Plasmonic nanolaser holds great potential in breaking down the diffraction limit of conventional optics to the deep sub‐wavelength regime and in ultrafast lasing dynamics. However, plasmonic laser ...devices are constrained in practical applications due to their high cost and high thresholds. All‐inorganic cesium lead halide perovskites are promising solutions for their excellent optical gain properties and high emission efficiency. In this work, high‐quality single‐crystalline CsPbBr3 perovskite nanowires (NWs) are synthesized by chemical vapor deposition method. The plasmonic lasing is achieved from the CsPbBr3 nanowire based plasmonic devices with lasing threshold down to ≈6.5 µJ cm−2 at room temperature. The highly polarized emission parallel to nanowire axis and polarization‐sensitive pump response confirm the plasmonic characteristic in these devices. Furthermore, time‐resolved photoluminescence study suggests that the radiative recombination lifetime of CsPbBr3 NW is shortened by a factor of ≈6.14 due to Purcell effect. The lasing threshold of plasmonic device increases along with the nanowire length, indicating greater potential in small size and integration in plasmonic device than its photonic counterparts. The results not only provide a solution to fabricate low‐cost nanowire based plasmonic lasers, but also advocate the prospect of all‐inorganic perovskite nanowires as promising candidates in plasmonic‐based devices.
Plasmonic nanolaser holds great potential in breaking down the diffraction limit of conventional optics to deep sub‐wavelength regime. Herein, all‐inorganic CsPbBr3 nanowire based plasmonic lasers are demonstrated at room tempearutre with threshold ≈6.5 µJ cm−2. The lasing threshold of plasmonic device increases along with the nanowire length, indicating greater potential in plasmonic integration device than its photonic couterparts.
The guided waveguide structures based on surface plasmons can be used to miniaturize microwave devices. By simply introducing a series of periodic truncation slits in the SSPP (spoof surface plasmon ...polariton) waveguide, three frequency regions, namely radiating spatial wave region, guiding SSPP mode region, and the cut-off region, are formed. In the frequency region of radiation, the SSPP mode can be transitioned to spatial wave. Consequently, double-port leaky wave antenna based on SSPP waveguide is realized with beam sweep function. Furthermore, a single-port antenna is demonstrated by symmetrical halving of the dual-port antenna. The half-sized single-port antenna exhibits beam steering capability and improved directivity. The proposed SSPP leakage antenna can be applied to the fifth-generation (5G) mobile communication systems.
Using combined genetic mapping, Illumina sequencing, bioinformatics analyses, and experimental validation, we identified 60 essential genes from 104 lethal mutations in two genomic regions of
...totalling approximately 14 Mb on chromosome III(mid) and chromosome V(left). Five of the 60 genes had not previously been shown to have lethal phenotypes by RNA interference depletion. By analyzing the regions around the lethal missense mutations, we identified four putative new protein functional domains. Furthermore, functional characterization of the identified essential genes shows that most are enzymes, including helicases, tRNA synthetases, and kinases in addition to ribosomal proteins. Gene Ontology analysis indicated that essential genes often encode for enzymes that conduct nucleic acid binding activities during fundamental processes, such as intracellular DNA replication, transcription, and translation. Analysis of essential gene shows that they have fewer paralogs, encode proteins that are in protein interaction hubs, and are highly expressed relative to non-essential genes. All these essential gene traits in
are consistent with those of human disease genes. Most human orthologs (90%) of the essential genes in this study are related to human diseases. Therefore, functional characterization of essential genes underlines their importance as proxies for understanding the biological functions of human disease genes.
