The full repertoire of Drosophila gustatory receptors for detecting an aversive compound.

The ability to detect toxic compounds in foods is essential for animal survival. However, the minimal subunit composition of gustatory receptors required for sensing aversive chemicals in Drosophila is unknown. Here we report that three gustatory receptors, GR8a, GR66a and GR98b function together in the detection of L-canavanine, a plant-derived insecticide. Ectopic co-expression of Gr8a and Gr98b in Gr66a-expressing, bitter-sensing gustatory receptor neurons (GRNs) confers responsiveness to L-canavanine. Furthermore, misexpression of all three Grs enables salt- or sweet-sensing GRNs to respond to L-canavanine. Introduction of these Grs in sweet-sensing GRNs switches L-canavanine from an aversive to an attractive compound. Co-expression of GR8a, GR66a and GR98b in Drosophila S2 cells induces an L-canavanine-activated nonselective cation conductance. We conclude that three GRs collaborate to produce a functional L-canavanine receptor. Thus, our results clarify the full set of GRs underlying the detection of a toxic tastant that drives avoidance behaviour in an insect

Objective Function and Parameter Calibrations of Flood Forecasting Models

Source: ICHE Conference Archive - https://mdi-de.baw.de/icheArchiv

Associations Among the Opioid Receptor Gene (OPRM1) A118G Polymorphism, Psychiatric Symptoms, and Quantitative EEG in Korean Males with Gambling Disorder: A Pilot Study

Background and aims: A single nucleotide polymorphism of A118G (SNP; rs1799971) in the opioid receptor μ-1 (OPRM1) gene is a missense variant that influences the affinity of μ-opioid receptors. This study aimed to investigate the associations among the A118G polymorphism in the OPRM1 gene, psychiatric symptoms, and quantitative electroencephalography (qEEG) findings in patients with gambling disorder. Methods: Fifty-five male patients with gambling disorder aged between 18 and 65 years old participated in the study. The A118G polymorphism was genotyped into the AA, GA, and GG groups by the polymerase chain reaction/restriction fragment length polymorphism method. Resting-state qEEG was recorded with the eyes closed, and the absolute power of the delta (1–4 Hz), theta (4–8 Hz), alpha (8–12 Hz), and beta (12–30 Hz) frequency bands was analyzed. Psychiatric symptoms, including depression, anxiety, impulsivity and severity of gambling, were assessed by a self-rating scale. Results: There were no significant differences in psychiatric symptoms among the three genotype groups (AA, GA, and GG). However, the frequency band power of qEEG showed significant differences among the three genotype groups. The absolute power of the beta and theta bands in the frontal lobe was higher in G allele carriers. Discussion and conclusion: Based on the findings of this study, the polymorphism in the OPRM1 gene might affect the neurophysiological process in patients with gambling disorder

Positional Effects of Fluorination in Conjugated Side Chains on Photovoltaic Properties of Donor-Acceptor Copolymers

The position at which conjugated side chains were fluorinated, the meta- or ortho-position in phenyl side chains, was varied to investigate the positional effects of fluorination on the energy levels, crystalline ordering, and photovoltaic properties of the polymers. The fluorine in the ortho-position achieved a lower HOMO energy level than that in the meta-position, but reduced the chain rigidity.1116Ysciescopu

EEG correlates associated with the severity of gambling disorder and serum BDNF levels in patients with gambling disorder

Background and aims This study aimed to evaluate the association between the severity of pathological gambling, serum brain-derived neurotrophic factor (BDNF) level, and the characteristics of quantitative electroencephalography (EEG) in patients with gambling disorder. Methods A total of 55 male patients aged 18–65 with gambling disorder participated. The severity of pathological gambling was assessed with the nine-item Problem Gambling Severity Index from the Canadian Problem Gambling Index (CPGI-PGSI). The Beck Depression Inventory and Lubben Social Network Scale were also assessed. Serum BDNF levels were assessed from blood samples. The resting-state EEG was recorded while the eyes were closed, and the absolute power of five frequency bands was analyzed: delta (1–4 Hz), theta (4–8 Hz), alpha (8–12 Hz), beta (12–30 Hz), and gamma (30–50 Hz). Results Serum BDNF level was positively correlated with theta power in the right parietal region (P4, r = .403, p = .011), beta power in the right parietal region (P4, r = .456, p = .010), and beta power in the right temporal region (T8, r = .421, p = .008). Gambling severity (CPGI-PGSI) was positively correlated with absolute beta power in the left frontal region (F7, r = .284, p = .043) and central region [(C3, r = .292, p = .038), (C4, r = .304, p = .030)]. Conclusions These findings support the hypothesis that right-dominant lateralized correlations between BDNF and beta and theta power reflect right-dominant brain activation in addiction. The positive correlations between beta power and the severity of gambling disorder may be associated with hyperexcitability and increased cravings. These findings contribute to a better understanding of brain-based electrophysiological changes and BDNF levels in patients with pathological gambling

