Large-language models facilitate discovery of the molecular signatures regulating sleep and activity.

Sleep, locomotor and social activities are essential animal behaviors, but their reciprocal relationships and underlying mechanisms remain poorly understood. Here, we elicit information from a cutting-edge large-language model (LLM), generative pre-trained transformer (GPT) 3.5, which interprets 10.2-13.8% of Drosophila genes known to regulate the 3 behaviors. We develop an instrument for simultaneous video tracking of multiple moving objects, and conduct a genome-wide screen. We have identified 758 fly genes that regulate sleep and activities, including mre11 which regulates sleep only in the presence of conspecifics, and NELF-B which regulates sleep regardless of whether conspecifics are present. Based on LLM-reasoning, an educated signal web is modeled for understanding of potential relationships between its components, presenting comprehensive molecular signatures that control sleep, locomotor and social activities. This LLM-aided strategy may also be helpful for addressing other complex scientific questions.

Enrichment of microbial consortia for MEOR in crude oil phase of reservoir-produced liquid and their response to environmental disturbance.

Developing microbial consortiums is necessary for microbial enhanced oil recovery (MEOR) in heavy crude oil production. The aqueous phase of produced fluid has long been considered an ideal source of microorganisms for MEOR. However, it is recently found that rich microorganisms (including hydrocarbon-degrading bacteria) are present in the crude oil phase, which is completely different from the aqueous phase of produced fluid. So, in this study, the microbial consortia from the crude oil phase of produced fluids derived from four wells were enriched, respectively. The microbial community structure during passage was dynamically tracked, and the response of enriched consortia to successive disturbance of environmental factors was investigated. The results showed the crude oil phase had high microbial diversity, and the original microbial community structure from four wells was significantly different. After ten generations of consecutive enrichment, different genera were observed in the four enriched microbial consortia, namely, Geobacillus, Bacillus, Brevibacillus, Chelativorans, Ureibacillus, and Ornithinicoccus. In addition, two enriched consortia (eG1614 and eP30) exhibited robustness to temperature and oxygen perturbations. These results further suggested that the crude oil phase of produced fluids can serve as a potential microbial source for MEOR.

Methylmercury promotes oxidative stress and autophagy in rat cerebral cortex: Involvement of PI3K/AKT/mTOR or AMPK/TSC2/mTOR pathways and attenuation by N-acetyl-L-cysteine.

Methylmercury (MeHg) is a potent neurotoxicant that could induce oxidative stress and autophagy. However, the underlying mechanisms through which MeHg affects the central nervous system have not been fully elucidated, and little has been known of the interaction between oxidative stress and autophagy. Therefore, rats were administrated with different MeHg concentrations to evaluate the neurotoxic effects and autophagy in cerebral cortex. Moreover, we have investigated the neuroprotective role of N-acetyl-L-cysteine (NAC) against MeHg-induced neurotoxicity in order to estimate the regulation effects of oxidative stress on autophagy. A total of 64 rats, 40 of which were randomly divided into control and MeHg-treated (4, 8 and 12 µ mol/kg) groups. The remaining 24 rats were divided into control, NAC control (1 mmol/kg), 12 µ mol/kg MeHg, and NAC pretreatment. Administration of 12 µ mol/kg MeHg significantly increased behavioral and pathological abnormalities, and autophagy levels. In addition, the oxidative stress levels increased, together with abnormal expression of autophagy-related molecules. Pretreatment with NAC significantly prevented MeHg-induced oxidative stress and PI3K/AKT/mTOR or AMPK/TSC2/mTOR-mediated autophagy. In conclusion, the present study suggested that oxidative stress can regulate autophagy through PI3K/AKT/mTOR or AMPK/TSC2/mTOR pathways. This study provides a theoretical basis for the study and treatment of MeHg-induced neurotoxicity.

SRH suppressed P-G-I design for very long-wavelength infrared HgCdTe photodiodes.

