# SYNTAXIN OF PLANTS132 Regulates Root Meristem Activity and Stem Cell Niche Maintenance via RGF-PLT Pathways

## TL;DR

This study shows that the SYP132 gene in plants is crucial for maintaining root stem cells and regulating root growth through specific molecular pathways.

## Contribution

The study reveals a novel role of SYP132 in connecting auxin-PLT and RGF-PLT pathways for root stem cell maintenance.

## Key findings

- SYP132 knockdown disrupts root meristem activity and stem cell niche identity in Arabidopsis.
- SYP132 regulates auxin distribution and PLT gene expression through vesicle transport of PIN proteins.
- RGF1 application partially rescues defects in syp132 mutants, linking auxin-PLT and RGF-PLT pathways.

## Abstract

Root growth and development are contingent upon continuous cell division and differentiation in root tips. In this study, we found that the knockdown of the syntaxin gene SYNTAXIN OF PLANTS132 (SYP132) in Arabidopsis thaliana resulted in a significant reduction in root meristem activity and disruption of root stem cell niche (SCN) identity. The SYP132 knockdown mutant exhibits a compromised SCN characterized by an increased number of quiescent center (QC) cells, abnormal columella stem cells (CSCs), reduced meristem size, and subsequent inhibition of root growth. In syp132, vesicle transport of PIN proteins is disrupted, leading to altered auxin distribution and decreased expression of the auxin-response transcription factors PLETHORA 1 (PLT1) and PLETHORA 2 (PLT2). Furthermore, the transcription level of the precursor of root meristem growth factor 1 (RGF1) is also modified in syp132. The reduction in PLT2 transcription and protein levels along with defects in the root SCN are partially rescued by the application of synthesized RGF1. This finding suggests that both the auxin-PLT and RGF-PLT pathways are interconnected through SYP132-mediated vesicle transport. Collectively, our findings indicate that SYP132 regulates the PLT pathway to maintain the root stem cell niche (SCN) in an RGF1-dependent manner.