# ARABIDOPSIS HOMOLOG OF TRITHORAX1 impacts lateral root development by epigenetic regulation of targets involved in root system architecture

## TL;DR

This study shows how the ATX1 protein in Arabidopsis affects root development by controlling gene activity through epigenetic changes.

## Contribution

The study identifies a novel epigenetic mechanism linking ATX1 to root system architecture via PRX35 regulation.

## Key findings

- ATX1 mutants show abnormal lateral root development due to altered growth and cell cycle delays.
- PRX35 is a key target of ATX1, with reduced expression and H3K4me3 levels in mutants.
- Downregulated genes in atx1setm are linked to cell wall and H2O2 metabolism.

## Abstract

Developmental processes are regulated at multiple levels, including the epigenetic level. Among the epigenetic factors, histone H3 lysine 4 (H3K4) methyltransferases contribute to active transcription of target genes, and here, we explored how the H3K4 methyltransferase ARABIDOPSIS HOMOLOG OF TRITHORAX1 (ATX1) affects Arabidopsis thaliana lateral root (LR) primordium (LRP) morphogenesis.We examined LR development in a loss‐of‐function null mutant (atx1‐1) and a mutant affected in the ATX1 catalytic domain (atx1setm) through bright‐field and long‐term time‐lapse confocal microscopy, transcriptomics, and chromatin immunoprecipitation.LRP morphogenesis in both mutants was severely abnormal, resulting from altered principal growth directions, and was accompanied by extended cell cycle durations and slower transitions between LRP stages. Among the differentially expressed genes downregulated in atx1setm, the most enriched Gene Ontology categories were cell wall organization and H2O2 metabolism, the latter of which included PEROXIDASE35 (PRX35). The LRP morphogenesis abnormalities were similar in prx35 and atx1 mutants. Both the deposition of H3K4me3 at the PRX35 promoter and the PRX35 expression in the atx1setm mutant were significantly reduced.Our results reveal a link between LR development and a redox homeostasis controlled by ATX1 at epigenetic level by maintaining active transcription of PRX35 and thereby impacting root system formation.

Developmental processes are regulated at multiple levels, including the epigenetic level. Among the epigenetic factors, histone H3 lysine 4 (H3K4) methyltransferases contribute to active transcription of target genes, and here, we explored how the H3K4 methyltransferase ARABIDOPSIS HOMOLOG OF TRITHORAX1 (ATX1) affects Arabidopsis thaliana lateral root (LR) primordium (LRP) morphogenesis.

We examined LR development in a loss‐of‐function null mutant (atx1‐1) and a mutant affected in the ATX1 catalytic domain (atx1setm) through bright‐field and long‐term time‐lapse confocal microscopy, transcriptomics, and chromatin immunoprecipitation.

LRP morphogenesis in both mutants was severely abnormal, resulting from altered principal growth directions, and was accompanied by extended cell cycle durations and slower transitions between LRP stages. Among the differentially expressed genes downregulated in atx1setm, the most enriched Gene Ontology categories were cell wall organization and H2O2 metabolism, the latter of which included PEROXIDASE35 (PRX35). The LRP morphogenesis abnormalities were similar in prx35 and atx1 mutants. Both the deposition of H3K4me3 at the PRX35 promoter and the PRX35 expression in the atx1setm mutant were significantly reduced.

Our results reveal a link between LR development and a redox homeostasis controlled by ATX1 at epigenetic level by maintaining active transcription of PRX35 and thereby impacting root system formation.