Biology subjects

Qiu, Y.

Publications and source records attributed to Qiu, Y..

At least 127 records · Page 7Linked to original sources

bioRxiv2023

Rhythmic lipid and gene expression responses to chilling in panicoid grasses

Chilling stress threatens plant growth and development, particularly affecting membrane fluidity and cellular integrity. Understanding plant membrane responses to chilling stress is important for unraveling the molecular mechanisms of stress tolerance. Whereas core transcriptional responses to chilling stress and stress tolerance are conserved across species, the associated changes in membrane lipids appear to be less conserved, as which lipids are affected by chilling stress varies by species. Here, we investigated changes in gene expression and membrane lipids in response to chilling stress during one diurnal cycle in sorghum (Sorghum bicolor), Urochloa (browntop signal grass, Urochloa fusca) (lipids only), and foxtail millet (Setaria italica), leveraging their evolutionary relatedness and differing levels of chilling-stress tolerance. We show that most chilling-induced lipid changes are conserved across the three species, while we observed distinct, time-specific responses in chilling-tolerant foxtail millet, indicating the presence of a finely orchestrated adaptive mechanism. We detected diurnal rhythmicity in lipid responses to chilling stress in the three grasses, which were also present in Arabidopsis (Arabidopsis thaliana), suggesting the conservation of rhythmic patterns across species and highlighting the importance of accounting for diurnal effects. When integrating lipid datasets with gene expression profiles, we identified potential candidate genes that showed corresponding transcriptional changes in response to chilling stress, providing insights into the differences in regulatory mechanisms between chilling-sensitive sorghum and chilling-tolerant foxtail millet. Significance StatementPlants respond to low-temperature stress in myriad ways. While core transcriptional changes are conserved across species, specific adaptive strategies do exist. However, membrane lipid responses during chilling do not appear to be conserved. Here, we collected samples from control and chilling stress-treated seedlings [PSC4] to assess gene expression and membrane lipids in three panicoid grasses to show that lipid metabolic changes follow a daily rhythm. Lipid changes in chilling-tolerant foxtail millet occurred at specific time points, partly explaining the difficulty in finding conserved chilling-induced lipid changes in previous reports. We identified specific orthologs in sorghum and foxtail millet that showed a correlation between gene expression and lipid metabolic changes; these orthologs may be used as potential target genes for developing chilling-tolerant sorghum varieties.

plant biology↗

bioRxiv2023

Inhibiting Glutamine Metabolism Blocks Coronavirus Replication in Mammalian Cells

Developing therapeutic strategies against COVID-19 has gained widespread interest given the likelihood that new viral variants will continue to emerge. Here we describe one potential therapeutic strategy which involves targeting members of the glutaminase family of mitochondrial metabolic enzymes (GLS and GLS2), which catalyze the first step in glutamine metabolism, the hydrolysis of glutamine to glutamate. We show three examples where GLS expression increases during coronavirus infection of host cells, and another in which GLS2 is upregulated. The viruses hijack the metabolic machinery responsible for glutamine metabolism to generate the building blocks for biosynthetic processes and satisfy the bioenergetic requirements demanded by the glutamine addiction of virus-infected host cells. We demonstrate how genetic silencing of glutaminase enzymes reduces coronavirus infection and that newer members of two classes of small molecule allosteric inhibitors targeting these enzymes, designated as SU1, a pan-GLS/GLS2 inhibitor, and UP4, which is specific for GLS, block viral replication in mammalian epithelial cells. Overall, these findings highlight the importance of glutamine metabolism for coronavirus replication in human cells and show that glutaminase inhibitors can block coronavirus infection and thereby may represent a novel class of anti-viral drug candidates. TeaserInhibitors targeting glutaminase enzymes block coronavirus replication and may represent a new class of anti-viral drugs.

