TY  - JOUR
A1  - Schäbler, Stefan
A1  - Amatobi, Kelechi M.
A1  - Horn, Melanie
A1  - Rieger, Dirk
A1  - Helfrich‑Förster, Charlotte
A1  - Mueller, Martin J.
A1  - Wegener, Christian
A1  - Fekete, Agnes
T1  - Loss of function in the Drosophila clock gene period results in altered intermediary lipid metabolism and increased susceptibility to starvation
JF  - Cellular and Molecular Life Sciences
N2  - The fruit fly Drosophila is a prime model in circadian research, but still little is known about its circadian regulation of metabolism. Daily rhythmicity in levels of several metabolites has been found, but knowledge about hydrophobic metabolites is limited. We here compared metabolite levels including lipids between period\(^{01}\) (per\(^{01}\)) clock mutants and Canton-S wildtype  (WT\(_{CS}\)) flies in an isogenic and non-isogenic background using LC–MS. In the non-isogenic background, metabo-lites with differing levels comprised essential amino acids, kynurenines, pterinates, glycero(phospho)lipids, and fatty acid esters. Notably, detectable diacylglycerols (DAG) and acylcarnitines (AC), involved in lipid metabolism, showed lower levels in per\(^{01}\) mutants. Most of these differences disappeared in the isogenic background, yet the level differences for AC as well as DAG were consistent for fly bodies. AC levels were dependent on the time of day in WTCS in phase with food consumption under LD conditions, while DAGs showed weak daily oscillations. Two short-chain ACs continued to cycle even in constant darkness. per\(^{01}\) mutants in LD showed no or very weak diel AC oscillations out of phase with feeding activity. The low levels of DAGs and ACs in per\(^{01}\) did not correlate with lower total food consumption, body mass or weight. Clock mutant flies showed higher sensitivity to starvation independent of their background-dependent activity level. Our results suggest that neither feeding, energy storage nor mobilisation is significantly affected in per\(^{01}\) mutants, but point towards impaired mitochondrial activity, supported by upregulation of the mitochondrial stress marker 4EBP in the clock mutants
KW  - circadian rhythms
KW  - metabolomics
KW  - mitochondrial activity
KW  - tryptophan
KW  - acylcarnitine
KW  - feeding
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-232432
SN  - 1420-682X
VL  - 77
ER  - 
TY  - JOUR
A1  - Ferber, Elena
A1  - Gerhards, Julian
A1  - Sauer, Miriam
A1  - Krischke, Markus
A1  - Dittrich, Marcus T.
A1  - Müller, Tobias
A1  - Berger, Susanne
A1  - Fekete, Agnes
A1  - Mueller, Martin J.
T1  - Chemical Priming by Isothiocyanates Protects Against Intoxication by Products of the Mustard Oil Bomb
JF  - Frontiers in Plant Science
N2  - In Brassicaceae, tissue damage triggers the mustard oil bomb i.e., activates the degradation of glucosinolates by myrosinases leading to a rapid accumulation of isothiocyanates at the site of damage. Isothiocyanates are reactive electrophilic species (RES) known to covalently bind to thiols in proteins and glutathione, a process that is not only toxic to herbivores and microbes but can also cause cell death of healthy plant tissues. Previously, it has been shown that subtoxic isothiocyanate concentrations can induce transcriptional reprogramming in intact plant cells. Glutathione depletion by RES leading to breakdown of the redox potential has been proposed as a central and common RES signal transduction mechanism. Using transcriptome analyses, we show that after exposure of Arabidopsis seedlings (grown in liquid culture) to subtoxic concentrations of sulforaphane hundreds of genes were regulated without depletion of the cellular glutathione pool. Heat shock genes were among the most highly up-regulated genes and this response was found to be dependent on the canonical heat shock factors A1 (HSFA1). HSFA1-deficient plants were more sensitive to isothiocyanates than wild type plants. Moreover, pretreatment of Arabidopsis seedlings with subtoxic concentrations of isothiocyanates increased resistance against exposure to toxic levels of isothiocyanates and, hence, may reduce the autotoxicity of the mustard oil bomb by inducing cell protection mechanisms.
KW  - autotoxicity
KW  - heat shock response
KW  - isothiocyanates
KW  - mustard oil bomb
KW  - reactive electrophilic species
KW  - redox homeostasis
KW  - sulforaphane
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-207104
SN  - 1664-462X
VL  - 11
ER  -