The TaNHLP1-TaRACK1A module regulates tillering via abscisic acid signaling in wheat

Yaoqi Si (), Shuiquan Tian, Jianqing Niu, Qiao Lu, Qiushuang Shang, Shengwei Ma, Zhimeng Zhang, Tingting Du, Huilan Wu, Jundong Li, Xiansheng Zhang, Fang Wang (), Hong-Qing Ling () and Shusong Zheng ()
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Yaoqi Si: Chinese Academy of Sciences
Shuiquan Tian: Chinese Academy of Sciences
Jianqing Niu: Yazhouwan National Laboratory
Qiao Lu: Chinese Academy of Sciences
Qiushuang Shang: Shandong Agricultural University
Shengwei Ma: Yazhouwan National Laboratory
Zhimeng Zhang: Chinese Academy of Sciences
Tingting Du: Chinese Academy of Sciences
Huilan Wu: Chinese Academy of Sciences
Jundong Li: Yunnan University
Xiansheng Zhang: Shandong Agricultural University
Fang Wang: Shandong Agricultural University
Hong-Qing Ling: Chinese Academy of Sciences
Shusong Zheng: Chinese Academy of Sciences

Nature Communications, 2025, vol. 16, issue 1, 1-17

Abstract: Abstract Wheat tillering is an important agronomic trait influencing grain yield. Here, we identify an NHL repeat-containing protein, TaNHLP1, which positively regulates tiller number in wheat. We discovered that the core components of the abscisic acid (ABA) signaling pathway, type 2C protein phosphatase TaPP2C and SNF1-related protein kinase TaSnRK2, interact with TaNHLP1 to regulate its abundance. Furthermore, TaNHLP1 interacts with the Receptor for Activated C Kinase 1 (TaRACK1A), an ABA pathway negative regulator, and influences its subcellular localization. Importantly, both the TaNHLP1 and TaRACK1A mutations promote ABA accumulation in the shoot bases and tiller buds. Notably, the NHLP1-RACK1 module is conserved across monocots and eudicots, and natural variations in the promoter of TaNHLP1-A enhance its transcriptional activity, leading to increased tiller number and yield. Collectively, these findings elucidate the genetic mechanism of NHLP1-mediated tillering regulation and highlight its potential as a target for improving crop plant architecture.

Date: 2025
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DOI: 10.1038/s41467-025-62654-5

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