title: Selenite-induced hormonal and signalling mechanisms during root growth of Arabidopsis thaliana L.
abstract: Selenium excess can cause toxicity symptoms, e.g. root growth inhibition in non-hyperaccumulator plants such as Arabidopsis. Selenite-induced hormonal and signalling mechanisms in the course of development are poorly understood; therefore this study set out to investigate the possible hormonal and signalling processes using transgenic and mutant Arabidopsis plants. Significant alterations were observed in the root architecture of the selenite-treated plants, due to the loss of cell viability in the root apex. During mild selenite excess, the plants showed symptoms of the morphogenic response: primary root (PR) shortening and increased initiation of laterals, ensuring better nutrient and water uptake and stress acclimation. As well as lower meristem cell activity, the second reason for the Se-induced growth hindrance is the hormonal imbalance, since the in situ expression of the auxin-responsive DR5::GUS, and consequently the auxin levels, significantly decreased, while that of the cytokinin-inducible ARR5::GUS and the ethylene biosynthetic ACS8::GUS increased. It is assumed that auxin and ethylene might positively regulate selenium tolerance, since reduced levels of them resulted in sensitivity. Moreover, high cytokinin levels caused notable selenite tolerance. During early seedling development, nitric oxide (NO) contents decreased but hydrogen peroxide levels increased reflecting the antagonism between the two signal molecules during Se excess. High levels of NO in gsnor1-3, lead to selenite tolerance, while low NO production in nia1nia2 resulted in selenite sensitivity. Consequently, NO derived from the root nitrate reductase activity is responsible for the large-scale selenite tolerance in Arabidopsis.
authors.affiliation: Department of Plant Biology, Faculty of Science and Informatics, University of Szeged, Szeged, Hungary. lehotai.nora@gmail.com
authors.forename: Nóra
authors.initials: N
authors.lastname: Lehotai
authors.forename: Zsuzsanna
authors.initials: Z
authors.lastname: Kolbert
authors.forename: Andrea
authors.initials: A
authors.lastname: Peto
authors.forename: Gábor
authors.initials: G
authors.lastname: Feigl
authors.forename: Attila
authors.initials: A
authors.lastname: Ördög
authors.forename: Devanand
authors.initials: D
authors.lastname: Kumar
authors.forename: Irma
authors.initials: I
authors.lastname: Tari
authors.forename: László
authors.initials: L
authors.lastname: Erdei
mesh_terms: D017360:Arabidopsis / Q000187:drug effects* / Q000235:genetics / Q000254:growth & development / Q000502:physiology; D029681:Arabidopsis Proteins / Q000235:genetics; D002470:Cell Survival; D003583:Cytokinins / Q000378:metabolism; D005030:Ethylenes / Q000378:metabolism; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D006706:Homeostasis / Q000187:drug effects*; D006861:Hydrogen Peroxide / Q000378:metabolism; D007210:Indoleacetic Acids / Q000378:metabolism; D018519:Meristem / Q000187:drug effects / Q000235:genetics / Q000254:growth & development / Q000502:physiology; D009154:Mutation; D009569:Nitric Oxide / Q000378:metabolism; D010937:Plant Growth Regulators / Q000378:metabolism*; D018517:Plant Roots / Q000187:drug effects* / Q000235:genetics / Q000254:growth & development / Q000502:physiology; D018520:Plant Shoots / Q000187:drug effects / Q000235:genetics / Q000254:growth & development / Q000502:physiology; D020887:Selenious Acid / Q000494:pharmacology*; D012643:Selenium / Q000032:analysis / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013312:Stress, Physiological / Q000187:drug effects
chemical_list: D029681:Arabidopsis Proteins; D003583:Cytokinins; D005030:Ethylenes; D007210:Indoleacetic Acids; D010937:Plant Growth Regulators; D009569:Nitric Oxide; C036216:ethylene; D006861:Hydrogen Peroxide; D020887:Selenious Acid; D012643:Selenium