STOP1 attenuates the auxin response to maintain root stem cell niche identity
Jiajia Liu,
Huiyu Tian,
Mengxin Zhang,
Yi Sun,
Junxia Wang,
Qianqian Yu,
Zhaojun Ding
Affiliations
Jiajia Liu
The Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, Shandong, China
Huiyu Tian
The Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, Shandong, China
Mengxin Zhang
The Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, Shandong, China
Yi Sun
The Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, Shandong, China
Junxia Wang
The Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, Shandong, China
Qianqian Yu
College of Life Sciences, Liaocheng University, Liaocheng, Shandong, China
Zhaojun Ding
The Key Laboratory of Plant Development and Environmental Adaptation Biology, Ministry of Education, School of Life Sciences, Shandong University, Qingdao, Shandong, China; Corresponding author
Summary: In plant roots, the identity of the stem cell niche (SCN) is maintained by an auxin gradient with its maximum in the quiescent center (QC). Optimal levels of auxin signaling are essential for root SCN identity, but the regulatory mechanisms that control this pathway in root are largely unknown. Here, we find that the zinc finger transcription factor sensitive to proton rhizotoxicity 1 (STOP1) regulates root SCN identity by negative feedback of auxin signaling in root tips. Mutation and overexpression of STOP1 both affect QC cell division and distal stem cell differentiation in the root. We find that auxin treatment stabilizes STOP1 via MPK3/6-dependent phosphorylation. Accumulating STOP1 can compete with AUX/IAAs to interact with, and enhance the repressive activity of, auxin-repressive response factor ARF2. Overall, we show that the MPK3/6-STOP1-ARF2 module prevents excessive auxin signaling in the presence of auxin to maintain root SCN identity.
