Unmodificated stepless regulation of CRISPR/Cas12a multi-performance.

As CRISPR technology is promoted to more fine-divided molecular biology applications, its inherent performance finds it increasingly difficult to cope with diverse needs in these different fields, and how to more accurately control the performance has become a key issue to develop CRISPR technology to a new stage. Herein, we propose a CRISPR/Cas12a regulation strategy based on the powerful programmability of nucleic acid nanotechnology. Unlike previous difficult and rigid regulation of core components Cas nuclease and crRNA, only a simple switch of different external RNA accessories is required to change the reaction kinetics or thermodynamics, thereby finely and almost steplessly regulating multi-performance of CRISPR/Cas12a including activity, speed, specificity, compatibility, programmability and sensitivity. In particular, the significantly improved specificity is expected to mark advance the accuracy of molecular detection and the safety of gene editing. In addition, this strategy was applied to regulate the delayed activation of Cas12a, overcoming the compatibility problem of the one-pot assay without any physical separation or external stimulation, and demonstrating great potential for fine-grained control of CRISPR. This simple but powerful CRISPR regulation strategy without any component modification has pioneering flexibility and versatility, and will unlock the potential for deeper applications of CRISPR technology in many finely divided fields.

Epidemiology, pathogenesis, immune evasion mechanism and vaccine development of porcine Deltacoronavirus.

Coronaviruses have been identified as pathogens of gastrointestinal and respiratory diseases in humans and various animal species. In recent years, the global spread of new coronaviruses has had profound influences for global public health and economies worldwide. As highly pathogenic zoonotic viruses, coronaviruses have become the focus of current research. Porcine Deltacoronavirus (PDCoV), an enterovirus belonging to the family of coronaviruses, has emerged on a global scale in the past decade and significantly influenced the swine industry. Moreover, PDCoV infects not only pigs but also other species, including humans, chickens and cattles, exhibiting a broad host tropism. This emphasizes the need for in-depth studies on coronaviruses to mitigate their potential threats. In this review, we provided a comprehensive summary of the current studies on PDCoV. We first reviewed the epidemiological investigations on the global prevalence and distribution of PDCoV. Then, we delved into the studies on the pathogenesis of PDCoV to understand the mechanisms how the virus impacts its hosts. Furthermore, we also presented some exploration studies on the immune evasion mechanisms of the virus to enhance the understanding of host-virus interactions. Despite current limitations in vaccine development for PDCoV, we highlighted the inhibitory effects observed with certain substances, which offers a potential direction for future research endeavors. In conclusion, this review summarized the scientific findings in epidemiology, pathogenesis, immune evasion mechanisms and vaccine development of PDCoV. The ongoing exploration of potential vaccine candidates and the insights gained from inhibitory substances have provided a solid foundation for future vaccine development to prevent and control diseases associated with PDCoV.

Aspartyl proteases identified as candidate genes of a fiber length QTL, qFLD05, that regulates fiber length in cotton (Gossypium hirsutum L.).

KEY MESSAGE: GhAP genes were identified as the candidates involved in cotton fiber length under the scope of fine mapping a stable fiber length QTL, qFLD05. Moreover, the transcription factor GhWRKY40 positively regulated GhAP3 to decrease fiber length. Fiber length (FL) is an economically important fiber quality trait. Although several genes controlling cotton fiber development have been identified, our understanding of this process remains limited. In this study, an FL QTL (qFLD05) was fine-mapped to a 216.9-kb interval using a secondary F2:3 population derived from the upland hybrid cultivar Ji1518. This mapped genomic segment included 15 coding genes, four of which were annotated as aspartyl proteases (GhAP1-GhAP4). GhAPs were identified as candidates for qFLD05 as the sequence variations in GhAPs were associated with FL deviations in the mapping population, and functional validation of GhAP3 and GhAP4 indicated a longer FL following decreases in their expression levels through virus-induced gene silencing (VIGS). Subsequently, the potential involvement of GhWRKY40 in the regulatory network was revealed: GhWRKY40 positively regulated GhAP3's expression according to transcriptional profiling, VIGS, yeast one-hybrid assays and dual-luciferase experiments. Furthermore, alterations in the expression of the eight previously reported cotton FL-responsive genes from the above three VIGS lines (GhAP3, GhAP4 and GhWRKY40) implied that MYB5_A12 was involved in the GhWRKY40-GhAP network. In short, we unveiled the unprecedented FL regulation roles of GhAPs in cotton, which was possibly further regulated by GhWRKY40. These findings will reveal the genetic basis of FL development associated with qFLD05 and be beneficial for the marker-assisted selection of long-staple cotton.

