title: The beta-subunit of the Arabidopsis G protein negatively regulates auxin-induced cell division and affects multiple developmental processes.
abstract: Plant cells respond to low concentrations of auxin by cell expansion, and at a slightly higher concentration, these cells divide. Previous work revealed that null mutants of the alpha-subunit of a putative heterotrimeric G protein (GPA1) have reduced cell division. Here, we show that this prototypical G protein complex acts mechanistically by controlling auxin sensitivity toward cell division. Loss-of-function G protein mutants have altered auxin-mediated cell division throughout development, especially during the auxin-induced formation of lateral and adventitious root primordia. Ectopic expression of the wild-type Galpha-subunit phenocopies the Gbeta mutants (auxin hypersensitivity), probably by sequestering the Gbetagamma-subunits, whereas overexpression of Gbeta reduces auxin sensitivity and a constitutively active (Q222L) mutant Galpha behaves like the wild type. These data are consistent with a model in which Gbetagamma acts as a negative regulator of auxin-induced cell division. Accordingly, basal repression of approximately one-third of the identified auxin-regulated genes (47 of 150 upregulated genes among 8300 quantitated) is lost in the Gbeta transcript-null mutant. Included among these are genes that encode proteins proposed to control cell division in root primordia formation as well as several novel genes. These results suggest that although auxin-regulated cell division is not coupled directly by a G protein, the Gbeta-subunit attenuates this auxin pathway upstream of the control of mRNA steady state levels.
authors.affiliation: Department of Biology, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-3280, USA.
authors.forename: Hemayet
authors.initials: H
authors.lastname: Ullah
authors.forename: Jin-Gui
authors.initials: JG
authors.lastname: Chen
authors.forename: Brenda
authors.initials: B
authors.lastname: Temple
authors.forename: Douglas C
authors.initials: DC
authors.lastname: Boyes
authors.forename: José M
authors.initials: JM
authors.lastname: Alonso
authors.forename: Keith R
authors.initials: KR
authors.lastname: Davis
authors.forename: Joseph R
authors.initials: JR
authors.lastname: Ecker
authors.forename: Alan M
authors.initials: AM
authors.lastname: Jones
mesh_terms: D000483:Alleles; D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics* / Q000254:growth & development; D029681:Arabidopsis Proteins / Q000235:genetics* / Q000378:metabolism; D002455:Cell Division / Q000187:drug effects; D044385:GTP-Binding Protein alpha Subunits; D044387:GTP-Binding Protein beta Subunits; D020869:Gene Expression Profiling / Q000379:methods; D018506:Gene Expression Regulation, Plant; D005816:Genetic Complementation Test; D020962:Heterotrimeric GTP-Binding Proteins / Q000235:genetics* / Q000378:metabolism; D007210:Indoleacetic Acids / Q000494:pharmacology*; D008027:Light; D008958:Models, Molecular; D009154:Mutation; D010641:Phenotype; D010937:Plant Growth Regulators / Q000494:pharmacology; D018517:Plant Roots / Q000187:drug effects / Q000235:genetics / Q000254:growth & development
chemical_list: C089590:AGB1 protein, Arabidopsis; D029681:Arabidopsis Proteins; C429765:GPA1 protein, Arabidopsis; D044385:GTP-Binding Protein alpha Subunits; D044387:GTP-Binding Protein beta Subunits; D007210:Indoleacetic Acids; D010937:Plant Growth Regulators; D020962:Heterotrimeric GTP-Binding Proteins