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Intolerance of uncertainty (IU) has been suggested to be associated with emotional perceptions and evaluations. Several studies have also revealed that IU is related to cognitive preferences, in particular gain-relevant risk preference. Nevertheless, it is still unclear whether both prospective and inhibitory IU, two dimensions of IU, predict gain-related and moreover, loss-relevant risky preference. More importantly, it is unknown whether the associations between IU and risk preference are modulated by biological factors (e.g., genes). Therefore, the current study investigated whether prospective and inhibitory IU were associated with gain-/loss-related risk preference and whether the associations were modulated by an impulsivity control-related gene, tryptophan hydroxylase 1 (TPH1) gene (A779C, rs1799913) through recruiting 222 healthy Chinese participants. Results showed that prospective IU was correlated with gain-relevant risk averse. There was not a significant association between IU and loss-relevant risk preference. Nevertheless, further analysis revealed that the association was modulated by the TPH1 genotype. Prospective and inhibitory IU predicted loss-relevant risk averse specifically for TPH1 AC genotype carriers but not for other genotype carriers (i.e., AA or CC). The findings emphasize the associations between IU and risk preference depending on frame and genetic variance., Author(s): Huiyan Lin [sup.1] [sup.2] , Junkai Yang [sup.1] , Jianping Hu [sup.1] Author Affiliations: (1) https://ror.org/04grzdh47, grid.464294.9, 0000 0004 1805 7312, Laboratory for Behavioral and Regional Finance, Guangdong University [...]

Author(s): Ole Herud-Sikimic [sup.1] , Andre C. Stiel [sup.1] [sup.2] , Martina Kolb [sup.1] , Sooruban Shanmugaratnam [sup.1] [sup.3] , Kenneth W. Berendzen [sup.4] , Christian Feldhaus [sup.1] , Birte [...], One of the most important regulatory small molecules in plants is indole-3-acetic acid, also known as auxin. Its dynamic redistribution has an essential role in almost every aspect of plant life, ranging from cell shape and division to organogenesis and responses to light and gravity.sup.1,2. So far, it has not been possible to directly determine the spatial and temporal distribution of auxin at a cellular resolution. Instead it is inferred from the visualization of irreversible processes that involve the endogenous auxin-response machinery.sup.3-7; however, such a system cannot detect transient changes. Here we report a genetically encoded biosensor for the quantitative in vivo visualization of auxin distribution. The sensor is based on the Escherichia coli tryptophan repressor.sup.8, the binding pocket of which is engineered to be specific to auxin. Coupling of the auxin-binding moiety with selected fluorescent proteins enables the use of a fluorescence resonance energy transfer signal as a readout. Unlike previous systems, this sensor enables direct monitoring of the rapid uptake and clearance of auxin by individual cells and within cell compartments in planta. By responding to the graded spatial distribution along the root axis and its perturbation by transport inhibitors--as well as the rapid and reversible redistribution of endogenous auxin in response to changes in gravity vectors--our sensor enables real-time monitoring of auxin concentrations at a (sub)cellular resolution and their spatial and temporal changes during the lifespan of a plant. A genetically encoded sensor for the quantitative visualization of auxin distribution in plants enables real-time monitoring of its uptake and clearance by individual cells and within cellular compartments.

Chlamydia trachomatis is spread by close social contact or sexual activity. Worldwide, C. trachomatis is the leading preventable cause of blindness and bacterial sexually transmitted infections (STIs). Various typing techniques [...]

Buchnera aphidicola BCc has lost its symbiotic role as the tryptophan supplier to the aphid Cinara cedri. We report the presence of a plasmid in this endosymbiont that contains the trpEG genes. The remaining genes for the pathway (trpDCBA) are located on the chromosome of the secondary endosymbiont 'Candidatus Serratia symbiotica.' Thus, we propose that a symbiotic consortium is necessary to provide tryptophan.

Voltage-dependent calcium channels consist of a pore-forming subunit ([Ca.sub.v][[alpha].sub.1]) that includes all the molecular determinants of a voltage-gated channel, and several accessory subunits. The ancillary [beta]-subunit ([Ca.sub.v][beta]) is a potent activator of voltage-dependent calcium channels, but the mechanisms and structural bases of this regulation remain elusive. [Ca.sub.v][beta] binds reversibly to a conserved consensus sequence in [Ca.sub.v][[alpha].sub.1], the [[alpha].sub.1]-interaction domain (AID), which forms an [alpha]-helix when complexed with [Ca.sub.v][beta]. Conserved aromatic residues face to one side of the helix and strongly interact with a hydrophobic pocket on [Ca.sub.v][beta]. Here, we studied the effect of mutating residues located opposite to the AID-[Ca.sub.v[[beta] contact surface in [Ca.sub.v]l.2. Substitution of AID-exposed residues by the corresponding amino acids present in other [Ca.sub.v][[alpha].sub.1] subunits (E462R, K465N, D469S, and Q473K) hinders [Ca.sub.v][beta]'s ability to increase ionic-current to charge-movement ratio (I/Q) without changing the apparent affinity for [Ca.sub.v][beta]. At the single channel level, these [Ca.sub.v]l.2 mutants coexpressed with [Ca.sub.v][beta].sub.2a], visit high open probability mode less frequently than wildtype channels. On the other hand, [Ca.sub.v]l.2 carrying either a mutation in the conserved tryptophan residue (W470S, which impairs [Ca.sub.v][beta] binding), or a deletion of the whole AID sequence, does not exhibit [Ca.sub.v][beta]- induced increase in I/Q. In addition, we observed a shift in the voltage dependence of activation by +12 mV in the AID-deleted channel in the absence of [Ca.sub.v][beta], suggesting a direct participation of these residues in the modulation of channel activation. Our results show that [Ca.sub.v][beta]-dependent potentiation arises primarily from changes in the modal gating behavior. We envision that [Ca.sub.v][beta] spatially reorients AID residues that influence the channel gate. These findings provide a new framework for understanding modulation of VDCC gating by [Ca.sub.v][beta].

