TY - JOUR A1 - Schroeder, Florian A1 - Lisso, Janina A1 - Obata, Toshihiro A1 - Erban, Alexander A1 - Maximova, Eugenia A1 - Giavalisco, Patrick A1 - Kopka, Joachim A1 - Fernie, Alisdair R. A1 - Willmitzer, Lothar A1 - Muessig, Carsten T1 - Consequences of induced brassinosteroid deficiency in Arabidopsis leaves JF - BMC plant biology N2 - Background: The identification of brassinosteroid (BR) deficient and BR insensitive mutants provided conclusive evidence that BR is a potent growth-promoting phytohormone. Arabidopsis mutants are characterized by a compact rosette structure, decreased plant height and reduced root system, delayed development, and reduced fertility. Cell expansion, cell division, and multiple developmental processes depend on BR. The molecular and physiological basis of BR action is diverse. The BR signalling pathway controls the activity of transcription factors, and numerous BR responsive genes have been identified. The analysis of dwarf mutants, however, may to some extent reveal phenotypic changes that are an effect of the altered morphology and physiology. This restriction holds particularly true for the analysis of established organs such as rosette leaves. Results: In this study, the mode of BR action was analysed in established leaves by means of two approaches. First, an inhibitor of BR biosynthesis (brassinazole) was applied to 21-day-old wild-type plants. Secondly, BR complementation of BR deficient plants, namely CPD (constitutive photomorphogenic dwarf)-antisense and cbb1 (cabbage1) mutant plants was stopped after 21 days. BR action in established leaves is associated with stimulated cell expansion, an increase in leaf index, starch accumulation, enhanced CO2 release by the tricarboxylic acid cycle, and increased biomass production. Cell number and protein content were barely affected. Conclusion: Previous analysis of BR promoted growth focused on genomic effects. However, the link between growth and changes in gene expression patterns barely provided clues to the physiological and metabolic basis of growth. Our study analysed comprehensive metabolic data sets of leaves with altered BR levels. The data suggest that BR promoted growth may depend on the increased provision and use of carbohydrates and energy. BR may stimulate both anabolic and catabolic pathways. KW - Brassinosteroids KW - Arabidopsis KW - Tricarboxylic acid cycle KW - Biomass KW - Cell expansion KW - Growth Y1 - 2014 U6 - https://doi.org/10.1186/s12870-014-0309-0 SN - 1471-2229 VL - 14 PB - BioMed Central CY - London ER - TY - JOUR A1 - Schröder, Florian A1 - Lisso, Janina A1 - Muessig, Carsten T1 - Exordium-Like1 promotes growth during low carbon availability in arabidopsis JF - Plant physiology : an international journal devoted to physiology, biochemistry, cellular and molecular biology, biophysics and environmental biology of plants N2 - Little is known about genes that control growth and development under low carbon (C) availability. The Arabidopsis (Arabidopsis thaliana) EXORDIUM-LIKE1 (EXL1) gene (At1g35140) was identified as a brassinosteroid-regulated gene in a previous study. We show here that the EXL1 protein is required for adaptation to C-and energy-limiting growth conditions. In-depth analysis of EXL1 transcript levels under various environmental conditions indicated that EXL1 expression is controlled by the C and energy status. Sugar starvation, extended night, and anoxia stress induced EXL1 gene expression. The C status also determined EXL1 protein levels. These results suggested that EXL1 is involved in the C-starvation response. Phenotypic changes of an exl1 loss-of-function mutant became evident only under corresponding experimental conditions. The mutant showed diminished biomass production in a short-day/low-light growth regime, impaired survival during extended night, and impaired survival of anoxia stress. Basic metabolic processes and signaling pathways are presumed to be barely impaired in exl1, because the mutant showed wild-type levels of major sugars, and transcript levels of only a few genes such as QUA-QUINE STARCH were altered. Our data suggest that EXL1 is part of a regulatory pathway that controls growth and development when C and energy supply is poor. Y1 - 2011 U6 - https://doi.org/10.1104/pp.111.177204 SN - 0032-0889 VL - 156 IS - 3 SP - 1620 EP - 1630 PB - American Society of Plant Physiologists CY - Rockville ER - TY - JOUR A1 - Lisso, Janina A1 - Schröder, Florian A1 - Fisahn, Joachim A1 - Muessig, Carsten T1 - NFX1-LIKE2 (NFXL2) Suppresses Abscisic Acid Accumulation and Stomatal Closure in Arabidopsis thaliana JF - PLoS one N2 - The NFX1-LIKE1 (NFXL1) and NFXL2 genes were identified as regulators of salt stress responses. The NFXL1 protein is a nuclear factor that positively affects adaptation to salt stress. The nfxl1-1 loss-of-function mutant displayed reduced survival rates under salt and high light stress. In contrast, the nfxl2-1 mutant, defective in the NFXL2 gene, and NFXL2-antisense plants exhibited enhanced survival under these conditions. We show here that the loss of NFXL2 function results in abscisic acid (ABA) overaccumulation, reduced stomatal conductance, and enhanced survival under drought stress. The nfxl2-1 mutant displayed reduced stomatal aperture under all conditions tested. Fusicoccin treatment, exposition to increasing light intensities, and supply of decreasing CO2 concentrations demonstrated full opening capacity of nfxl2-1 stomata. Reduced stomatal opening presumably is a consequence of elevated ABA levels. Furthermore, seedling growth, root growth, and stomatal closure were hypersensitive to exogenous ABA. The enhanced ABA responses may contribute to the improved drought stress resistance of the mutant. Three NFXL2 splice variants were cloned and named NFXL2-78, NFXL2-97, and NFXL2-100 according to the molecular weight of the putative proteins. Translational fusions to the green fluorescent protein suggest nuclear localisation of the NFXL2 proteins. Stable expression of the NFXL2-78 splice variant in nfxl2-1 plants largely complemented the mutant phenotype. Our data show that NFXL2 controls ABA levels and suppresses ABA responses. NFXL2 may prevent unnecessary and costly stress adaptation under favourable conditions. Y1 - 2011 U6 - https://doi.org/10.1371/journal.pone.0026982 SN - 1932-6203 VL - 6 IS - 11 PB - PLoS CY - San Fransisco ER -