The very long wavelength infrared (VLWIR, >14 µm) spectral band is an indispensable part of new-generation infrared remote sensing. Mercury cadmium telluride (HgCdTe or MCT) has shown excellent potential across the entire infrared band. However, the dark current, which is extremely sensitive to the technological level and small Cd composition, severely limits the performance of VLWIR HgCdTe photodiodes. In this study, cut-off wavelengths of up to 15 µm for HgCdTe devices with novel P-G-I (including wide bandgap p-type cap layer, grading layer and intrinsic absorption layer) designs have been reported. Compared with a device with a double-layer heterojunction (DLHJ) structure, the designed P-G-I structure successfully reduced dark current by suppressing the Shockley-Read-Hall process. Considering the balance of quantum efficiency and dark current, with the introduction of an approximately 0.8 µm thickness Cd composition grading layer, the device can achieve a high detectivity of up to 2.5×1011 cm Hz1/2 W-1. Experiments show that the P-G-I-T device has a lower dark current and a better SRH process suppressing ability than DLHJ devices, the measured detectivity achieved 8.7×1010 cm Hz1/2 W-1. According to additional research, the trap-assisted tunneling current is the primary component of the dark current. Controlling the trap concentration to as low as 1×1013 cm-3 will be continuous and meaningful work. The proposed study provides guidance for VLWIR HgCdTe photodetectors.

First report of Coniella vitis causing white rot on Virginia creeper (Parthenocissus quinquefolia [L.] Planch.) in China.

Virginia creeper (Parthenocissus quinquefolia [L.] Planch.) belongs to the genus of Parthenocissus and Vitaceae family, which is very common in vineyards and where wild grape occurs (Bergh et al., 2011). In September of 2021, a severe white rot disease was observed on Virginia creeper around the vineyard of wine grapevine (Cabernet Sauvignon) located in Penglai city (37º 75'38" N, 120º 84'28" E), Shandong province of China. The disease incidence was about 75%, and infected leaf of Virginia creeper exhibited irregular necrotic lesion with brown center, and most lesion occurred on leaf margin, black pycnidia were also observed on the infected leaf at the late stage of infection. To determine the causal agent, symptomatic leaves with typical lesions were cut into small pieces (5 mm × 3 mm), surface sterilized with 75% ethanol for 1 min, followed by three times rinsed in sterile water. Leaf sections were plated onto potato dextrose agar (PDA) medium and incubated at 28°C for 3 days. Totally, five isolates (referred to as JD01, JD07, JD09, JD12 and JD16) were collected and transferred on to fresh PDA medium for incubation at 28°C. Seven days later, colonies on PDA plates had crenulated edges with concentric rings, the upper surface of colonies was mostly flat and white with many pycnidia. The conidia were hyaline at immature and became brown later, spherical or ellipsoid, aseptate, and 7.92 ± 1.20 µm × 5.18 ± 0.61 µm (n=50), length : width ratio is nearly 2. Morphologically, the isolates were identified as Coniella vitis (Chethana et al., 2017). Further to confirm the fungal species, the internal transcribed spacer region (ITS) of the ribosomal RNA gene, large subunit rRNA gene (LSU) and the translation elongation factor 1-alpaha gene (TEF1-α) were amplified using primers ITS1/ ITS4, LR7/ LROR, and TEF1- 728F/ TEF1- 986R (Chethana et al., 2017; Raudabaugh et al., 2018). The amplification products were sequenced and deposited in GenBank database. The sequences were compared to type sequences in GenBank. The results showed that ITS (GenBank accession numbers ON329769, ON329770, ON329771, ON329772 and ON329773), LSU (ON358423，ON358424, ON358425, ON358426 and ON358427) and TEF (ON297671, ON229071, ON229072, ON229073 and ON297672) sequences of the five isolates were 99.66%, 96.90% and 98.79% identical with the sequences data from C. vitis isolates in GeneBank (MFLUCC 18-0093, JZB3700020 and MFLUCC 18-0093, respectively). Furthermore, concatenated sequences of the three genes (ITS, LSU and TEF) were used to conduct a phylogenetic tree using maximum likehood MEGA-X (Raudabaugh et al., 2018). The phylogenetic analysis showed that the five isolates (JD01, JD07, JD09, JD12 and JD16) belong to C. vitis clade among the 41strains of Coniella spp. In the pathogenicity tests, detached leaves of Virginia creeper (1-year-old) were inoculated with mycelia plugs (5 mm diameter) (form 3-day-old of isolate JD07 culture), and control were inoculated with PDA plugs (5 mm diameter). Virginia creeper live plants (1-year-old) were inoculated with conidial suspension (2.5×106 spores/ml) of the isolate JD07 of one week old, and control plants were inoculated with sterile water. All treated Virginia creeper plants (detached leaves) were placed in a greenhouse maintained at 28°C and 95% relative humidity. Virginia creeper plants (detached leaves) inoculated with the conidial suspension (fungal mycelia) had brown lesion on leaves, the disease symptoms were similar to those observed in field. No such symptoms were observed on control plants (detached leaves). The pathogen was reisolated from inoculated Virginia creeper plants and re-identified, thus fulfilling Koch's postulates. C. vitis had been reported to cause grape white rot in China (Chethana et al., 2017). Virginia creeper, as an excellent host of C. vitis, will increase the transmission risk of the pathogens. To our knowledge, this is the first report of C. vitis causing white rot on Virginia creeper, and this finding will provide useful information for developing effective control strategies for white rot disease.