Association between diurnal temperature range and outpatient visits for urticaria disease in Lanzhou, China: a distributed lag nonlinear analysis.

BACKGROUND: A growing number of epidemiological studies have shown that daily temperatures are associated with urticaria. However, the relationship between daily changes in temperature and urticaria is unclear. OBJECTIVES: To assess the diurnal temperature difference (DTR) effects on urticaria outpatient visits in Lanzhou, China. METHODS: Urticaria outpatient visits data during 2011-2019 were collected from three major tertiary hospitals in Lanzhou. Daily temperature data from the official website of China Meteorological Administration. Assessment of the relationship between urticaria outpatient volume and DTR in Lanzhou City using a distributed lag nonlinear model. RESULTS: A total of 83,022 urticaria visits were enrolled. There was a nonlinear relationship between DTR and urticaria outpatient visits and a lagged effect of DTR impact. The effects of high DTR on urticaria visits were not seen in all populations but in the male population and in the 15-59 age group. High DTR (P95: 18.2 °C) was associated with a 27% (95% CI: 0.01, 60.53%) and 31% (95% CI: 1.60, 68.99%) increase in the number of urticaria visits in the 21-day lag effect for the male cohort and the 15-59 year old cohort, respectively, compared with 11.5 °C, respectively. CONCLUSIONS: Our study suggests that DTR is a potential risk factor for urticaria. The results of this study may provide a scientific basis for local governments to improve preventive measures in the health care system.

LRRK2 plays essential roles in maintaining lung homeostasis and preventing the development of pulmonary fibrosis.

Perturbation of lung homeostasis is frequently associated with progressive and fatal respiratory diseases, such as pulmonary fibrosis. Leucine-rich repeat kinase 2 (LRRK2) is highly expressed in healthy lungs, but its functions in lung homeostasis and diseases remain elusive. Herein, we showed that LRRK2 expression was clearly reduced in mammalian fibrotic lungs, and LRRK2-deficient mice exhibited aggravated bleomycin-induced pulmonary fibrosis. Furthermore, we demonstrated that in bleomycin-treated mice, LRRK2 expression was dramatically decreased in alveolar type II epithelial (AT2) cells, and its deficiency resulted in profound dysfunction of AT2 cells, characterized by impaired autophagy and accelerated cellular senescence. Additionally, LRRK2-deficient AT2 cells showed a higher capacity of recruiting profibrotic macrophages via the CCL2/CCR2 signaling, leading to extensive macrophage-associated profibrotic responses and progressive pulmonary fibrosis. Taken together, our study demonstrates that LRRK2 plays a crucial role in preventing AT2 cell dysfunction and orchestrating the innate immune responses to protect against pulmonary fibrosis.

ABRO1 promotes NLRP3 inflammasome activation through regulation of NLRP3 deubiquitination.

Deubiquitination of NLRP3 has been suggested to contribute to inflammasome activation, but the roles and molecular mechanisms are still unclear. We here demonstrate that ABRO1, a subunit of the BRISC deubiquitinase complex, is necessary for optimal NLRP3-ASC complex formation, ASC oligomerization, caspase-1 activation, and IL-1ß and IL-18 production upon treatment with NLRP3 ligands after the priming step, indicating that efficient NLRP3 activation requires ABRO1. Moreover, we report that ABRO1 deficiency results in a remarkable attenuation in the syndrome severity of NLRP3-associated inflammatory diseases, including MSU- and Alum-induced peritonitis and LPS-induced sepsis in mice. Mechanistic studies reveal that LPS priming induces ABRO1 binding to NLRP3 in an S194 phosphorylation-dependent manner, subsequently recruiting the BRISC to remove K63-linked ubiquitin chains of NLRP3 upon stimulation with activators. Furthermore, deficiency of BRCC3, the catalytically active component of BRISC, displays similar phenotypes to ABRO1 knockout mice. Our findings reveal an ABRO1-mediated regulatory signaling system that controls activation of the NLRP3 inflammasome and provide novel potential targets for treating NLRP3-associated inflammatory diseases.

