title: DNA damage inhibits lateral root formation by up-regulating cytokinin biosynthesis genes in Arabidopsis thaliana.
abstract: Lateral roots (LRs) are an important organ for water and nutrient uptake from soil. Thus, control of LR formation is crucial in the adaptation of plant growth to environmental conditions. However, the underlying mechanism controlling LR formation in response to external factors has remained largely unknown. Here, we found that LR formation was inhibited by DNA damage. Treatment with zeocin, which causes DNA double-strand breaks, up-regulated several DNA repair genes in the LR primordium (LRP) through the signaling pathway mediated by the transcription factor SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1). Cell division was severely inhibited in the LRP of zeocin-treated sog1-1 mutant, which in turn inhibited LR formation. This result suggests that SOG1-mediated maintenance of genome integrity is crucial for proper cell division during LRP development. Furthermore, zeocin induced several cytokinin biosynthesis genes in a SOG1-dependent manner, thereby activating cytokinin signaling in the LRP. LR formation was less inhibited by zeocin in mutants defective in cytokinin biosynthesis or signaling, suggesting that elevated cytokinin signaling is crucial for the inhibition of LR formation in response to DNA damage. We conclude that SOG1 regulates DNA repair and cytokinin signaling separately and plays a key role in controlling LR formation under genotoxic stress.
authors.affiliation: Graduate School of Biological Sciences, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara, 630-0192, Japan.
authors.forename: La Ode Muhammad Muchdar
authors.initials: OM
authors.lastname: Davis
authors.affiliation: Graduate School of Biological Sciences, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara, 630-0192, Japan.
authors.forename: Nobuo
authors.initials: N
authors.lastname: Ogita
authors.affiliation: Graduate School of Biological Sciences, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara, 630-0192, Japan.
authors.forename: Soichi
authors.initials: S
authors.lastname: Inagaki
authors.affiliation: Graduate School of Biological Sciences, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara, 630-0192, Japan.
authors.forename: Naoki
authors.initials: N
authors.lastname: Takahashi
authors.affiliation: Graduate School of Biological Sciences, Nara Institute of Science and Technology, Takayama 8916-5, Ikoma, Nara, 630-0192, Japan.|JST, CREST, Takayama 8916-5, Ikoma, Nara, 630-0192, Japan.
authors.forename: Masaaki
authors.initials: M
authors.lastname: Umeda
mesh_terms: D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics* / Q000254:growth & development; D029681:Arabidopsis Proteins / Q000378:metabolism; D064007:Ataxia Telangiectasia Mutated Proteins / Q000378:metabolism; D001761:Bleomycin / Q000494:pharmacology; D002455:Cell Division / Q000235:genetics; D003583:Cytokinins / Q000096:biosynthesis / Q000235:genetics*; D004249:DNA Damage; D018744:DNA, Plant; D018506:Gene Expression Regulation, Plant; D018745:Genome, Plant; D009154:Mutation; D018517:Plant Roots / Q000187:drug effects / Q000254:growth & development*; D015398:Signal Transduction; D014157:Transcription Factors / Q000378:metabolism
chemical_list: C576589:ATM protein, Arabidopsis; D029681:Arabidopsis Proteins; D003583:Cytokinins; D018744:DNA, Plant; C561308:SOG1 protein, Arabidopsis; D014157:Transcription Factors; D001761:Bleomycin; C105427:Zeocin; D064007:Ataxia Telangiectasia Mutated Proteins