Intragenic suppression of a trafficking-defective brassinosteroid receptor mutant in arabidopsis

Youssef Belkhadir, Amanda Durbak, Michael Wierzba, Robert J. Schmitz, Andrea Aguirre, Rene Michel, Scott Rowe, Shozo Fujioka, Frans E. Tax

Research output: Contribution to journalArticle

16 Scopus citations

Abstract

The cell surface receptor kinase BRASSINOSTEROID-INSENSITIVE-1 (BRI1) is the major receptor for steroid hormones in Arabidopsis. Plants homozygous for loss-of-function mutations in BRI1 display a reduction in the size of vegetative organs, resulting in dwarfism. The recessive bri1-5 mutation produces receptors that do not accumulate to wild-type levels and are retained mainly in the endoplasmic reticulum. We have isolated a dominant suppressor of the dwarf phenotype of bri1-5 plants. We show that this suppression is caused by a second-site mutation in BRI1, bri1-5R1. The bri1-5R1 mutation partially rescues the phenotypes of bri1-5 in many tissues and enhances bri1-5 phenotypes above wild-type levels in several other tissues. We demonstrate that the phenotypes of bri1-5R1 plants are due to both increased cell expansion and increased cell division. To test the mechanism of bri1-5 suppression, we assessed whether the phenotypic suppression in bri1-5R1 was dependent on ligand availability and the integrity of the signaling pathway. Our results indicate that the suppression of the dwarf phenotypes associated with bri1-5R1 requires both BR biosynthesis and the receptor kinase BRI1-ASSOCIATED KINASE-1 (BAK1). Finally, we show that bri1-5R1 partially restores the accumulation and plasma membrane localization of BRI1. Collectively, our results point toward a model in which bri1-R1 compensates for the protein-folding abnormalities caused by bri1-5, restoring accumulation of the receptor and its delivery to the cell surface.

Original languageEnglish (US)
Pages (from-to)1283-1296
Number of pages14
JournalGenetics
Volume185
Issue number4
DOIs
StatePublished - Aug 1 2010

ASJC Scopus subject areas

  • Genetics

Fingerprint Dive into the research topics of 'Intragenic suppression of a trafficking-defective brassinosteroid receptor mutant in arabidopsis'. Together they form a unique fingerprint.

  • Cite this

    Belkhadir, Y., Durbak, A., Wierzba, M., Schmitz, R. J., Aguirre, A., Michel, R., Rowe, S., Fujioka, S., & Tax, F. E. (2010). Intragenic suppression of a trafficking-defective brassinosteroid receptor mutant in arabidopsis. Genetics, 185(4), 1283-1296. https://doi.org/10.1534/genetics.109.111898