The Pseudomonas aeruginosa type III secretion system (T3SS) is known to be a very important virulence factor in acute human infections, but it is less important in maintaining chronic infections in which T3SS genes are downregulated. In vitro, the activation of T3SS expression involves a positive activating loop that acts on the transcriptional regulator ExsA. We have observed that in vivo T3SS expression is cell density-dependent in a manner that does not need known quorumsensing (QS) signals. In addition, stationary-phase culture supernatants added to exponentialphase growing strains can inhibit T3SS expression. The analysis of transposon insertion mutants showed that the production of such T3SS-inhibiting signals might depend on tryptophan synthase and hence tryptophan, which is the precursor of signalling molecules such as indole-3-acetic acid (IAA), kynurenine and Pseudomonas quinolone signal (PQS). Commercially available tryptophan-derived molecules were tested for their role in the regulation of T3SS expression. At millimolar concentrations, IAA, 1-naphthalacetic acid (NAA) and 3-hydroxykynurenine inhibited T3SS expression. Inactivation of the tryptophan dioxygenase-encoding kynA gene resulted in a decrease in the T3SS-inhibiting activity of supernatants. These observations suggest that tryptophan catabolites are involved in the downregulation of T3SS expression in the transition from a low- to a high-cell-density state.

The Bacillus subtilis anti-TRAP protein regulates the ability of the tryptophan-activated TRAP protein to bind to trp operon leader RNA and promote transcription termination. AT synthesis is regulated both transcriptionally and translationally by uncharged tRN[A.sup.Trp]. In this study, we examined the roles of AT synthesis and tRN[A.sup.Trp] charging in mediating physiological responses to tryptophan starvation. Adding excess phenylalanine to wild-type cultures reduced the charged tRN[A.sup.Trp] level from 80% to 40%; the charged level decreased further, to 25%, in an AT-deficient mutant. Adding tryptophan with phenylalanine increased the charged tRN[A.sup.Trp] level, implying that phenylalanine, when added alone, reduces the availability of tryptophan for tRN[A.sup.Trp] charging. Changes in the charged tRN[A.sup.Trp] level observed during growth with added phenylalanine were associated with increased transcription of the genes of tryptophan metabolism. Nutritional shift experiments, from a medium containing tryptophan to a medium with phenylalanine and tyrosine, showed that wild-type cultures gradually reduced their charged tRN[A.sup.Trp] level. When this shift was performed with an AT-deficient mutant, the charged tRN[A.sup.Trp] level decreased even further. Growth rates for wild-type and mutant strains deficient in AT or TRAP or that overproduce AT were compared in various media. A lack of TRAP or overproduction of AT resulted in phenylalanine being required for growth. These findings reveal the importance of AT in maintaining a balance between the synthesis of tryptophan versus the synthesis of phenylalanine, with the level of charged tRN[A.sup.Trp] acting as the crucial signal regulating AT production.

Phosphoribosyl amine (PRA) is an intermediate in purine biosynthesis and also required for thiamine biosynthesis in Salmonella enterica. PRA is normally synthesized by phosphoribosyl pyrophosphate amidotransferase, a high-turnover enzyme of the purine biosynthetic pathway encoded by purF. However, PurFindependent PRA synthesis has been observed in strains having different genetic backgrounds and growing under diverse conditions. Genetic analysis has shown that the anthranilate synthase-phosphoribosyltransferase (AS-PRT) enzyme complex, involved in the synthesis of tryptophan, can playa role in the synthesis of PRA. This work describes the in vitro synthesis of PRA in the presence of the purified components of the AS-PRT complex. Results from in vitro assays and in vivo studies indicate that the cellular accumulation of phosphoribosyl anthranilate can result in nonenzymatic PRA formation sufficient for thiamine synthesis. These studies have uncovered a mechanism used by cells to redistribute metabolites to ensure thiamine synthesis and may define a general paradigm of metabolic robustness.

Conserved trp genes encode enzymes that catalyze tryptophan biosynthesis in all three biological domains, and studies of their expression in Bacteria and eukaryotes have revealed a variety of different regulatory mechanisms. The results reported here provide the first detailed description of an archaeal trp gene regulatory system. We have established that the trpEGCFBAD operon in Methanothermobacter thermautotrophicus is transcribed divergently from a gene (designated trpY) that encodes a tryptophan-sensitive transcription regulator. TrpY binds to TRP box sequences (consensus, TGTACA) located in the overlapping promoter regions between trpY and trpE, inhibiting trpY transcription in the absence of tryptophan and both trpY and trpEGCFBAD transcription in the presence of tryptophan. TrpY apparently inhibits trpY transcription by blocking RNA polymerase access to the site of trpY transcription initiation and represses trpEGCFBAD transcription by preventing TATA box binding protein (TBP) binding to the TATA box sequence. Given that residue 2 (W2) is the only tryptophan in TrpY and in TrpY homologues in other Euryarchaea and that there is only one tryptophan codon in the entire trpEGCFBAD operon (trpB encodes W175), expression of the trp operon may also be regulated in vivo by the supply of charged tRN[A.sup.Trp] available to translate the second codon of the trpY mRNA.