@article{JonesHuangHedrichetal.2022,
  author    = {Jones, Jeffrey J. and Huang, Shouguang and Hedrich, Rainer and Geilfus, Christoph-Martin and Roelfsema, M. Rob G.},
  title     = {The green light gap: a window of opportunity for optogenetic control of stomatal movement},
  series = {New Phytologist},
  volume    = {236},
  journal   = {New Phytologist},
  number    = {4},
  doi       = {10.1111/nph.18451},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-293724},
  pages     = {1237 -- 1244},
  year      = {2022},
  abstract  = {Green plants are equipped with photoreceptors that are capable of sensing radiation in the ultraviolet-to-blue and the red-to-far-red parts of the light spectrum. However, plant cells are not particularly sensitive to green light (GL), and light which lies within this part of the spectrum does not efficiently trigger the opening of stomatal pores. Here, we discuss the current knowledge of stomatal responses to light, which are either provoked via photosynthetically active radiation or by specific blue light (BL) signaling pathways. The limited impact of GL on stomatal movements provides a unique option to use this light quality to control optogenetic tools. Recently, several of these tools have been optimized for use in plant biological research, either to control gene expression, or to provoke ion fluxes. Initial studies with the BL-activated potassium channel BLINK1 showed that this tool can speed up stomatal movements. Moreover, the GL-sensitive anion channel GtACR1 can induce stomatal closure, even at conditions that provoke stomatal opening in wild-type plants. Given that crop plants in controlled-environment agriculture and horticulture are often cultivated with artificial light sources (i.e. a combination of blue and red light from light-emitting diodes), GL signals can be used as a remote-control signal that controls stomatal transpiration and water consumption.},
  language  = {en}
}
@article{BazihizinaBoehmMessereretal.2022,
  author    = {Bazihizina, Nadia and B{\"o}hm, Jennifer and Messerer, Maxim and Stigloher, Christian and M{\"u}ller, Heike M. and Cuin, Tracey Ann and Maierhofer, Tobias and Cabot, Joan and Mayer, Klaus F. X. and Fella, Christian and Huang, Shouguang and Al-Rasheid, Khaled A. S. and Alquraishi, Saleh and Breadmore, Michael and Mancuso, Stefano and Shabala, Sergey and Ache, Peter and Zhang, Heng and Zhu, Jian-Kang and Hedrich, Rainer and Scherzer, S{\"o}nke},
  title     = {Stalk cell polar ion transport provide for bladder-based salinity tolerance in Chenopodium quinoa},
  series = {New Phytologist},
  volume    = {235},
  journal   = {New Phytologist},
  number    = {5},
  doi       = {10.1111/nph.18205},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-287222},
  pages     = {1822 -- 1835},
  year      = {2022},
  abstract  = {Chenopodium quinoa uses epidermal bladder cells (EBCs) to sequester excess salt. Each EBC complex consists of a leaf epidermal cell, a stalk cell, and the bladder. Under salt stress, sodium (Na\(^{+}\)), chloride (Cl\(^{-}\)), potassium (K\(^{+}\)) and various metabolites are shuttled from the leaf lamina to the bladders. Stalk cells operate as both a selectivity filter and a flux controller. In line with the nature of a transfer cell, advanced transmission electron tomography, electrophysiology, and fluorescent tracer flux studies revealed the stalk cell's polar organization and bladder-directed solute flow. RNA sequencing and cluster analysis revealed the gene expression profiles of the stalk cells. Among the stalk cell enriched genes, ion channels and carriers as well as sugar transporters were most pronounced. Based on their electrophysiological fingerprint and thermodynamic considerations, a model for stalk cell transcellular transport was derived.},
  language  = {en}
}
@article{ScherzerHuangIosipetal.2022,
  author    = {Scherzer, S{\"o}nke and Huang, Shouguang and Iosip, Anda and Kreuzer, Ines and Yokawa, Ken and Al-Rasheid, Khaled A. S. and Heckmann, Manfred and Hedrich, Rainer},
  title     = {Ether anesthetics prevents touch-induced trigger hair calcium-electrical signals excite the Venus flytrap},
  series = {Scientific reports},
  volume    = {12},
  journal   = {Scientific reports},
  doi       = {10.1038/s41598-022-06915-z},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-300411},
  year      = {2022},
  abstract  = {Plants do not have neurons but operate transmembrane ion channels and can get electrical excited by physical and chemical clues. Among them the Venus flytrap is characterized by its peculiar hapto-electric signaling. When insects collide with trigger hairs emerging the trap inner surface, the mechanical stimulus within the mechanosensory organ is translated into a calcium signal and an action potential (AP). Here we asked how the Ca\(^{2+}\) wave and AP is initiated in the trigger hair and how it is feed into systemic trap calcium-electrical networks. When Dionaea muscipula trigger hairs matures and develop hapto-electric excitability the mechanosensitive anion channel DmMSL10/FLYC1 and voltage dependent SKOR type Shaker K\(^{+}\) channel are expressed in the sheering stress sensitive podium. The podium of the trigger hair is interface to the flytrap's prey capture and processing networks. In the excitable state touch stimulation of the trigger hair evokes a rise in the podium Ca2+ first and before the calcium signal together with an action potential travel all over the trap surface. In search for podium ion channels and pumps mediating touch induced Ca\(^{2+}\) transients, we, in mature trigger hairs firing fast Ca\(^{2+}\) signals and APs, found OSCA1.7 and GLR3.6 type Ca\(^{2+}\) channels and ACA2/10 Ca\(^{2+}\) pumps specifically expressed in the podium. Like trigger hair stimulation, glutamate application to the trap directly evoked a propagating Ca\(^{2+}\) and electrical event. Given that anesthetics affect K\(^+\) channels and glutamate receptors in the animal system we exposed flytraps to an ether atmosphere. As result propagation of touch and glutamate induced Ca\(^{2+}\) and AP long-distance signaling got suppressed, while the trap completely recovered excitability when ether was replaced by fresh air. In line with ether targeting a calcium channel addressing a Ca\(^{2+}\) activated anion channel the AP amplitude declined before the electrical signal ceased completely. Ether in the mechanosensory organ did neither prevent the touch induction of a calcium signal nor this post stimulus decay. This finding indicates that ether prevents the touch activated, glr3.6 expressing base of the trigger hair to excite the capture organ.},
  language  = {en}
}