Comparative genomic and functional analyses of Paenibacillus peoriae ZBSF16 with biocontrol potential against grapevine diseases, provide insights into its genes related to plant growth-promoting and biocontrol mechanisms.

Paenibacillus peoriae is a plant growth-promoting rhizobacteria (PGPR) widely distributed in various environments. P. peoriae ZBFS16 was isolated from the wheat rhizosphere and significantly suppressed grape white rot disease caused by Coniella vitis. Here, we present the complete genome sequence of P. peoriae ZBFS16, which consists of a 5.83 Mb circular chromosome with an average G + C content of 45.62%. Phylogenetic analyses showed that ZBFS16 belongs to the genus P. peoriae and was similar to P. peoriae ZF390, P. peoriae HS311 and P. peoriae HJ-2. Comparative analysis with three closely related sequenced strains of P. peoriae identified the conservation of genes involved in indole-3-acetic acid production, phosphate solubilization, nitrogen fixation, biofilm formation, flagella and chemotaxis, quorum-sensing systems, two-component systems, antimicrobial substances and resistance inducers. Meanwhile, in vitro experiments were also performed to confirm these functions. In addition, the strong colonization ability of P. peoriae ZBFS16 was observed in soil, which provides it with great potential for use in agriculture as a PGPR. This study will be helpful for further studies of P. peoriae on the mechanisms of plant growth promotion and biocontrol.

Unbalanced ER-mitochondrial calcium homeostasis promotes mitochondrial dysfunction and associated apoptotic pathways activation in methylmercury exposed rat cortical neurons.

Methylmercury (MeHg) is a cumulative environmental pollutant that can easily cross the blood-brain barrier and cause damage to the brain, mainly targeting the central nervous system. The purpose of this study is to investigate the role of calcium ion (Ca2+ ) homeostasis between the endoplasmic reticulum (ER) and mitochondria in MeHg-induced neurotoxicity. Rat primary cortical neurons exposed to MeHg (0.25-1 µm) underwent dose-dependent cell damage, accompanied by increased Ca2+ release from the ER and elevated levels of free Ca2+ in cytoplasm and mitochondria. MeHg also increased the protein and messenger RNA expressions of the inositol 1,4,5-triphosphate receptor, ryanodine receptor 2, and mitochondrial calcium uniporter. Ca2+ channel inhibitors 2-aminoethyl diphenylborinate and procaine reduced the release of Ca2+ from ER, while RR and 4,4'-diisothiocyanatostilbene-2,2'-disulfonate inhibited Ca2+ uptake from mitochondria. In addition, pretreatment with Ca2+ chelator BAPTA-AM effectively restored mitochondrial membrane potential levels, inhibited over opening of mitochondrial permeability transition pore, and maintained mitochondrial function stability. Meanwhile, the expression of mitochondrial apoptosis-related proteins recovered to some extent, along with the reduction of the early apoptosis ratio. These results suggest that Ca2+ homeostasis plays an essential role in mitochondrial damage and apoptosis induced by MeHg, which may be one of the important mechanisms of MeHg-induced neurotoxicity.

Microbial communities in crude oil phase and filter-graded aqueous phase from a Daqing oilfield after polymer flooding.

AIMS: The aim was to characterize indigenous micro-organisms in oil reservoirs after polymer flooding (RAPF). METHODS: The microbial communities in the crude oil phase (Oil) and in the filter-graded aqueous phases Aqu0.22 (>0.22 µm) and Aqu0.1 (0.1-0.22 µm) were investigated by 16S rRNA gene high-throughput sequencing. RESULTS: Indigenous micro-organisms related to hydrocarbon degradation prevailed in the three phases of each well. However, obvious differences in bacterial compositions were observed amongst the three phases of the same well and amongst the same phase of different wells. The crude oil and Aqu0.22 shared many dominant bacteria. Aqu0.1 contained a unique bacterial community in each well. Most bacteria in Aqu0.1 were affiliated to culturable genera, suggesting that they may adapt to the oil reservoir environment by reduction of cell size. Contrary to the bacterial genera, archaeal genera were similar in the three phases but varied in relative abundances. The observed microbial differences may be driven by specific environmental factors in each oil well. CONCLUSIONS: The results suggest an application potential of microbial enhanced oil recovery (MEOR) technology in RAPF. The crude oil and Aqu0.1 contain many different functional micro-organisms related to hydrocarbon degradation. Both should not be overlooked when investing and exploring the indigenous micro-organisms for MEOR. SIGNIFICANCE AND IMPACT OF THE STUDY: This work facilitates the understanding of microbial community structures in RAPF and provides information for microbial control in oil fields.