A Spatially Controlled Proximity Split Tweezer Switch for Enhanced DNA Circuit Construction and Multifunctional Transduction.

DNA strand displacement reactions are vital for constructing intricate nucleic acid circuits, owing to their programmability and predictability. However, the scarcity of effective methods for eliminating circuit leakages has hampered the construction of circuits with increased complexity. Herein, a versatile strategy is developed that relies on a spatially controlled proximity split tweezer (PST) switch to transduce the biomolecular signals into the independent oligonucleotides. Leveraging the double-stranded rigidity of the tweezer works synergistically with the hindering effect of the hairpin lock, effectively minimizing circuit leakage compared with sequence-level methods. In addition, the freely designed output strand is independent of the target binding sequence, allowing the PST switch conformation to be modulated by nucleic acids, small molecules, and proteins, exhibiting remarkable adaptability to a wide range of targets. Using this platform, established logical operations between different types of targets for multifunctional transduction are successfully established. Most importantly, the platform can be directly coupled with DNA catalytic circuits to further enhance transduction performance. The uniqueness of this platform lies in its design straightforwardness, flexibility, scalable intricacy, and system compatibility. These attributes pave a broad path toward nucleic acid-based development of sophisticated transduction networks, making them widely applied in basic science research and biomedical applications.

Enhanced light output from deep ultraviolet light-emitting diodes enabled by high-order modes on a photonic crystal surface.

The authors demonstrate the enhanced light output from 275-nm AlGaN-based deep ultraviolet (DUV) light-emitting diode (LED) structures via the in-plane modulation of shallow photonic crystal (PC) patterns that were fabricated on the p-AlGaN contact layer surface. The employed PC lattice constants are in the range of 270-780 nm, much larger than the fundamental Bragg order lattice constant (∼95 nm). As compared to the unpatterned sample, the intensity of the top (or bottom) emission can be enhanced by up to 331% (or 246%), attributed to the high-order coherent diffraction of the internal trapped light and also the Purcell enhancement of spontaneous emission. The findings in this Letter suggest an easier way for the realization of more energy-efficient DUV LEDs which offer the advantage of high emission for various applications in disinfection and sterilization.

Elevated FAM134B expression induces radiation-sensitive in hepatocellular carcinoma.

BACKGROUND: Previous studies have shown that Family with sequence similarity 134 member B (FAM134B) was involved in the occurrence and development of malignancy, however, the function and molecular mechanism of FAM134B in Hepatocellular Carcinoma (HCC) radiotherapy resistance remain unclear. Therefore, it may clinical effective to clarify the molecular mechanism and identify novel biomarker to overcome radiotherapy resistance in HCC. METHODS: The protein and mRNA expression of FAM134B were determined using Real-time PCR and Western blot, respectively. IHC assay was performed to investigate the association between FAM134B expression and the clinicopathological characteristics of 132 HCC patients. Functional assays, such as in situ model, colon formation, FACS, and Tunel assay were used to determine the oncogenic role of FAM134B in human HCC progression. Furthermore, western blotting and luciferase assay were used to determine the mechanism of FAM134B promotes radiation-sensitive in HCC cells. RESULTS: We noted that FAM134B was downregulated in HCC, which was correlated with the radiation resistance in patients with HCC. Overexpression of FAM134B contribute to radiation sensitive in HCC; however, inhibition of FAM134B confers HCC cell lines to radiation resistance both in vitro and in vivo. Moreover, we found that FAM134B interacts with FMS related receptor tyrosine kinase 3 (FLT3) and downregulation of FAM134B activated JAK/Stat3 signaling pathway. Importantly, pharmacological inhibition of JAK/Stat3 signaling pathway significantly counteracted downregulation of FAM134B-induced radiation resistance and enhanced radiation therapeutic efficacy in HCC. CONCLUSIONS: Our findings suggest that FAM134B may be a potential therapeutic biomarker for the treatment of HCC patients with radiotherapy tolerance.

Metal-Phenolic Networks Assembled on TiO2 Nanospikes for Antimicrobial Peptide Deposition and Osteoconductivity Enhancement in Orthopedic Applications.

