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Cooperative adaptive cruise control (CACC) for human and autonomous self-driving aims to achieve active safe driving that avoids vehicle accidents or traffic jam by exchanging the road traffic information (e.g., traffic flow, traffic density, velocity variation, etc.) among neighbor vehicles. However, in CACC, the butterfly effect is encountered while exhibiting asynchronous brakes that easily lead to backward shock-waves and are difficult to remove. Several critical issues should be addressed in CACC, including (i) difficulties with adaptive steering of the inter-vehicle distances among neighbor vehicles and the vehicle speed, (ii) the butterfly effect, (iii) unstable vehicle traffic flow, etc. To address the above issues in CACC, this paper proposes the mobile edge computing-based vehicular cloud of the cooperative adaptive driving (CAD) approach to avoid shock-waves efficiently in platoon driving. Numerical results demonstrate that the CAD approach outperforms the compared techniques in the number of shock-waves, average vehicle velocity, average travel time and time to collision (TTC). Additionally, the adaptive platoon length is determined according to the traffic information gathered from the global and local clouds.

This study investigated several visualizations, including enhancing relevant information and impairing distracting information, that harnessed the visual salience effect with augmented reality (AR) to assist people in searching for targets. The experiment used a scenario of shopping for food products where participants searched for the target product wearing an AR head-mounted display that presented the visualizations. In addition, the field-dependent (FD) and field-independent (FI) cognitive styles of users were investigated. First, FI participants completed the product selection tasks more quickly than FD participants when using the visualizations of enhancing relevant information but not the visualizations of impairing distracting information. Second, the visualizations of impairing irrelevant information improved the search speed but not the accuracy of FD participants compared to the visualizations of enhancing relevant information. Third, participants perceived a higher clarity of the highlighted items when they were highlighted with a frame rather than an overlay. [ABSTRACT FROM AUTHOR]

SETX (senataxin) is an RNA/DNA helicase that has been implicated in transcriptional regulation and the DNA damage response through resolution of R-loop structures. Mutations in SETX result in either of two distinct neurodegenerative disorders. SETX dominant mutations result in a juvenile form of amyotrophic lateral sclerosis (ALS) called ALS4, whereas recessive mutations are responsible for ataxia called ataxia with oculomotor apraxia type 2 (AOA2). How mutations in the same protein can lead to different phenotypes is still unclear. To elucidate AOA2 disease mechanisms, we first examined gene expression changes following SETX depletion. We observed the effects on both transcription and RNA processing, but surprisingly observed decreased R-loop accumulation in SETX-depleted cells. Importantly, we discovered a strong connection between SETX and the macroautophagy/autophagy pathway, reflecting a direct effect on transcription of autophagy genes. We show that SETX depletion inhibits the progression of autophagy, leading to an accumulation of ubiquitinated proteins, decreased ability to clear protein aggregates, as well as mitochondrial defects. Analysis of AOA2 patient fibroblasts also revealed a perturbation of the autophagy pathway. Our work has thus identified a novel function for SETX in the regulation of autophagy, whose modulation may have a therapeutic impact for AOA2. Abbreviations: 3ʹREADS: 3ʹ region extraction and deep sequencing; ACTB: actin beta; ALS4: amyotrophic lateral sclerosis type 4; AOA2: ataxia with oculomotor apraxia type 2; APA: alternative polyadenylation; AS: alternative splicing; ATG7: autophagy-related 7; ATP6V0D2: ATPase H+ transporting V0 subunit D2; BAF: bafilomycin A1; BECN1: beclin 1; ChIP: chromatin IP; Chloro: chloroquine; CPT: camptothecin; DDR: DNA damage response; DNMT1: DNA methyltransferase 1; DRIP: DNA/RNA IP; DSBs: double strand breaks; EBs: embryoid bodies; FTD: frontotemporal dementia; GABARAP: GABA type A receptor-associated protein; GO: gene ontology; HR: homologous recombination; HTT: huntingtin; IF: immunofluorescence; IP: immunoprecipitation; iPSCs: induced pluripotent stem cells; KD: knockdown; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MN: motor neuron; MTORC1: mechanistic target of rapamycin kinase complex 1; PASS: PolyA Site Supporting; PFA: paraformaldehyde; RNAPII: RNA polymerase II; SCA: spinocerebellar ataxia; SETX: senataxin; SMA: spinal muscular atrophy; SMN1: survival of motor neuron 1, telomeric; SQSTM1/p62: sequestosome 1; TFEB: transcription factor EB; TSS: transcription start site; TTS: transcription termination site; ULK1: unc-51 like autophagy activating kinase 1; WB: western blot; WIPI2: WD repeat domain, phosphoinositide interacting 2; XRN2: 5ʹ-3ʹ exoribonuclease 2. [ABSTRACT FROM AUTHOR]

