Waymarking in Social Robots: Environment Signaling Using Human–Robot Interaction

Travellers use the term waymarking to define the action of posting signs, or waymarks, along a route. These marks are intended to be points of reference during navigation for the environment. In this research, we will define waymarking as the skill of a robot to signal the environment or generate information to facilitate localization and navigation, both for its own use and for other robots as well. We present an automated environment signaling system using human–robot interaction and radio frequency identification (RFID) technology. The goal is for the robot, through human–robot interaction, to obtain information from the environment and use this information to carry out the signaling or waymarking process. HRI will play a key role in the signaling process since this type of communication makes it possible to exchange more specific and enriching information. The robot uses common phrases such as “Where am I?” and “Where can I go?”, just as we humans do when we ask other people for information about the environment. It is also possible to guide the robot and “show” it the environment to carry out the task of writing the signs. The robot will use the information received to create, update, or improve the navigation data in the RFID signals. In this paper, the signaling process will be described, how the robot acquires the information for signals, writing and updating process and finally, the implementation and integration in a real social robot in a real indoor environment.

Charismatic Tour-Guiding: Scale Development and Validation

Charismatic leadership has been conceptualized as a signaling process whereby a leader influences followers to achieve effective management. Although there have been many studies on charismatic leadership, no scale exists to measure tour leaders’ charismatic guiding. Thus, the purpose of this study was to develop a valid and reliable charismatic-guiding scale for tour leaders, from the perspectives of both tour leaders and tour members. Through a rigorous development process, the study’s 20-item, 4-dimensional tour leaders’ charismatic-guiding scale was proven to be valid and reliable. The novel scale may function as a tool for tour leaders to measure their charismatic guiding as well as for travel agencies in their assignment of tour leaders. This study applied charismatic leadership theory to tourism, furthering knowledge of charismatic guiding in tour leaders and establishing a foundation for future theoretical development.

ASFV pD345L protein negatively regulates NF-kB signaling through inhibiting IKK kinase activity

The NF-κB pathway is an essential signaling process against viral infection including African swine fever virus (ASFV). ASFV encodes for more than 151 proteins by its own transcription machinery and possesses a great capacity to evade or subvert antiviral innate immune responses. A couple of such viral proteins have been reported, but many remain unknown. Here, we showed that pD345L, an ASFV-encoded lambda-like exonuclease, is an inhibitor of cGAS/STING mediated NF-κB sig-naling by blocking IKKα/β kinase activity. Specifically, we showed that overexpression of pD345L suppresses cGAS/STING induced IFNβ and NF-κB activation, resulting in decreased transcription of IFNβ and several pro-inflammatory cytokines, including IL-1α, IL-6, IL-8, and TNFα. In addition, we showed that pD345L targeted at or downstream of IKK and upstream of p65. Importantly, we found that pD345L associates with KD and HLH domains of IKKα and LZ domain of IKKβ, and thus interrupts their kinase activity on downstream substrate IκBα. Finally, we showed that pD345L inhibition of NF-κB signaling was independent of its exonuclease activity. Taken together, we concluded that pD345L blocks IKKα/β kinase activity by protein-protein interaction and thus disrupts cGAS/STING mediated NF-κB signaling.

Homeostatic Depression Shows Heightened Sensitivity to Synaptic Calcium

Synapses and circuits rely on homeostatic forms of regulation in order to transmit meaningful information. The Drosophila melanogaster neuromuscular junction (NMJ) is a well-studied synapse that shows robust homeostatic control of function. Most prior studies of homeostatic plasticity at the NMJ have centered on presynaptic homeostatic potentiation (PHP). PHP happens when postsynaptic muscle neurotransmitter receptors are impaired, triggering retrograde signaling that causes an increase in presynaptic neurotransmitter release. As a result, normal levels of evoked excitation are maintained. The counterpart to PHP at the NMJ is presynaptic homeostatic depression (PHD). Overexpression of the Drosophila vesicular glutamate transporter (VGlut) causes an increase in the amplitude of spontaneous events. PHD happens when the synapse responds to the challenge by decreasing quantal content (QC) during evoked neurotransmission—again, resulting in normal levels of postsynaptic excitation. We hypothesized that there may exist a class of molecules that affects both PHP and PHD. Impairment of any such molecule could hurt a synapse’s ability to respond to any significant homeostatic challenge. We conducted an electrophysiology-based screen for blocks of PHD. We did not observe a block of PHD in the genetic conditions screened, but we found loss-of-function conditions that led to a substantial deficit in evoked amplitude when combined with VGlut overexpression. The conditions causing this phenotype included a double heterozygous loss-of-function condition for genes encoding the inositol trisphosphate receptor (IP3R —itpr) and ryanodine receptor (RyR). IP3Rs and RyRs gate calcium release from intracellular stores. Pharmacological agents targeting IP3R and RyR recapitulated the genetic losses of these factors, as did lowering calcium levels from other sources. Our data are consistent with the idea that the homeostatic signaling process underlying PHD is especially sensitive to levels of calcium at the presynapse.