The lack of antimicrobial and osteoconductive activities of titanium (Ti) for orthopedic implants has led to problems such as infection and structural looseness, which bring physical and psychological sufferings to patients as well as economic burden on the healthcare system. To endow Ti implants with anti-infective function and bioactivity, in this study, we successfully constructed TiO2 nanospike (TNS) structure on the surface of Ti followed by assembling metal-polyphenol networks (MPNs) and depositing antimicrobial peptides (AMPs). The TNSs' structure can disrupt the bacteria by physical puncture, and it was also proved to have excellent photothermal conversion performance upon near-infrared light irradiation. Furthermore, with the assistance of contact-active chemo bactericidal efficacy of AMPs, TNS-MPN-AMP nanocoating achieved physical/photothermal/chemo triple-synergistic therapy against pathogenic bacteria. The anti-infective efficiency of this multimodal treatment was obviously improved, with an antibacterial ratio of >99.99% in vitro and 95.03% in vivo. Moreover, the spike-like nanostructure of TNSs and the bioactive groups from MPNs and AMPs not only demonstrated desirable biocompatibility but also promoted the surface hydroxyapatite formation in simulated body fluid for further osseointegration enhancement. Altogether, this multifaceted TNS-MPN-AMP nanocoating endowed Ti implants with enhanced antibacterial activity, excellent cytocompatibility, and desirable osteoconductive ability.

LncRNA SLC7A11-AS1 promotes the progression of hepatocellular carcinoma by mediating KLF9 ubiquitination.

Hepatocellular carcinoma (HCC) is a malignant tumor, which seriously threatens the life of patients. LncRNA SLC7A11-AS1 was reported to be abnormally expressed in HCC. Here, the functions and relative molecular regulatory mechanism of SLC7A11-AS1 in HCC were investigated. Nude mice and HCC cells were used as the experimental subjects. Knockdown or overexpression of exogenous genes was conducted in HCC cells. RT-qPCR, IHC, and western blot were employed to evaluate the abundance of genes and proteins. The malignant behaviors were evaluated using CCK-8, clone formation, wound-healing, and Transwell. The locations of SLC7A11-AS1 and KLF9 in cells were determined by FISH and IF assays. The total m6A level was evaluated by dot-blot assay. m6A modification of SLC7A11-AS1 was detected using RNA MeRIP. The interactions among molecules were validated by RIP, ChIP, dual luciferase reporter assay, and co-IP. SLC7A11-AS1 was elevated apparently in HCC cells and HCC tissues from mice. SLC7A11-AS1 silencing could suppress HCC progression, which was validated in in vivo and in vitro experiments. Furthermore, METTL3 mediated m6A modification of SLC7A11-AS1 to elevate its expression. In addition, SLC7A11-AS1 downregulated KLF9 expression by affecting STUB1-mediated ubiquitination degradation and KLF9 enhanced PHLPP2 expression to inactivate the AKT pathway. Eventually, rescue experiments revealed that KLF9 knockdown abolished SLC7A11-AS1 silencing-mediated suppression of HCC progression in vivo and in vitro. Our results unveiled that m6A-modified SLC7A11-AS1 promoted HCC progression by regulating the STUB1/KLF9/PHLPP2/AKT axis, indicating that targeting SLC7A11-AS1 might alleviate HCC progression.

Digital technology and national entrepreneurship: An ecosystem perspective.

Although the importance of digital technology has been recognized in the entrepreneurship literature, we know relatively little about how and to what extent it influences a nation's entrepreneurial activities. Drawing on the concept of entrepreneurial ecosystem, this study developed a conceptual model to explain the impact of digital technology on national entrepreneurship and the interactions between digital technology and other ecosystem elements. The hypotheses are tested by using unbalanced panel data of 101 countries from 2001 to 2018. The empirical results show that the level of digital technology is positively associated with the output of national entrepreneurial ecosystems, and this positive relationship is strengthened in nations with a supportive culture, high-quality institutions, supportive policies, accessible resources, and well-developed service industries. The findings highlight the importance of digital technology, provide fresh insights into the interdependence between elements and causal mechanisms in national entrepreneurial ecosystems.

Genetic mapping, transcriptomic sequencing and metabolic profiling indicated a glutathione S-transferase is responsible for the red-spot-petals in Gossypium arboreum.