molecular biology↗

bioRxiv2023

Structural insights into abscisic acid exporter AtABCG25

Cellular hormone homeostasis is essential for the precise spatial and temporal signaling responses and plant fitness. Abscisic acid (ABA) plays pivotal roles in orchestrating various developmental and stress responses and confers fitness benefits over ecological and evolutionary timescales in terrestrial plants. Cellular ABA levels is regulated by complex processes including biosynthesis, catabolism, and transport. AtABCG25 is the first identified ABA exporter through genetic screen which affects diverse ABA responses. Resolving the structure basis of ABCG25 in ABA exporting is critical for further manipulating ABA homeostasis and plant fitness. We utilized cryo-electron microscopy to elucidate the structural dynamics of AtABCG25, and successfully characterized different states including apo AtABCG25, ABA-bound AtABCG25 and ATP-bound AtABCG25(E232Q). Notably, AtABCG25 forms a homodimer, featuring a deep, slit-like cavity in the transmembrane domain. The critical residues in the cavity where ABA binds are precisely characterized. Moreover, ATP binding triggers the closure of nucleotide-binding domains and conformational transitions in the transmembrane domains. Collectively, these findings provide valuable insights into the intricate substrate recognition and transport mechanisms of ABA exporter ABCG25, paving the way towards genetical manipulating of ABA homeostasis and plant fitness.

plant biology↗

bioRxiv2023

Metabotropic signaling within somatostatin interneurons regulates thalamocortical inputs during development

During brain development, neural circuits undergo major activity-dependent restructuring. Circuit wiring mainly occurs through synaptic strengthening following the Hebbian "fire together, wire together" precept. However, select connections, essential for circuit development, are transient. They are effectively connected early in development, but strongly diminish during maturation. The mechanisms by which transient connectivity recedes are unknown. To investigate this process, we characterize transient thalamocortical inputs, which depress onto somatostatin inhibitory interneurons during development, by employing optogenetics, chemogenetics, transcriptomics and CRISPR-based strategies. We demonstrate that in contrast to typical activity-dependent mechanisms, transient thalamocortical connectivity onto somatostatin interneurons is non-canonical and involves metabotropic signaling. Specifically, metabotropic-mediated transcription, of guidance molecules in particular, supports the elimination of this connectivity. Remarkably, we found that this developmental process impacts the development of normal exploratory behaviors of adult mice.

neuroscience↗

bioRxiv2023

VirEvol platform:accurate prediction and visualization of SARS-CoV-2 evolutionary trajectory based on protein language model, structural information and immunological recognition mechanism

Predicting the mutation direction of SARS-CoV-2 using exploratory computational methods presents a challenging, yet prospective, research avenue. However, existing research methods often ignore the effects of protein structure and multi-source viral information on mutation prediction, making it difficult to accurately predict the evolutionary trend of the SARS-CoV-2 S protein receptor-binding domain (RBD). To overcome this limitation, we proposed an interpretable language model combining structural, sequence and immune information. The dual utility of this model lies in its ability to predict SARS-CoV-2s affinity for the ACE2 receptor, and to assess its potential for immune evasion. Additionally, it explores the mutation trend of SARS-CoV-2 via a genetic algorithm-directed evolution. The model exhibits high accuracy in both regards and has displayed promising early warning capabilities, effectively identifying 13 out of 14 high-risk strains, marking a success rate of 93%.". This study provides a novel method for discerning the molecular evolutionary pattern, as well as predicting the evolutionary trend of SARS-CoV-2 which is of great significance for vaccine design and drug development of new coronaviruses. We further developed VirEvol, a unique platform designed to visualize the evolutionary trajectories of novel SARS-CoV-2 strains, thereby facilitating real-time predictive analysis for researchers. The methodologies adopted in this work may inspire new strategies and offer technical support for addressing challenges posed by other highly mutable viruses.