Among many essential genes in the nematode Caenorhabditis elegans, let‐330 is located on the left arm of chromosome V and was identified as the largest target of a mutagen in this region. However, ...let‐330 gene has not been characterized at the molecular level. Here, we report that two sequenced let‐330 alleles are nonsense mutations of ketn‐1, a previously characterized gene encoding kettin. Kettin is a large actin‐binding protein of 472 kDa with 31 immunoglobulin domains and is expressed in muscle cells in C. elegans. let‐330/ketn‐1 mutants are homozygous lethal at the first larval stage with mild defects in body elongation. These mutants have severe defects in sarcomeric actin and myosin assembly in striated muscle. However, α‐actinin and vinculin, which are components of the dense bodies anchoring actin to the membranes, were not significantly disorganized by let‐330/ketn‐1 mutation. Kettin localizes to embryonic myofibrils before α‐actinin is expressed, and α‐actinin deficiency does not affect kettin localization in larval muscle. Depletion of vinculin minimally affects kettin localization but significantly reduces colocalization of actin with kettin in embryonic muscle cells. These results indicate that kettin is an essential protein for sarcomeric assembly of actin filaments in muscle cells.
Genetic studies in C. elegans can shed light on the molecular function of genes that are essential in developmental processes. In this study performed by Shoichiro Ono and colleagues, analysis of genetic mapping data revealed that let‐330 alleles are nonsense mutations of ketn‐1, a gene encoding kettin. Kettin is a large actin‐binding protein that is expressed in nematode muscle cells. Mutations in let‐330/ketn‐1 cause lethality during larval development and, at the molecular level, these mutants display severe disorganization of sarcomeric actin and myosin in striated muscle. These results indicate that kettin is essential for muscle sarcomeric assembly in C. elegans.
The water-insolubility of a potentially versatile photoresponsive 'turn-on' fluorescence probe was overcome by incorporating it into a nano-assembly containing an upconverting nanoparticle wrapped in ...an amphiphilic polymer. The appeal of the nano-system is not only in the ability to turn "on" and "off" the fluorescence from the organic chromophore using UV and visible light, it is in the fact that the nanoparticle acts as a static probe because it emits red and green light when excited by near infrared light, which is not effected by UV and visible light. This dual-functioning emission behaviour was demonstrated in live organisms.
Precise arrangement of actin, myosin, and other regulatory components in a sarcomeric pattern is critical for producing contractile forces in striated muscles. Actin-interacting protein 1 (AIP1), ...also known as WD-repeat protein 1 (WDR1), is one of essential factors that regulate sarcomeric assembly of actin filaments. In the nematode Caenorhabditis elegans, mutation in unc-78, encoding one of the two AIP1 isoforms, causes severe disorganization of sarcomeric actin filaments and near paralysis, but mutation in sup-13 suppresses the unc78-mutant phenotypes to restore nearly normal sarcomeric actin organization and worm motility. Here, we identified that sup- 13 is a nonsense allele of arrd-15 encoding an alpha-arrestin. The sup-13/arrd-15 mutation suppressed the phenotypes of unc-78 null mutant but required aipl-1 that encodes a second AIP1 isoform. aipl-1 was normally expressed highly in embryos and downregulated in mature muscle. However, in the sup-13/arrd-15 mutant, the AIPL-1 protein was maintained at high levels in adult muscle to compensate for the absence of the UNC-78 protein. The sup-13/arrd-15 mutation caused accumulation of ubiquitinated AIPL-1 protein, suggesting that a normal function of sup-13/arrd-15 is to enhance degradation of ubiquitinated AIPL-1, thereby promoting transition of AIP1 isoforms from AIPL-1 to UNC-78 in developing muscle. These results suggest that alpha- arrestin is a novel factor to promote isoform turnover by enhancing protein degradation. Keywords: actin, actin-interacting protein 1 (AIP1), alpha-arrestin, sarcomere, ubiquitination
Precise arrangement of actin, myosin, and other regulatory components in a sarcomeric pattern is critical for producing contractile forces in striated muscles. Actin-interacting protein 1 (AIP1), ...also known as WD-repeat protein 1 (WDR1), is one of essential factors that regulate sarcomeric assembly of actin filaments. In the nematode
, mutation in
, encoding one of the two AIP1 isoforms, causes severe disorganization of sarcomeric actin filaments and near paralysis, but mutation in
suppresses the
mutant phenotypes to restore nearly normal sarcomeric actin organization and worm motility. Here, we identified that
is a nonsense allele of
encoding an α-arrestin. The
mutation suppressed the phenotypes of
null mutant but required
that encodes a second AIP1 isoform.