Suppression of Grape White Rot Caused by Coniella vitis Using the Potential Biocontrol Agent Bacillus velezensis GSBZ09.

Grape white rot caused by Coniella vitis is prevalent in almost all grapevines worldwide and results in a yield loss of 10-20% annually. Bacillus velezensis is a reputable plant growth-promoting bacterial. Strain GSBZ09 was isolated from grapevine cv. Red Globe (Vitis vinifera) and identified as B. velezensis according to morphological, physiological, biochemical characteristics and a multilocus gene sequence analysis (MLSA) based on six housekeeping genes (16S rRNA, gyrB, rpoD, atpD, rho and pgk). B. velezensis GSBZ09 was screened for antifungal activity against C. vitis under in vitro and in vivo conditions. GSBZ09 presented broad spectrum antifungal activity and produced many extracellular enzymes that remarkably inhibited the mycelial growth and spore germination of C. vitis. Furthermore, GSBZ09 had a high capacity for indole-3-acetic acid (IAA) production, siderophore production, and mineral phosphate solubilization. Pot experiments showed that the application of GSBZ09 significantly decreased the disease index of the grape white rot, directly promoted the growth of grapes, and upregulated defense-related enzymes. Overall, the features of B. velezensis GSBZ09 make it a potential strain for application as a biological control agent against C. vitis.

Shedding new light on methylmercury-induced neurotoxicity through the crosstalk between autophagy and apoptosis.

Methylmercury (MeHg) is a bio-accumulative global environmental contaminant present in fish and seafood. MeHg accumulates in the aquatic environment and eventually reaches the human system via the food chain by bio-magnification. The central nervous system is the primary target of toxicity and is particularly vulnerable during development. It is well documented that developmental MeHg exposure can lead to neurological alterations, including cognitive and motor dysfunction. Apoptosis is a primary characteristic of MeHg-induced neurotoxicity, and may be regulated by autophagic activity. However, mechanisms mediating the interaction between apoptosis and autophagy remains to be explored. Autophagy is an adaptive response under stressful conditions, and the basal level of autophagy ensures the physiological turnover of old and damaged organelles. Autophagy can regulate cell fate through different crosstalk signaling pathways. A complex interplay between autophagy and apoptosis determines the degree of apoptosis and the progression of MeHg-induced neurotoxicity as demonstrated by pre-clinical models and clinical trials. This review summarizes recent advances in the roles of autophagy and apoptosis in MeHg neurotoxicity and thoroughly explores the relationship between them. The autophagic pathway may be a potential therapeutic target in MeHg neurotoxicity through modulation of apoptosis.

Advances on the Influence of Methylmercury Exposure during Neurodevelopment.

Mercury (Hg) is a toxic heavy-metal element, which can be enriched in fauna and flora and transformed into methylmercury (MeHg). MeHg is a widely distributed environmental pollutant that may be harmful to fish-eating populations through enrichment of aquatic food chains. The central nervous system is a primary target of MeHg. Embryos and infants are more sensitive to MeHg, and exposure to MeHg during gestational feeding can significantly impair the homeostasis of offspring, leading to long-term neurodevelopmental defects. At present, MeHg-induced neurodevelopmental toxicity has become a hotspot in the field of neurotoxicology, but its mechanisms are not fully understood. Some evidence point to oxidative damage, excitotoxicity, calcium ion imbalance, mitochondrial dysfunction, epigenetic changes, and other molecular mechanisms that play important roles in MeHg-induced neurodevelopmental toxicity. In this review, advances in the study of neurodevelopmental toxicity of MeHg exposure during pregnancy and the molecular mechanisms of related pathways are summarized, in order to provide more scientific basis for the study of neurodevelopmental toxicity of MeHg.

The effects of mTOR or Vps34-mediated autophagy on methylmercury-induced neuronal apoptosis in rat cerebral cortex.

