMIEL gene was highly expressed in the flower petals,stamens,and pistils and was expressed the lowest in the peach buds during endodormancy.Subcellular localization showed that PpMIEL1 was localized in the nucleus and cytoplasm.Overexpression of PpMIEL1 promoted seed germination of transgenic Arabidopsis thaliana. |