Plasmodesmata-localized proteins and ROS orchestrate light-induced rapid systemic signaling in Arabidopsis

Systemic signaling and systemic acquired acclimation (SAA) are key to the survival of plants during episodes of abiotic stress. These processes depend on a continuous chain of cell-to-cell signaling events that extends from the initial tissue that senses the stress (the local tissue) to the entire plant (systemic tissues). Reactive oxygen species (ROS) and Ca2+ are key signaling molecules thought to be involved in this cell-to-cell mechanism. Here, we report that the systemic response of Arabidopsis thaliana to a local treatment of high light stress, which resulted in local ROS accumulation, required ROS generated by respiratory burst oxidase homolog D (RBOHD). ROS increased cell-to-cell transport and plasmodesmata (PD) pore size in a manner dependent on PD-localized protein 1 (PDLP1) and PDLP5, and this process was required for the propagation of the systemic ROS signals and SAA. Furthermore, aquaporins and several Ca2+-permeable channels in the glutamate receptor–like (GLR), mechanosensitive small conductance–like (MSL), and cyclic nucleotide–gated (CNGC) families were involved in this systemic signaling process. However, we determined that these channels were required primarily to amplify the systemic signal in each cell along the path of the systemic ROS wave, as well as to establish local and systemic acclimation. Thus, PD and RBOHD-generated ROS orchestrate light stress–induced rapid cell-to-cell spread of systemic signals in Arabidopsis.

Enhanced Production of the Mical Redox Domain for Enzymology and F-actin Disassembly Assays

To change their behaviors, cells require actin proteins to assemble together into long polymers/filaments—and so a critical goal is to understand the factors that control this actin filament (F-actin) assembly and stability. We have identified a family of unusual actin regulators, the MICALs, which are flavoprotein monooxygenase/hydroxylase enzymes that associate with flavin adenine dinucleotide (FAD) and use the co-enzyme nicotinamide adenine dinucleotide phosphate (NADPH) in Redox reactions. F-actin is a specific substrate for these MICAL Redox enzymes, which oxidize specific amino acids within actin to destabilize actin filaments. Furthermore, this MICAL-catalyzed reaction is reversed by another family of Redox enzymes (SelR/MsrB enzymes)—thereby revealing a reversible Redox signaling process and biochemical mechanism regulating actin dynamics. Interestingly, in addition to the MICALs’ Redox enzymatic portion through which MICALs covalently modify and affect actin, MICALs have multiple other domains. Less is known about the roles of these other MICAL domains. Here we provide approaches for obtaining high levels of recombinant protein for the Redox only portion of Mical and demonstrate its catalytic and F-actin disassembly activity. These results provide a ground state for future work aimed at defining the role of the other domains of Mical — including characterizing their effects on Mical’s Redox enzymatic and F-actin disassembly activity.

Structure, Activation and Regulation of NLRP3 and AIM2 Inflammasomes

The inflammasome is a three-component (sensor, adaptor, and effector) filamentous signaling platform that shields from multiple pathogenic infections by stimulating the proteolytical maturation of proinflammatory cytokines and pyroptotic cell death. The signaling process initiates with the detection of endogenous and/or external danger signals by specific sensors, followed by the nucleation and polymerization from sensor to downstream adaptor and then to the effector, caspase-1. Aberrant activation of inflammasomes promotes autoinflammatory diseases, cancer, neurodegeneration, and cardiometabolic disorders. Therefore, an equitable level of regulation is required to maintain the equilibrium between inflammasome activation and inhibition. Recent advancement in the structural and mechanistic understanding of inflammasome assembly potentiates the emergence of novel therapeutics against inflammasome-regulated diseases. In this review, we have comprehensively discussed the recent and updated insights into the structure of inflammasome components, their activation, interaction, mechanism of regulation, and finally, the formation of densely packed filamentous inflammasome complex that exists as micron-sized punctum in the cells and mediates the immune responses.

Photosensitive tyrosine analogues unravel site-dependent phosphorylation in TrkA initiated MAPK/ERK signaling

Tyrosine kinase A (TrkA) is a membrane receptor which, upon ligand binding, activates several pathways including MAPK/ERK signaling, implicated in a spectrum of human pathologies; thus, TrkA is an emerging therapeutic target in treatment of neuronal diseases and cancer. However, mechanistic insights into TrKA signaling are lacking due to lack of site-dependent phosphorylation control. Here we engineer two light-sensitive tyrosine analogues, namely p-azido-L-phenylalanine (AzF) and the caged-tyrosine (ONB), through amber codon suppression to optically manipulate the phosphorylation state of individual intracellular tyrosines in TrkA. We identify TrkA-AzF and ONB mutants, which can activate the ERK pathway in the absence of NGF ligand binding through light control. Our results not only reveal how TrkA site-dependent phosphorylation controls the defined signaling process, but also extend the genetic code expansion technology to enable regulation of receptor-type kinase activation by optical control at the precision of a single phosphorylation site. It paves the way for comprehensive analysis of kinase-associated pathways as well as screening of compounds intervening in a site-directed phosphorylation pathway for targeted therapy.