Methylmercury (MeHg) is a environmental contaminant, which can induce neurotoxic effects. So far, the exact molecular mechanisms of autophagy and its effect on apoptosis in MeHg-induced neurotoxicity have not been elucidated. Here, rats were exposed to MeHg (4, 8, or 12 µmol/kg) for 4 weeks to evaluate the dose-effect relationship between MeHg and apoptosis, or autophagy in cerebral cortex. On this basis, rapamycin (Rapa) or 3-methyladenine (3-MA) was administrated to further explore the regulatory mechanisms of autophagy on MeHg-induced neuronal apoptosis. The pathological changes, autophagy or apoptosis levels, expression of autophagic or apoptotic-associated factors such as mTOR, S6K1, 4EBP1, Vps34, Beclin1, p62, LC3, Bcl-2/Bax, caspase, or MAPKs were investigated. Results showed that MeHg dose-dependently induced pathological changes in cerebral cortex, and the levels of autophagy and apoptosis were increased. Furthermore, Rapa pretreatment antagonized MeHg-induced apoptosis, whereas 3-MA further aggravated apoptosis, which were supported by findings that Rapa activated mTOR-mediated autophagy while 3-MA inhibited Vps34-related autophagy, further affect neuronal apoptosis through regulation of apoptotic factors mentioned above. In conclusion, the findings indicated that MeHg dose-dependently induced autophagy or apoptosis, and mTOR or Vps34 may play important roles in mediating autophagy, which further regulated apoptosis through MAPKs or mitochondrial apoptosis pathways.

The Roles of Oxidative Stress in Regulating Autophagy in Methylmercury-induced Neurotoxicity.

Methylmercury (MeHg) is a potential neurotoxin that is highly toxic to the human central nervous system. Although MeHg neurotoxicity has been widely studied, the mechanism of MeHg neurotoxicity has not yet been fully elucidated. Some research evidence suggests that oxidative stress and autophagy are important molecular mechanisms of MeHg-induced neurotoxicity. Researchers have widely accepted that oxidative stress regulates the autophagy pathway. The current study reviews the activation of Nuclear factor-erythroid-2-related factor (Nrf2)-related oxidative stress pathways and autophagy signaling pathways in the case of MeHg neurotoxicity. In addition, autophagy mainly plays a role in the neurotoxicity of MeHg through mTOR-dependent and mTOR-independent autophagy signaling pathways. Finally, the regulation of autophagy by reactive oxygen species (ROS) and Nrf2 in MeHg neurotoxicity was explored in this review, providing a new concept for the study of the neurotoxicity mechanism of MeHg.

Mechanisms of oxidative stress in methylmercury-induced neurodevelopmental toxicity.

Methylmercury (MeHg) is a long-lasting organic environmental pollutant that poses a great threat to human health. Ingestion of seafood containing MeHg is the most important way by which it comes into contact with human body, where the central nervous system (CNS) is the primary target of MeHg toxicity. During periods of pre-plus postnatal, in particular, the brain of offspring is vulnerable to specific developmental insults that result in abnormal neurobehavioral development, even without symptoms in mothers. While many studies on neurotoxic effects of MeHg on the developing brain have been conducted, the mechanisms of oxidative stress in MeHg-induced neurodevelopmental toxicity is less clear. Hitherto, no single process can explain the many effects observed in MeHg-induced neurodevelopmental toxicity. This review summarizes the possible mechanisms of oxidative stress in MeHg-induced neurodevelopmental toxicity, highlighting modulation of Nrf2/Keap1/Notch1, PI3K/AKT, and PKC/MAPK molecular pathways as well as some preventive drugs, and thus contributes to the discovery of endogenous and exogenous molecules that can counteract MeHg-induced neurodevelopmental toxicity.

Optical Constants and Band Gap Evolution with Phase Transition in Sub-20-nm-Thick TiO2 Films Prepared by ALD.

Titanium dioxide (TiO2) ultrathin films with different thicknesses below 20 nm were grown by atomic layer deposition (ALD) on silicon substrates at 300 °C. Spectroscopic ellipsometry (SE) measurements were operated to investigate the effect of thickness on the optical properties of ultrathin films in the spectra range from 200 to 1000 nm with Forouhi-Bloomer (F-B) dispersion relation. It has been found that the refractive index and extinction coefficient of the investigated TiO2 ultrathin film increase while the band gap of TiO2 ultrathin film decreases monotonically with an increase in film thickness. Furthermore, with the purpose of studying the temperature dependence of optical properties of TiO2 ultrathin film, the samples were annealed at temperature from 400 to 900 °C in N2 atmosphere. The crystalline structure of deposited and annealed films was deduced by SE and supported by X-ray diffraction (XRD). It was revealed that the anatase TiO2 film started to transform into rutile phase when the annealing temperature was up to 800 °C. In this paper, a constructive and effective method of monitoring the phase transition in ultrathin films by SE has been proposed when the phase transition is not so obvious analyzed by XRD.

