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 Tax

Research output: Contribution to journalArticle

15 Citations (Scopus)

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 2010

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Brassinosteroids
Arabidopsis
Phenotype
Mutation
Phosphotransferases
Dwarfism
Organ Size
Steroid Receptors
Protein Folding
Cell Surface Receptors
Endoplasmic Reticulum
Cell Division
Cell Membrane
Hormones
Ligands

ASJC Scopus subject areas

  • Genetics

Cite this

Belkhadir, Y., Durbak, A., Wierzba, M., Schmitz, R. J., Aguirre, A., Michel, R., ... Tax, F. (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

Intragenic suppression of a trafficking-defective brassinosteroid receptor mutant in arabidopsis. / Belkhadir, Youssef; Durbak, Amanda; Wierzba, Michael; Schmitz, Robert J.; Aguirre, Andrea; Michel, Rene; Rowe, Scott; Fujioka, Shozo; Tax, Frans.

In: Genetics, Vol. 185, No. 4, 08.2010, p. 1283-1296.

Research output: Contribution to journalArticle

Belkhadir, Y, Durbak, A, Wierzba, M, Schmitz, RJ, Aguirre, A, Michel, R, Rowe, S, Fujioka, S & Tax, F 2010, 'Intragenic suppression of a trafficking-defective brassinosteroid receptor mutant in arabidopsis', Genetics, vol. 185, no. 4, pp. 1283-1296. https://doi.org/10.1534/genetics.109.111898
Belkhadir Y, Durbak A, Wierzba M, Schmitz RJ, Aguirre A, Michel R et al. Intragenic suppression of a trafficking-defective brassinosteroid receptor mutant in arabidopsis. Genetics. 2010 Aug;185(4):1283-1296. https://doi.org/10.1534/genetics.109.111898
Belkhadir, Youssef ; Durbak, Amanda ; Wierzba, Michael ; Schmitz, Robert J. ; Aguirre, Andrea ; Michel, Rene ; Rowe, Scott ; Fujioka, Shozo ; Tax, Frans. / Intragenic suppression of a trafficking-defective brassinosteroid receptor mutant in arabidopsis. In: Genetics. 2010 ; Vol. 185, No. 4. pp. 1283-1296.
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