@phdthesis{Schroeder2011,
  author    = {Schr{\"o}der, Florian},
  title     = {Funktionelle Charakterisierung der EXO/EXL-Proteinfamilie und NFXL2-Isoformen in Arabidopsis thaliana},
  address   = {Potsdam},
  pages     = {86 S.},
  year      = {2011},
  language  = {de}
}
@article{SchroederLissoMuessig2011,
  author    = {Schr{\"o}der, Florian and Lisso, Janina and Muessig, Carsten},
  title     = {Exordium-Like1 promotes growth during low carbon availability in arabidopsis},
  series = {Plant physiology : an international journal devoted to physiology, biochemistry, cellular and molecular biology, biophysics and environmental biology of plants},
  volume    = {156},
  journal   = {Plant physiology : an international journal devoted to physiology, biochemistry, cellular and molecular biology, biophysics and environmental biology of plants},
  number    = {3},
  publisher = {American Society of Plant Physiologists},
  address   = {Rockville},
  issn      = {0032-0889},
  doi       = {10.1104/pp.111.177204},
  pages     = {1620 -- 1630},
  year      = {2011},
  abstract  = {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.},
  language  = {en}
}
@article{LissoSchroederFisahnetal.2011,
  author    = {Lisso, Janina and Schr{\"o}der, Florian and Fisahn, Joachim and Muessig, Carsten},
  title     = {NFX1-LIKE2 (NFXL2) Suppresses Abscisic Acid Accumulation and Stomatal Closure in Arabidopsis thaliana},
  series = {PLoS one},
  volume    = {6},
  journal   = {PLoS one},
  number    = {11},
  publisher = {PLoS},
  address   = {San Fransisco},
  issn      = {1932-6203},
  doi       = {10.1371/journal.pone.0026982},
  pages     = {12},
  year      = {2011},
  abstract  = {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.},
  language  = {en}
}