BubR1 acetylation at prometaphase is required for modulating APC/C activity and timing of mitosis

Regulation of BubR1 is central to the control of APC/C activity. We have found that BubR1 forms a complex with PCAF and is acetylated at lysine 250. Using mass spectrometry and acetylated BubR1-specific antibodies, we have confirmed that BubR1 acetylation occurs at prometaphase. Importantly, BubR1 acetylation was required for checkpoint function, through the inhibition of ubiquitin-dependent BubR1 degradation. BubR1 degradation began before the onset of anaphase. It was noted that the pre-anaphase degradation was regulated by BubR1 acetylation. Degradation of an acetylation-mimetic form, BubR1–K250Q, was inhibited and chromosome segregation in cells expressing BubR1–K250Q was markedly delayed. By contrast, the acetylation-deficient mutant, BubR1–K250R, was unstable, and mitosis was accelerated in BubR1–K250R-expressing cells. Furthermore, we found that APC/C–Cdc20 was responsible for BubR1 degradation during mitosis. On the basis of our collective results, we propose that the acetylation status of BubR1 is a molecular switch that converts BubR1 from an inhibitor to a substrate of the APC/C complex, thus providing an efficient way to modulate APC/C activity and mitotic timing

Calsyntenins Function as Synaptogenic Adhesion Molecules in Concert with Neurexins

SummaryMultiple synaptic adhesion molecules govern synapse formation. Here, we propose calsyntenin-3/alcadein-β as a synapse organizer that specifically induces presynaptic differentiation in heterologous synapse-formation assays. Calsyntenin-3 (CST-3) is highly expressed during various postnatal periods of mouse brain development. The simultaneous knockdown of all three CSTs, but not CST-3 alone, decreases inhibitory, but not excitatory, synapse densities in cultured hippocampal neurons. Moreover, the knockdown of CSTs specifically reduces inhibitory synaptic transmission in vitro and in vivo. Remarkably, the loss of CSTs induces a concomitant decrease in neuron soma size in a non-cell-autonomous manner. Furthermore, α-neurexins (α-Nrxs) are components of a CST-3 complex involved in CST-3-mediated presynaptic differentiation. However, CST-3 does not directly bind to Nrxs. Viewed together, these data suggest that the three CSTs redundantly regulate inhibitory synapse formation, inhibitory synapse function, and neuron development in concert with Nrxs

ZnO nanoparticle growth on single-walled carbon nanotubes by atomic laye r deposition and a consequent lifetime elongation of nanotube field emission emission

ZnO nanoparticles were grown on single-walled carbon nanotubes (SWNTs) by atomic layer deposition using diethylzinc (DEZ) and water. The athors discuss that, because of chemical inertness of nanotubes to DEZ and water molecules, such nanoparticles are not likely to grow on the wall of clean and perfect nanotubes. Rather, the growth of ZnO nanoparticles should be attributed to imperfection of nanotubes, such as defects and carbonaceous impurities. Lifetime of field emission from SWNTs with the ZnO nanoparticles is 2.5 times longer than that from the as-grown nanotubes. It is thought that the protection of the defects or impurities by ZnO nanoparticles mainly contributed to the improvement of the field emission lifetime from SWNTs.open262

Deregulated DNA ADP-ribosylation impairs telomere replication

The recognition that DNA can be ADP ribosylated provides an unexpected regulatory level of how ADP-ribosylation contributes to genome stability, epigenetics and immunity. Yet, it remains unknown whether DNA ADP-ribosylation (DNA-ADPr) promotes genome stability and how it is regulated. Here, we show that telomeres are subject to DNA-ADPr catalyzed by PARP1 and removed by TARG1. Mechanistically, we show that DNA-ADPr is coupled to lagging telomere DNA strand synthesis, forming at single-stranded DNA present at unligated Okazaki fragments and on the 3′ single-stranded telomere overhang. Persistent DNA-linked ADPr, due to TARG1 deficiency, eventually leads to telomere shortening. Furthermore, using the bacterial DNA ADP-ribosyl-transferase toxin to modify DNA at telomeres directly, we demonstrate that unhydrolyzed DNA-linked ADP-ribose compromises telomere replication and telomere integrity. Thus, by identifying telomeres as chromosomal targets of PARP1 and TARG1-regulated DNA-ADPr, whose deregulation compromises telomere replication and integrity, our study highlights and establishes the critical importance of controlling DNA-ADPr turnover for sustained genome stability