生物
生长素
转录组
拟南芥
细胞生物学
基因敲除
代谢组
分生组织
RNA干扰
效应器
基因表达调控
调节器
基因调控网络
细胞命运测定
植物
基因
基因沉默
基因表达谱
遗传学
MYB公司
计算生物学
代谢组学
机制(生物学)
生长素极性运输
次生细胞壁
细胞壁
表型
作者
Lin Wang,Junping Gao,Chen Wang,Guoyun Xu,Zhen Ma,Shuaibin Wang,Zhaopeng Luo,Mingzhu Wu,Jianfeng Zhang,Jie Yang,Peijian Cao,Xiaodong Xie
摘要
Plant architecture is key to crop yield, with leaf angle being critical for high-density cultivation. Although TAC1 represents a promising regulator of leaf angle for breeding, its molecular mechanism remains poorly understood, particularly at single-nucleus resolution. Here, we performed single-nucleus RNA sequencing on NtTAC1 knockdown lines exhibiting reduced leaf angle. This analysis generated a transcriptional atlas comprising 20 distinct clusters corresponding to 14 cell types and identified the endodermis as a central regulatory hub. Weighted gene co-expression network analysis and trajectory inference revealed that the auxin transporter NtPIN3 acts as a key downstream effector of NtTAC1. The two genes are co-expressed in endodermal cells and promote their differentiation from meristematic cells. Spatial metabolomics further demonstrated that NtTAC1 suppression elevates auxin levels and alters its spatial distribution, resulting in asymmetric auxin accumulation preferentially in the abaxial region and consequent reduction in leaf angle. Silencing NtPIN3 recapitulated the NtTAC1 disruption phenotype, confirming that the NtTAC1-NtPIN3 axis regulates both auxin asymmetry and cell wall remodelling. Consistently, both knockdown lines exhibited enhanced lignin deposition, linking disrupted auxin flow to secondary wall thickening. Moreover, CRISPR/Cas9-mediated editing of SlTAC1 in tomato suppressed SlPIN3 expression, indicating evolutionary conservation of this module. Collectively, our findings uncover a cell-type-resolved mechanism underlying leaf angle regulation and provide a mechanistic framework for precision engineering of crop architecture adapted to high-density cultivation.
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