An allelic series of bak1 mutations differentially alter bir1 cell death, immune response, growth, and root development phenotypes in Arabidopsis thaliana

Michael P. Wierzba, Frans Tax

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Receptor-like kinases (RLKs) mediate cell-signaling pathways in Arabidopsis thaliana, including those controlling growth and development, immune response, and cell death. The RLK coreceptor BRI1-ASSOCIATED KINASE-1 (BAK1) partners with multiple ligand-binding RLKs and contributes to their signaling in diverse pathways. An additional RLK, BAK1-INTERACTING RECEPTOR-1 (BIR1), physically interacts with BAK1, and loss-of-function mutations in BIR1 display constitutive activation of cell death and immune response pathways and dwarfism and a reduction in lateral root number. Here we show that bir1 plants display defects in primary root growth, characterize bir1 lateral root defects, and analyze expression of BIR1 and BAK1 promoters within the root. Using an allelic series of bak1 mutations, we show that loss of BAK1 function in immune response pathways can partially suppress bir1 cell death, immune response, and lateral root phenotypes and that null bak1 alleles enhance bir1 primary root phenotypes. Based on our data, we propose a model in which BIR1 functions to regulate BAK1 participation in multiple pathways.

Original languageEnglish (US)
Pages (from-to)689-702
Number of pages14
JournalGenetics
Volume202
Issue number2
DOIs
StatePublished - Feb 1 2016

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Growth and Development
Arabidopsis
Cell Death
Phosphotransferases
Phenotype
Mutation
Dwarfism
Sexual Partners
Alleles
Ligands
Growth

Keywords

  • Cell death
  • Genetic suppression
  • Lateral roots
  • Receptor-like kinases

ASJC Scopus subject areas

  • Genetics

Cite this

An allelic series of bak1 mutations differentially alter bir1 cell death, immune response, growth, and root development phenotypes in Arabidopsis thaliana. / Wierzba, Michael P.; Tax, Frans.

In: Genetics, Vol. 202, No. 2, 01.02.2016, p. 689-702.

Research output: Contribution to journalArticle

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