KEY MESSAGE: A GST for red-spot-petals in Gossypium arboreum was identified as the candidate under the scope of multi-omics approaches. Colored petal spots are correlated with insect pollination efficiency in Gossypium species. However, molecular mechanisms concerning the formation of red spots on Gossypium arboreum flowers remain elusive. In the current study, the Shixiya1-R (SxyR, with red spots) × Shixiya1-W (SxyW, without red spots) segregating population was utilized to determine that the red-spot-petal phenotype was levered by a single dominant locus. This phenotype was expectedly related to the anthocyanin metabolites, wherein the cyanidin and delphinidin derivatives constituted the major partition. Subsequently, this dominant locus was narrowed to a 3.27 Mb range on chromosome 7 by genomic resequencing from the two parents and the two segregated progeny bulks that have spotted petals or not. Furthermore, differential expressed genes generated from the two bulks at either of three sequential flower developmental stages that spanning the spot formation were intersected with the annotated ones that allocated to the 3.27 Mb interval, which returned eight genes. A glutathione S-transferase-coding gene (Gar07G08900) out of the eight was the only one that exhibited simultaneously differential expression among all three developmental stages, and it was therefore considered to be the probable candidate. Finally, functional validation upon this candidate was achieved by the appearance of scattered petal spots with inhibited expression of Gar07G08900. In conclusion, the current report identified a key gene for the red spotted petal in G. arboreum under the scope of multi-omics approaches, such efforts and embedded molecular resources would benefit future applications underlying the flower color trait in cotton.

Human leukocyte antigen HLA-C, HLA-G, HLA-F, and HLA-E placental profiles are altered in early severe preeclampsia and preterm birth with chorioamnionitis.

BACKGROUND: The extravillous trophoblast expresses each of the nonclassical major histocompatibility complex class I antigens-human leukocyte antigens E, F, and G-and a single classical class I antigen, human leukocyte antigen C. We recently demonstrated dynamic expression patterns of human leukocyte antigens C, G, and F during early extravillous trophoblast invasion and placentation. OBJECTIVE: This study aimed to investigate the hypothesis that the immune inflammatory mediated complications of pregnancy such as early preeclampsia and preterm labor may show altered expression profiles of nonclassical human leukocyte antigens. STUDY DESIGN: Real-time quantitative polymerase chain reaction, western blot, and immunohistochemistry were performed on placental villous tissues and basal plate sections from term nonlaboring deliveries, preterm deliveries, and severe early-onset preeclampsia, both with and without small-for-gestational-age neonates. RESULTS: Human leukocyte antigen G is strongly and exclusively expressed by the extravillous trophoblast within the placental basal plate, and its levels increase in pregnancies complicated by severe early-onset preeclampsia with small-for-gestational-age neonates relative to those of healthy term controls. Human leukocyte antigen C shows a similar profile in the extravillous trophoblast of preeclamptic pregnancies, but significantly decreases in the villous placenta. Human leukocyte antigen F protein levels are decreased in both extravillous trophoblast and villous placenta of severe early-onset preeclamptic pregnancies, both with and without small-for-gestational-age neonates, compared with those found in term and preterm birth deliveries. Human leukocyte antigen E decreases in blood vessels in placentas from preeclamptic pregnancies relative to its levels in term and preterm birth deliveries. Placental levels of human leukocyte antigens F and C are increased in cases of preterm birth with chorioamnionitis relative to those of cases of idiopathic preterm birth. CONCLUSION: Dysregulation of placental human leukocyte antigen expression at the maternal-fetal interface may contribute to compromised maternal tolerance in preterm birth with chorioamnionitis and excessive maternal systemic inflammation associated with severe early-onset preeclampsia.

Dipeptidyl peptidase-8 induces sorafenib resistance via binding with c-Rel to mediate NF-κB signaling in hepatocellular carcinoma.

