title: ATR and MKP1 play distinct roles in response to UV-B stress in Arabidopsis.
abstract: Ultraviolet-B (UV-B) stress activates MAP kinases (MAPKs) MPK3 and MPK6 in Arabidopsis. MAPK activity must be tightly controlled in order to ensure an appropriate cellular outcome. MAPK phosphatases (MKPs) effectively control MAPKs by dephosphorylation of phosphothreonine and phosphotyrosine in their activation loops. Arabidopsis MKP1 is an important regulator of MPK3 and MPK6, and mkp1 knockout mutants are hypersensitive to UV-B stress, which is associated with reduced inactivation of MPK3 and MPK6. Here, we demonstrate that MPK3 and MPK6 are hyperactivated in response to UV-B in plants that are deficient in photorepair, suggesting that UV-damaged DNA is a trigger of MAPK signaling. This is not due to a block in replication, as, in contrast to atr, the mkp1 mutant is not hypersensitive to the replication-inhibiting drug hydroxyurea, hydroxyurea does not activate MPK3 and MPK6, and atr is not impaired in MPK3 and MPK6 activation in response to UV-B. We further show that mkp1 leaves and roots are UV-B hypersensitive, whereas atr is mainly affected at the root level. Tolerance to UV-B stress has been previously associated with stem cell removal and CYCB1;1 accumulation. Although UV-B-induced stem cell death and CYCB1;1 expression are not altered in mkp1 roots, CYCB1;1 expression is reduced in mkp1 leaves. We conclude that the MKP1 and ATR pathways operate in parallel, with primary roles for ATR in roots and MKP1 in leaves.
authors.affiliation: Department of Botany and Plant Biology, University of Geneva, Sciences III, CH-1211, Geneva 4, Switzerland.
authors.forename: Marina A
authors.initials: MA
authors.lastname: González Besteiro
authors.forename: Roman
authors.initials: R
authors.lastname: Ulm
mesh_terms: D017360:Arabidopsis / Q000187:drug effects / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects*; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism*; D064007:Ataxia Telangiectasia Mutated Proteins; D018797:Cell Cycle Proteins / Q000235:genetics / Q000378:metabolism*; D016923:Cell Death / Q000235:genetics / Q000528:radiation effects; D019926:Cyclin B / Q000235:genetics / Q000378:metabolism; D004249:DNA Damage / Q000502:physiology / Q000528:radiation effects; D004261:DNA Replication / Q000187:drug effects / Q000235:genetics; D004789:Enzyme Activation / Q000528:radiation effects; D018506:Gene Expression Regulation, Plant; D006918:Hydroxyurea / Q000494:pharmacology; D020929:Mitogen-Activated Protein Kinase Kinases / Q000235:genetics / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D009154:Mutation; D018515:Plant Leaves / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects; D018517:Plant Roots / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects; D030821:Plants, Genetically Modified; D017346:Protein Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism*; D017027:Protein Tyrosine Phosphatases; D013312:Stress, Physiological
chemical_list: D029681:Arabidopsis Proteins; D018797:Cell Cycle Proteins; C462528:CycB1 protein, Arabidopsis; D019926:Cyclin B; C576892:ATR protein, Arabidopsis; D064007:Ataxia Telangiectasia Mutated Proteins; D017346:Protein Serine-Threonine Kinases; C458516:AtMPK3 protein, Arabidopsis; C436293:MPK6 protein, Arabidopsis; D020928:Mitogen-Activated Protein Kinases; D020929:Mitogen-Activated Protein Kinase Kinases; C499612:MKP1 protein, Arabidopsis; D017027:Protein Tyrosine Phosphatases; D006918:Hydroxyurea