# Mutations in RABE1C suppress the spirrig mutant phenotype

## TL;DR

This paper shows that a mutation in RABE1C can rescue a plant cell shape defect caused by a mutation in SPIRRIG, suggesting a genetic link between these proteins.

## Contribution

The novel contribution is the discovery of a genetic interaction between RABE1C and SPIRRIG in plant cell morphogenesis.

## Key findings

- A dominant negative mutation in RABE1C rescues the trichome phenotype of the SPI mutant.
- RABE1C and SPI genetically interact in processes related to vesicle trafficking and cell morphogenesis.
- RABE1C localizes to the Golgi and functions in the same pathway as SPI.

## Abstract

The plant BEACH-domain protein SPIRRIG (SPI) is involved in regulating cell morphogenesis and salt stress responses in Arabidopsis thaliana, Arabis alpina, and Marchantia polymorpha and was reported to function in the context of two unrelated cellular processes: vesicular trafficking and P-body mediated RNA metabolism. To further explore the molecular function of SPI, we isolated a second-site mutant, specifically rescuing the spi mutant trichome phenotype. The molecular analysis of the corresponding gene revealed a dominant negative mutation in RABE1C, a ras-related small GTP-binding protein that localizes to Golgi. Taken together, our data identified the genetic interaction between RABE1C and SPI, which is beneficial for further dissecting the function of SPI in vesicle trafficking-associated cell morphogenesis.