Sorafenib is the important first-standard drug for patients with advanced hepatocellular carcinoma (HCC). A major obstacle to successful treatment is sorafenib resistance. However, the mechanism of sorafenib resistance is unclear. The present study aimed to determine the involvement of dipeptidyl peptidase-8 (DPP8) in sorafenib resistance. DPP8 expression was detected using quantitative real-time PCR (qPCR) and western blot analysis. The effect of DPP8 on sorafenib resistance was examined using terminal deoxynulceotidyl transferase nick-end-labeling (TUNEL), colony formation, flow cytometry, luciferase reporter, immunofluorescence, and immunoprecipitation (IP) assays. We found that DPP8 mRNA and protein levels were dramatically upregulated in HCC. Gene set enrichment analysis (GSEA) illustrated that DPP8 might be involved in apoptosis regulation. Downregulation of DPP8 substantially promoted the sensitivity of HCC cells to sorafenib. Further analysis showed that DPP8 might regulate nuclear factor kappa B (NF-κB) signaling, which was confirmed using a luciferase reporter assay. Downregulation of DPP8 decreased the expression levels of downstream genes of the NF-κB pathway. IP showed that DPP8 can interact with NF-κB subunit c-Rel, an important protein of NF-κB signaling. Finally, a drug combination of sorafenib and Val-boroPro induced higher mortality of HCC cells than sorafenib alone in DPP8-upregulated cells. Our findings indicated that using the inhibitor Val-boroPro might be a promising method to enhance sorafenib sensitivity in advanced HCC.

Metastasis to the Pancreas From Ductal Carcinoma In Situ of Breast Cancer: A Case Report and Review of Literature.

Background: The usual locations of metastatic breast neoplasms include the bones, the liver, the lung, and the brain. Breast cancer rarely metastasizes to the pancreas. However, pancreatic metastasis and primary pancreatic cancer are difficult to differentiate because of their similar clinical features and radiological characteristics. Case presentation: We report on a 49-year-old woman initially diagnosed with left breast ductal carcinoma in June 2008. The patient was admitted to the hospital with jaundice after 12 years. Computed tomography (CT) scan and magnetic resonance imaging (MRI) revealed a mass in the pancreas head. Histopathology and immunohistochemistry showed ductal carcinoma originating from breast cancer. She underwent pancreatoduodenectomy to relieve jaundice. The patient is still alive with a favorable prognosis. Conclusions: In this paper, we mainly discuss the clinical characteristics, diagnostic methods, and surgical treatment of pancreatic metastasis. When a pancreatic lesion is detected with a history of breast cancer, the pancreatic metastasis likely originates from breast cancer.

Reach-to-grasp kinematics and kinetics with and without visual feedback in early-stage Alzheimer's disease.

This study aimed to investigate the effects of early-stage Alzheimer's disease (AD) on the reach-to-grasp kinematics and kinetics with and without visual supervision of the grasping arm and hand. Seventeen patients who had been diagnosed with early-stage AD and 17 age- and gender-matched, cognitive normal (CN) adults participated in the experiment. A mirror operating system was designed to block the visual feedback of their grasping hand and forearms but to virtually show grasped targets. The target for reach-to-grasp kinematics was a reflective marker installed on a base; and the target for reach-to-grasp kinetics was a custom-made apparatus installed with two six-component force/torque transducers. Kinematics and kinetic parameters were used to quantify the reach-to-grasp performances. Results showed that the early-stage AD remarkably decreased the reaching speed, reduced the grasping accuracy and increased the transportation variability for reach-to-grasp kinematics. For kinetic analysis, early-stage AD extended the preload duration, disturbed the grip and lift forces coordination, and increased the feedforward proportion in the grasping force control. The AD-related changes in the reach-to-grasp kinematic and kinetic parameters depended on visual feedback and were associated with nervous system function according to correlation analyses with the neuropsychological testing. These results suggest that the abnormal kinematic and kinetic characteristics may correlate with the neuropsychological status of early-stage AD, and that the reach-to-grasp kinematic and kinetic maneuver could potentially be used as a novel tool for non-invasive screening or evaluation of early-stage AD.

A Lightweight and Privacy-Friendly Data Aggregation Scheme against Abnormal Data.

Abnormal electricity data, caused by electricity theft or meter failure, leads to the inaccuracy of aggregation results. These inaccurate results not only harm the interests of users but also affect the decision-making of the power system. However, the existing data aggregation schemes do not consider the impact of abnormal data. How to filter out abnormal data is a challenge. To solve this problem, in this study, we propose a lightweight and privacy-friendly data aggregation scheme against abnormal data, in which the valid data can correctly be aggregated but abnormal data will be filtered out during the aggregation process. This is more suitable for resource-limited smart meters, due to the adoption of lightweight matrix encryption. The automatic filtering of abnormal data without additional processes and the detection of abnormal data sources are where our protocol outperforms other schemes. Finally, a detailed security analysis shows that the proposed scheme can protect the privacy of users' data. In addition, the results of extensive simulations demonstrate that the additional computation cost to filter the abnormal data is within the acceptable range, which shows that our proposed scheme is still very effective.

