BIG Modulates Stem Cell Niche and Meristem Development via SCR/SHR Pathway in Arabidopsis Roots

Int J Mol Sci. 2022 Jun 17;23(12):6784. doi: 10.3390/ijms23126784.

Abstract

BIG, a regulator of polar auxin transport, is necessary to regulate the growth and development of Arabidopsis. Although mutations in the BIG gene cause severe root developmental defects, the exact mechanism remains unclear. Here, we report that disruption of the BIG gene resulted in decreased quiescent center (QC) activity and columella cell numbers, which was accompanied by the downregulation of WUSCHEL-RELATED HOMEOBOX5 (WOX5) gene expression. BIG affected auxin distribution by regulating the expression of PIN-FORMED proteins (PINs), but the root morphological defects of big mutants could not be rescued solely by increasing auxin transport. Although the loss of BIG gene function resulted in decreased expression of the PLT1 and PLT2 genes, genetic interaction assays indicate that this is not the main reason for the root morphological defects of big mutants. Furthermore, genetic interaction assays suggest that BIG affects the stem cell niche (SCN) activity through the SCRSCARECROW (SCR)/SHORT ROOT (SHR) pathway and BIG disruption reduces the expression of SCR and SHR genes. In conclusion, our findings reveal that the BIG gene maintains root meristem activity and SCN integrity mainly through the SCR/SHR pathway.

Keywords: BIG; PLETHORA; SCARECROW; SHORT ROOT; polar auxin transport; stem cell niche.

MeSH terms

  • Arabidopsis Proteins* / genetics
  • Arabidopsis Proteins* / metabolism
  • Arabidopsis* / metabolism
  • Calmodulin-Binding Proteins / metabolism
  • Cell Division
  • Gene Expression Regulation, Plant
  • Indoleacetic Acids / metabolism
  • Meristem
  • Plant Roots / metabolism
  • Stem Cell Niche / genetics
  • Ubiquitin-Protein Ligases / metabolism

Substances

  • Arabidopsis Proteins
  • BIG protein, Arabidopsis
  • Calmodulin-Binding Proteins
  • Indoleacetic Acids
  • BIG BROTHER protein, Arabidopsis
  • Ubiquitin-Protein Ligases