Lily bulbils, which serve as advantageous axillary organs for vegetative propagation, have not been extensively studied in terms of the mechanism of bulbil initiation. The function of auxin and sucrose metabolism have been implicated in axillary organ development, but their relationship in regulating bulbil initiation remains unclear. In this study, exogenous indole-3-acetic acid (IAA) treatment increased the endogenous auxin levels at leaf axils and significantly decreased bulbil number, whereas treatment with the auxin polar transport inhibitor N-1-naphthylphthalamic acid (NPA), which resulted in a low auxin concentration at leaf axils, stimulated bulbil initiation and increased bulbil number. A low level of auxin caused by NPA spraying or silencing of auxin biosynthesis genes YUCCA FLAVIN MONOOXYGENASE-LIKE6 (LlYUC6) and TRYPTOPHAN AMINO-TRANSFERASE1 (LlTAR1) facilitated sucrose metabolism by activating the expression of LlSusy1 and LlCWIN2, resulting in enhanced bulbil initiation. Silencing SUCROSE SYNTHASES1 (LlSusy1) or CELL WALL INVERTASE2 (LlCWIN2) hindered bulbil initiation. Moreover, the transcription factor BASIC-HELIX-LOOP-HELIX35 (LlbHLH35) directly bound the promoter of LlSusy1, but not the promotor of LlCWIN2, and activated its transcription in response to the auxin content, bridging the gap between auxin and sucrose metabolism. In conclusion, our results reveal a LlbHLH35-LlSusy1 module mediates auxin-regulated sucrose metabolism during bulbil initiation.

中文翻译：

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生长素通过介导百合蔗糖代谢来调节珠芽起始

百合珠芽是营养繁殖的有利腋生器官，但其珠芽起始机制尚未得到广泛研究。生长素和蔗糖代谢的功能与腋窝器官的发育有关，但它们在调节珠芽起始中的关系仍不清楚。在这项研究中，外源吲哚-3-乙酸（IAA）处理增加了叶腋的内源生长素水平，并显着减少了珠芽数量，而用生长素极性运输抑制剂N-1-萘基邻苯二甲酸（NPA）处理，导致叶腋处生长素浓度低，刺激珠芽萌生并增加珠芽数量。NPA喷洒或沉默生长素生物合成基因YUCCA FLAVIN MONOOXYGENASE-LIKE6 (LlYUC6)和色氨酸氨基转移酶1 (LlTAR1)引起的低水平生长素通过激活LlSusy1和LlCWIN2的表达促进蔗糖代谢，从而增强珠芽起始。沉默蔗糖合成酶 1 (LlSusy1) 或细胞壁反转酶 2 (LlCWIN2) 会阻碍珠芽的启动。此外，转录因子BASIC-HELIX-LOOP-HELIX35 (LlbHLH35)直接结合LlSusy1的启动子，但不结合LlCWIN2的启动子，并响应生长素含量激活其转录，弥合了生长素和蔗糖代谢之间的差距。总之，我们的结果揭示了 LlbHLH35-LlSusy1 模块在珠芽起始过程中介导生长素调节的蔗糖代谢。