Genome-wide analysis of ATP-binding cassette transporter provides insight to genes related to bioactive metabolite transportation in Salvia miltiorrhiza.

BACKGROUND: ATP-binding cassette (ABC) transporters have been found to play important roles in metabolic transport in plant cells, influencing subcellular compartmentalisation and tissue distribution of these metabolic compounds. Salvia miltiorrhiza Bunge, known as Danshen in traditional Chinese medicine, is a highly valued medicinal plant used to treat cardiovascular and cerebrovascular diseases. The dry roots and rhizomes of S. miltiorrhiza contain biologically active secondary metabolites of tanshinone and salvianolic acid. Given an assembled and annotated genome and a set of transcriptome data of S. miltiorrhiza, we analysed and identified the candidate genes that likely involved in the bioactive metabolite transportation of this medicinal plant, starting with the members of the ABC transporter family. RESULTS: A total of 114 genes encoding ABC transporters were identified in the genome of S. miltiorrhiza. All of these ABC genes were divided into eight subfamilies: 3ABCA, 31ABCB, 14ABCC, 2ABCD, 1ABCE, 7ABCF, 46ABCG, and 10 ABCI. Gene expression analysis revealed tissue-specific expression profiles of these ABC transporters. In particular, we found 18 highly expressed transporters in the roots of S. miltiorrhiza, which might be involved in transporting the bioactive compounds of this medicinal plant. We further investigated the co-expression profiling of these 18 genes with key enzyme genes involved in tanshinone and salvianolic acid biosynthetic pathways using quantitative reverse transcription polymerase chain reaction (RT-qPCR). From this RT-qPCR validation, we found that three ABC genes (SmABCG46, SmABCG40, and SmABCG4) and another gene (SmABCC1) co-expressed with the key biosynthetic enzymes of these two compounds, respectively, and thus might be involved in tanshinone and salvianolic acid transport in root cells. In addition, we predicted the biological functions of S. miltiorrhiza ABC transporters using phylogenetic relationships and analysis of the transcriptome to find biological functions. CONCLUSIONS: Here, we present the first systematic analysis of ABC transporters in S. miltiorrhiza and predict candidate transporters involved in bioactive compound transportation in this important medicinal plant. Using genome-wide identification, transcriptome profile analysis, and phylogenetic relationships, this research provides a new perspective on the critical functions of ABC transporters in S. miltiorrhiza.

The cellulose synthase (CesA) gene family in four Gossypium species: phylogenetics, sequence variation and gene expression in relation to fiber quality in Upland cotton.

Cellulose synthases (CesAs) are multi-subunit enzymes found on the plasma membrane of plant cells and play a pivotal role in cellulose production. The cotton fiber is mainly composed of cellulose, and the genetic relationships between CesA genes and cotton fiber yield and quality are not fully understood. Through a phylogenetic analysis, the CesA gene family in diploid Gossypium arboreum and Gossypium raimondii, as well as tetraploid Gossypium hirsutum ('TM-1') and Gossypium barbadense ('Hai-7124' and '3-79'), was divided into 6 groups and 15 sub-groups, with each group containing two to five homologous genes. Most CesA genes in the four species are highly collinear. Among the five cotton genomes, 440 and 1929 single nucleotide polymorphisms (SNPs) in the CesA gene family were identified in exons and introns, respectively, including 174 SNPs resulting in amino acid changes. In total, 484 homeologous SNPs between the A and D genomes were identified in diploids, while 142 SNPs were detected between the two tetraploids, with 32 and 82 SNPs existing within G. hirsutum and G. barbadense, respectively. Additionally, 74 quantitative trait loci near 18 GhCesA genes were associated with fiber quality. One to four GhCesA genes were differentially expressed (DE) in ovules at 0 and 3 days post anthesis (DPA) between two backcross inbred lines having different fiber lengths, but no DE genes were identified between these lines in developing fibers at 10 DPA. Twenty-seven SNPs in above DE CesA genes were detected among seven cotton lines, including one SNP in Ghi_A08G03061 that was detected in four G. hirsutum genotypes. This study provides the first comprehensive characterization of the cotton CesA gene family, which may play important roles in determining cotton fiber quality.