TY  - JOUR
A1  - Huang, Shouguang
A1  - Ding, Meiqi
A1  - Roelfsema, M. Rob G.
A1  - Dreyer, Ingo
A1  - Scherzer, Sönke
A1  - Al-Rasheid, Khaled A. S
A1  - Gao, Shiqiang
A1  - Nagel, Georg
A1  - Hedrich, Rainer
A1  - Konrad, Kai R.
T1  - Optogenetic control of the guard cell membrane potential and stomatal movement by the light-gated anion channel GtACR1
JF  - Science Advances
N2  - Guard cells control the aperture of plant stomata, which are crucial for global fluxes of CO\(_2\) and water. In turn, guard cell anion channels are seen as key players for stomatal closure, but is activation of these channels sufficient to limit plant water loss? To answer this open question, we used an optogenetic approach based on the light-gated anion channelrhodopsin 1 (GtACR1). In tobacco guard cells that express GtACR1, blue- and green-light pulses elicit Cl\(^-\) and NO\(_3\)\(^-\) currents of -1 to -2 nA. The anion currents depolarize the plasma membrane by 60 to 80 mV, which causes opening of voltage-gated K+ channels and the extrusion of K+. As a result, continuous stimulation with green light leads to loss of guard cell turgor and closure of stomata at conditions that provoke stomatal opening in wild type. GtACR1 optogenetics thus provides unequivocal evidence that opening of anion channels is sufficient to close stomata.
KW  - abscisic-acid activation
KW  - Arabidopsis thaliana
KW  - H+-atpase
KW  - signal transduction
KW  - potassium channel
KW  - intact plants
KW  - K+ channels
KW  - R-type
KW  - CO2
KW  - SLAC1
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-260925
VL  - 7
IS  - 28
ER  - 
TY  - JOUR
A1  - Kucka, Kirstin
A1  - Lang, Isabell
A1  - Zhang, Tengyu
A1  - Siegmund, Daniela
A1  - Medler, Juliane
A1  - Wajant, Harald
T1  - Membrane lymphotoxin-α\(_2\)β is a novel tumor necrosis factor (TNF) receptor 2 (TNFR2) agonist
JF  - Cell Death & Disease
N2  - In the early 1990s, it has been described that LTα and LTβ form LTα\(_2\)β and LTαβ\(_2\) heterotrimers, which bind to TNFR1 and LTβR, respectively. Afterwards, the LTαβ\(_2\)–LTβR system has been intensively studied while the LTα\(_2\)β–TNFR1 interaction has been ignored to date, presumably due to the fact that at the time of identification of the LTα\(_2\)β–TNFR1 interaction one knew already two ligands for TNFR1, namely TNF and LTα. Here, we show that LTα\(_2\)β interacts not only with TNFR1 but also with TNFR2. We furthermore demonstrate that membrane-bound LTα\(_2\)β (memLTα\(_2\)β), despite its asymmetric structure, stimulates TNFR1 and TNFR2 signaling. Not surprising in view of its ability to interact with TNFR2, LTα\(_2\)β is inhibited by Etanercept, which is approved for the treatment of rheumatoid arthritis and also inhibits TNF and LTα.
KW  - cytokines
KW  - signal transduction
Y1  - 2021
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-260077
VL  - 12
IS  - 4
ER  -