This study involved developing a time-division multiplexing monopulse antenna system for tracking the DVB-SH signal operated in S-band. Such a system consists of a mode-former circuit and a stacked circularly polarized antenna array, which was implemented using planar-printed circuit technology. In the mode-former circuit, a four-way power splitter comprising Wilkinson power dividers and four switched-line phase shifters were employed to provide 0^\circ/180^\circ phase angles at each output port. The sum-and-difference angle discriminators were implemented along vertical and horizontal planes for detecting the incident elevation and azimuth angles. The stacked circularly polarized antenna array, composed of four edge-fed patches on the bottom layer and four corresponding parasitic patches, were exploited on the top layer to increase the axial ratio bandwidth. The experimental results revealed that, at 2.185 GHz, the null depth of the difference patterns were -34.2 dB and -33.2 dB along the two principal planes. [ABSTRACT FROM PUBLISHER]

Ribosome structure and activity are challenged at high temperatures, often demanding modifications to ribosomal RNAs (rRNAs) to retain translation fidelity. LC-MS/MS, bisulfite-sequencing, and high-resolution cryo-EM structures of the archaeal ribosome identified an RNA modification, N 4, N 4-dimethylcytidine (m 4 2 C), at the universally conserved C918 in the 16S rRNA helix 31 loop. Here, we characterize and structurally resolve a class of RNA methyltransferase that generates m 4 2 C whose function is critical for hyperthermophilic growth. m 4 2 C is synthesized by the activity of a unique family of RNA methyltransferase containing a Rossman-fold that targets only intact ribosomes. The phylogenetic distribution of the newly identified m 4 2 C synthase family implies that m 4 2 C is biologically relevant in each domain. Resistance of m 4 2 C to bisulfite-driven deamination suggests that efforts to capture m 5 C profiles via bisulfite sequencing are also capturing m 4 2 C., Competing Interests: Competing interests statement:K.A.F., P.S.H., V.T., L.E., J.S., H.P.F., R.C., and T.J.S. do not have any competing financial interests nor conflicts of interest to report. N.D., E.J.W., R.T.F., Y.-L.T., G.B.R., and I.R.C. are employed and funded by New England Biolabs, Inc., a manufacturer and vendor of molecular biology reagents, including nucleic acid modifying and synthesis enzymes. The authors state that this affiliation does not affect their impartiality, objectivity of data generation or interpretation, adherence to journal standards and policies, or availability of data.

Dysregulation of the DNA/RNA-binding protein FUS causes certain subtypes of ALS/FTD by largely unknown mechanisms. Recent evidence has shown that FUS toxic gain of function due either to mutations or to increased expression can disrupt critical cellular processes, including mitochondrial functions. Here, we demonstrate that in human cells overexpressing wild-type FUS or expressing mutant derivatives, the protein associates with multiple mRNAs, and these are enriched in mRNAs encoding mitochondrial respiratory chain components. Notably, this sequestration leads to reduced levels of the encoded proteins, which is sufficient to bring about disorganized mitochondrial networks, reduced aerobic respiration and increased reactive oxygen species. We further show that mutant FUS associates with mitochondria and with mRNAs encoded by the mitochondrial genome. Importantly, similar results were also observed in fibroblasts derived from ALS patients with FUS mutations. Finally, we demonstrate that FUS loss of function does not underlie the observed mitochondrial dysfunction, and also provides a mechanism for the preferential sequestration of the respiratory chain complex mRNAs by FUS that does not involve sequence-specific binding. Together, our data reveal that respiratory chain complex mRNA sequestration underlies the mitochondrial defects characteristic of ALS/FTD and contributes to the FUS toxic gain of function linked to this disease spectrum., (© 2020 Tsai et al.; Published by Cold Spring Harbor Laboratory Press.)

Firefly luminescence is an intriguing phenomenon with potential technological applications, whose biochemistry background was only recently established. The physics side of this phenomenon, however, was still unclear, specifically as far as the oxygen supply mechanism for light flashing is concerned. This uncertainty is due to the complex microscopic structure of the tracheal system: without fully knowing its geometry, one cannot reliably test the proposed mechanisms. We solved this problem using synchrotron phase contrast microtomography and transmission x-ray microscopy, finding that the oxygen consumption corresponding to mitochondria functions exceeds the maximum rate of oxygen diffusion from the tracheal system to the photocytes. Furthermore, the flashing mechanism uses a large portion of this maximum rate. Thus, the flashing control requires passivation of the mitochondria functions, e.g., by nitric oxide, and switching of the oxygen supply from them to photoluminescence.