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  - 
TY  - JOUR
A1  - Lambour, Benjamin
A1  - Glenz, René
A1  - Forner, Carmen
A1  - Krischke, Markus
A1  - Mueller, Martin J.
A1  - Fekete, Agnes
A1  - Waller, Frank
T1  - Sphingolipid long-chain base phosphate degradation can be a rate-limiting step in long-chain base homeostasis
JF  - Frontiers in Plant Science
N2  - Sphingolipid long-chain bases (LCBs) are building blocks for membrane-localized sphingolipids, and are involved in signal transduction pathways in plants. Elevated LCB levels are associated with the induction of programmed cell death and pathogen-derived toxin-induced cell death. Therefore, levels of free LCBs can determine survival of plant cells. To elucidate the contribution of metabolic pathways regulating high LCB levels, we applied the deuterium-labeled LCB D-erythro-sphinganine-d7 (D7-d18:0), the first LCB in sphingolipid biosynthesis, to Arabidopsis leaves and quantified labeled LCBs, LCB phosphates (LCB-Ps), and 14 abundant ceramide (Cer) species over time. We show that LCB D7-d18:0 is rapidly converted into the LCBs d18:0P, t18:0, and t18:0P. Deuterium-labeled ceramides were less abundant, but increased over time, with the highest levels detected for Cer(d18:0/16:0), Cer(d18:0/24:0), Cer(t18:0/16:0), and Cer(t18:0/22:0). A more than 50-fold increase of LCB-P levels after leaf incubation in LCB D7-d18:0 indicated that degradation of LCBs via LCB-Ps is important, and we hypothesized that LCB-P degradation could be a rate-limiting step to reduce high levels of LCBs. To functionally test this hypothesis, we constructed a transgenic line with dihydrosphingosine-1-phosphate lyase 1 (DPL1) under control of an inducible promotor. Higher expression of DPL1 significantly reduced elevated LCB-P and LCB levels induced by Fumonisin B1, and rendered plants more resistant against this fungal toxin. Taken together, we provide quantitative data on the contribution of major enzymatic pathways to reduce high LCB levels, which can trigger cell death. Specifically, we provide functional evidence that DPL1 can be a rate-limiting step in regulating high LCB levels.
KW  - sphingolipid
KW  - long-chain base
KW  - plant sphingolipid metabolism
KW  - cell death
KW  - metabolic flux analysis
KW  - dihydrosphingosine-1-phosphate lyase
KW  - LC–MS/MS
Y1  - 2022
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-277679
SN  - 1664-462X
VL  - 13
ER  -