Barrier layer induced channeling effect of As ion implantation in HgCdTe and its influences on electrical properties of p-n junctions.

The HgCdTe layers (xCd∼0.285 and 0.225) were grown by molecular beam epitaxy and liquid phase epitaxy, respectively, followed by the deposition of CdTe and ZnS films as barrier layers by thermal evaporation. Then, the p-on-n photodiodes were fabricated by AS ion implantation, Hg overpressure annealing, passivation, and metallization. The secondary ion mass spectrometry and transmission electron microscopy results indicate that the evaporated CdTe layer with a column structure induces the channeling effect of As ion implantation causing the device performance degradation. This effect could be suppressed by depositing a CdTe film with a layered structure through E-beam evaporation. Finally, the current-voltage (I-V) and capacitance-voltage (C-V) characteristics of these p-n junctions were estimated and analyzed.

Effective method to study the thickness-dependent dielectric functions of nanometal thin film.

A new method for measuring the dielectric functions change with the thickness of nanometal thin films was proposed. To confirm the accuracy and reliability of the method, a nano-thin wedge-shaped gold (Au) film with continuously varied thicknesses was designed and prepared on K9 glass by direct-current-sputtering (DC-sputtering). The thicknesses and the dielectric functions in the wavelength range of 300-1100 nm of the nano-thin Au films were obtained by fitting the ellipsometric parameters with the Drude and critical points model. Results show that while the real part of the dielectric function (ϵ1) changes marginally with increasing film thickness, the imaginary part (ϵ2) decreases drastically with the film thickness, approaching a stable value when the film thickness increases up to about 42 nm. This method is particularly useful in the study of thickness-dependent optical properties of nano-thin film.

The impact of thickness and thermal annealing on refractive index for aluminum oxide thin films deposited by atomic layer deposition.

The aluminum oxide (Al2O3) thin films with various thicknesses under 50 nm were deposited by atomic layer deposition (ALD) on silicon substrate. The surface topography investigated by atomic force microscopy (AFM) revealed that the samples were smooth and crack-free. The ellipsometric spectra of Al2O3 thin films were measured and analyzed before and after annealing in nitrogen condition in the wavelength range from 250 to 1,000 nm, respectively. The refractive index of Al2O3 thin films was described by Cauchy model and the ellipsometric spectra data were fitted to a five-medium model consisting of Si substrate/SiO2 layer/Al2O3 layer/surface roughness/air ambient structure. It is found that the refractive index of Al2O3 thin films decrease with increasing film thickness and the changing trend revised after annealing. The phenomenon is believed to arise from the mechanical stress in ALD-Al2O3 thin films. A thickness transition is also found by transmission electron microscopy (TEM) and SE after 900°C annealing.

Room-temperature photoconductivity far below the semiconductor bandgap.

A concept to stimulate photoconductivity in a semiconductor well below its bandgap in a metal-semiconductor-metal structure with sub-wavelength spacing is proposed. A potential well is induced in the semiconductor by external electromagnetic radiation to trap carriers from the metals. This opens an avenue to generate carriers by photons without adequate excitation energy and is expected to have great significance in modern materials.

Characterization of a novel type of HMW subunit of glutenin from Australopyrum retrofractum.

The Triticeae species Australopyrum retrofractum (genome WW) produces a single high molecular weight glutenin subunit (HMW-GS) in its endosperm. However, degenerate PCR amplification of its genome DNA revealed the presence of two related HMW-GS sequences, each consisting of an open reading frame. One of these (Glu-W1-2) has not previously been reported. Here, we sequenced Glu-W1-2 and showed that it encodes the same type of HMW-GS as Glu-W1-1, although its overall product length was much shorter, because the number of certain repetitive motifs was lower in its central region. Both A. retrofractum HMW-GSs have a unique repetitive motif, which differentiates them from other known x- and y-type subunits present in Triticeae species. We suggest that A. retrofractum must have diverged from the main Triticeae lineage prior to the Glu-1 duplication event which led to the evolution of the x- and y-type genes.