Shoot branching affects plant architecture. In strawberry (Fragaria L.), short branches (crowns) develop from dormant axillary buds to form inflorescences and flowers. While this developmental transition contributes greatly to perenniality and yield in strawberry, its regulatory mechanism remains unclear and understudied. In the woodland strawberry (Fragaria vesca), we identified and characterized two independent mutants showing more crowns. Both mutant alleles reside in FveMYB117a, a R2R3-MYB transcription factor gene highly expressed in shoot apical meristems, axillary buds and young leaves. Transcriptome analysis revealed that the expression of several cytokinin pathway genes was altered in the fvemyb117a mutant. Consistently, active cytokinins were significantly increased in the axillary buds of the fvemyb117a mutant. Exogenous application of cytokinin enhanced crown outgrowth in the wild type, whereas the cytokinin inhibitors suppressed crown outgrowth in the fvemyb117a mutant. FveMYB117a binds directly to the promoters of the cytokinin homeostasis genes FveIPT2 encoding an isopentenyltransferase and FveCKX1 encoding a cytokinin oxidase to regulate their expression. Conversely, the type-B Arabidopsis response regulators FveARR1 and FveARR2b can directly inhibit the expression of FveMYB117a, indicative of a negative feedback regulation. In conclusion, we identified FveMYB117a as a key repressor of crown outgrowth by inhibiting cytokinin accumulation and provide a mechanistic basis for bud fate transition in an herbaceous perennial plant.

中文翻译：

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林地草莓转录因子 FveMYB117a 通过调节细胞分裂素稳态抑制腋芽生长

枝条分枝影响植物结构。在草莓（Fragaria L.）中，短枝（冠）从休眠的腋芽发育成花序和花朵。虽然这种发育转变对草莓的多年生性和产量有很大贡献，但其调控机制仍不清楚且未被充分研究。在林地草莓（Fragaria vesca）中，我们鉴定并鉴定了两个显示更多冠的独立突变体。两个突变等位基因都存在于 FveMYB117a 中，FveMYB117a 是一种在茎尖分生组织、腋芽和幼叶中高度表达的 R2R3-MYB 转录因子基因。转录组分析显示，fvemyb117a 突变体中几个细胞分裂素途径基因的表达发生了改变。一致地，fvemyb117a 突变体的腋芽中活性细胞分裂素显着增加。外源应用细胞分裂素增强了野生型的冠生长，而细胞分裂素抑制剂抑制了 fvemyb117a 突变体的冠生长。 FveMYB117a 直接结合编码异戊烯基转移酶的细胞分裂素稳态基因 FveIPT2 和编码细胞分裂素氧化酶的 FveCKX1 的启动子来调节其表达。相反，B型拟南芥反应调节因子FveARR1和FveARR2b可以直接抑制FveMYB117a的表达，表明负反馈调节。总之，我们确定 FveMYB117a 通过抑制细胞分裂素积累而成为冠生长的关键抑制因子，并为多年生草本植物的芽命运转变提供了机制基础。