was normally expressed highly in embryos and downregulated in mature muscle. However, in the
mutant, the AIPL-1 protein was maintained at high levels in adult muscle to compensate for the absence of the UNC-78 protein. The
mutation caused accumulation of ubiquitinated AIPL-1 protein, suggesting that a normal function of
is to enhance degradation of ubiquitinated AIPL-1, thereby promoting transition of AIP1 isoforms from AIPL-1 to UNC-78 in developing muscle. These results suggest that α-arrestin is a novel factor to promote isoform turnover by enhancing protein degradation.
Abstract
Plasmonic nanolaser holds great potential in breaking down the diffraction limit of conventional optics to the deep sub‐wavelength regime and in ultrafast lasing dynamics. However, plasmonic ...laser devices are constrained in practical applications due to their high cost and high thresholds. All‐inorganic cesium lead halide perovskites are promising solutions for their excellent optical gain properties and high emission efficiency. In this work, high‐quality single‐crystalline CsPbBr
3
perovskite nanowires (NWs) are synthesized by chemical vapor deposition method. The plasmonic lasing is achieved from the CsPbBr
3
nanowire based plasmonic devices with lasing threshold down to ≈6.5 µJ cm
−2
at room temperature. The highly polarized emission parallel to nanowire axis and polarization‐sensitive pump response confirm the plasmonic characteristic in these devices. Furthermore, time‐resolved photoluminescence study suggests that the radiative recombination lifetime of CsPbBr
3
NW is shortened by a factor of ≈6.14 due to Purcell effect. The lasing threshold of plasmonic device increases along with the nanowire length, indicating greater potential in small size and integration in plasmonic device than its photonic counterparts. The results not only provide a solution to fabricate low‐cost nanowire based plasmonic lasers, but also advocate the prospect of all‐inorganic perovskite nanowires as promising candidates in plasmonic‐based devices.
Whole and partial chromosome losses or gains and structural chromosome changes are hallmarks of human tumors. Guanine-rich DNA, which has a potential to form a G-quadruplex (G4) structure, is ...particularly vulnerable to changes. In Caenorhabditis elegans, faithful transmission of G-rich DNA is ensured by the DOG-1/FANCJ deadbox helicase.
To identify a spectrum of mutations, after long-term propagation, we combined whole genome sequencing (WGS) and oligonucleotide array Comparative Genomic Hybridization (oaCGH) analysis of a C. elegans strain that was propagated, in the absence of DOG-1 and MDF-1/MAD1, for a total of 470 generations, with samples taken for long term storage (by freezing) in generations 170 and 270. We compared the genomes of F170 and F470 strains and identified 94 substitutions, 17 InDels, 3 duplications, and 139 deletions larger than 20 bp. These homozygous variants were predicted to impact 101 protein-coding genes. Phenotypic analysis of this strain revealed remarkable fitness recovery indicating that mutations, which have accumulated in the strain, are not only tolerated but also cooperate to achieve long-term population survival in the absence of DOG-1 and MDF-1. Furthermore, deletions larger than 20 bp were the only variants that frequently occurred in G-rich DNA. We showed that 126 of the possible 954 predicted monoG/C tracts, larger than 14 bp, were deleted in unc-46 mdf-1 such-4; dog-1 F470 (JNC170).
Here, we identified variants that accumulated in C. elegans' genome after long-term propagation in the absence of DOG-1 and MDF-1. We showed that DNA sequences, with G4-forming potential, are vulnerable to deletion-formation in this genetic background.
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![The [alpha]-arrestin SUP-13...](http://api.summon.serialssolutions.com/2.0.0/image/issn/XR4PS5YY4K/2752-6542/small "The [alpha]-arrestin SUP-13/ARRD-15 promotes isoform turnover of actin-interacting protein 1 in Caenorhabditis elegans striated muscle")
