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Auxin regulates bulbil initiation by mediating sucrose metabolism in Lilium lancifolium

文献类型： 外文期刊

作者： Xin, Yin 1 ; Chen, Xi 1 ; Liang, Jiahui 1 ; Wang, Shaokun 2 ; Pan, Wenqiang 2 ; Wu, Jingxiang 1 ; Zhang, Mingfang 1 ; Zaccai, Michele 4 ; Yu, Xiaonan 3 ; Zhang, Xiuhai 1 ; Wu, Jian 2 ; Du, Yunpeng 1 ;

作者机构： 1.Beijing Acad Agr & Forestry Sci, Inst Grassland Flowers & Ecol, Ornamental & Edible Lily Engn Res Ctr Natl Forestr, Beijing 100097, Peoples R China

2.China Agr Univ, Dept Ornamental Hort & Landscape Architecture, Beijing Key Lab Dev & Qual Control Ornamental Crop, Beijing 100193, Peoples R China

3.Beijing Forestry Univ, Natl Engn Res Ctr Floriculture, Beijing Key Lab Ornamental Plants Germplasm Innova, Beijing Lab Urban & Rural Ecol Environm,Coll Lands, Beijing 100083, Peoples R China

4.Ben Gurion Univ Negev, Dept Life Sci, IL-8410501 Beer Sheva, Israel

期刊名称：HORTICULTURE RESEARCH （ 影响因子：8.7； 五年影响因子：9.0 ）

ISSN： 2662-6810

年卷期： 2024 年 11 卷 4 期

页码：

收录情况： SCI

摘要： 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 functions 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-LIKE 6 (LlYUC6) and TRYPTOPHAN AMINOTRANSFERASERELATED 1 (LlTAR1) facilitated sucrose metabolism by activating the expression of SUCROSE SYNTHASES 1 (LlSusy1) and CELL WALL INVERTASE 2 (LlCWIN2), resulting in enhanced bulbil initiation. Silencing LlSusy1 or LlCWIN2 hindered bulbil initiation. Moreover, the transcription factor BASIC HELIX-LOOP-HELIX 35 (LlbHLH35) directly bound the promoter of LlSusy1, but not the promoter 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 that an LlbHLH35-LlSusy1 module mediates auxin-regulated sucrose metabolism during bulbil initiation.

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