bioinformatics↗

bioRxiv2023

Global and local adaptation to aridity in a desert plant Gymnocarpos przewalskii

In order to thrive and survive plant species need to combine stability in the long term and rapid response to environmental challenges in the short term. The former would be reflected by global adaptation across species and the latter by pronounced local adaptation among populations of the same species. It remains unclear how much overlap is to be expected between the parts of the genome associated to these two contrasted adaptation processes. In the present study, we generated a high-quality genome and re-sequenced 177 individuals for Gymnocarpos przewalskii, an important desert plant species from North-West China, to detect local adaptation. To test for global adaptation to aridity at the molecular level we compared genomic data of 15 species that vary in their ability to withstand drought. A total of 118 genes were involved in global adaptation to aridity. Sixty-five G. przewalskii genes were shared across all xerophytic species, of which sixty-three were under stabilizing selection and two under directional selection. While 20% of G. przewalskii genome showed signatures of local adaptation to aridity during population divergence, only 13 of those genes were also under global adaptation. Hence, our results suggest that long-term stability is crucial for adaptation to extreme environmental stress but is only maintained in a small group of highly pleiotropic genes while a rapid response to recent changes elicits a genome-wide response, including gene family expansion. The overlap between the two evolutionary mechanisms appears limited.

evolutionary biology↗

bioRxiv2023

The molecular basis of parental conflict driven regulation of endosperm cellularization

The endosperm is a seed tissue supporting embryo growth, similar to the placenta in mammals. It originates after fertilization of the maternal central cell by one of the paternal sperm cells. In the early stages of Arabidopsis thaliana seed development, nuclei divisions in the endosperm are not followed by cellularization. After a defined number of mitotic cycles, the endosperm cellularizes and stops dividing. The timing of endosperm cellularization impacts on final seed size and is differentially controlled by maternal and paternal genome contributions. While increased maternal genome dosage causes early endosperm cellularization and the formation of small seeds, the opposite is caused by increased paternal genome dosage. The parental factors controlling the differential timing of endosperm cellularization remain largely unexplored. Here, we show that a family of maternally expressed auxin response factors (ARFs) promotes endosperm cellularization and regulates final seed size. One-Sentence SummaryEndosperm cellularization is under antagonistic parental control that converges on Auxin Response Factors.

plant biology↗

bioRxiv2023

VIGA: an one-stop tool for eukaryotic Virus Identification and Genome Assembly from next-generation-sequencing data

Identification of viruses and further assembly of viral genomes from the next-generation-sequencing (NGS) data are essential steps in virome studies. This study presented an one-stop tool named VIGA (available at https://github.com/viralInformatics/VIGA) for eukaryotic virus identification and genome assembly from NGS data. It was composed of four modules including identification, taxonomic annotation, assembly and novel virus discovery which integrated the homology-based method for virus identification and both the reference-based and de novo assemblers for accurate and effective assembly of virus genomes. Evaluation on multiple simulated and real virome datasets showed that VIGA assembled more complete virus genomes than its competitors on both the metatranscriptomic and metagenomic data, and also performed well in assembling virus genomes at the strain level. Finally, VIGA was used to investigate the virome in metatranscriptomic data from the Human Microbiome Project and revealed different composition and positive rate of viromes in diseases of Prediabetes, Crohns disease and Ulcerative colitis. Overall, VIGA would help much in identification and characterization of viromes in future studies.

bioinformatics↗

bioRxiv2023

Hypoxia-induced circSTT3A maintains Breast Cancer Stem Cell formation by Stabilizing PGK1 protein

BackgroundHypoxia is a key feature of tumor microenvironment that can cause fundamental changes in cancer cells, and may also lead to the development of breast cancer stem cells (BCSCs) with self-renewal ability. However, the mechanism of hypoxia in inducing BCSCs is not fully understood. MethodsPerforming RNA sequence and bioinformatics analysis, a hypoxia specific circular RNA (circRNA), named circSTT3A, was identified in hypoxic breast cancer cells and tissues. The clinical significance of circSTT3A was investigated in breast cancer (BC) tissues and tissue array. The loss and acquisition of circSTT3A were carried out in vivo and in vitro to confirm its functional roles in BCSC stemness maintenance. HIF1 droved circSTT3A expression was evaluated by chromatin immunoprecipitation and dual luciferase reporter assays. RNA pull-down, RNA immunoprecipitation, silver staining detection, mass spectrographic analysis, co-immunoprecipitation assays and western blotting were exerted to determine circSTT3A directly binding with HSP70 and PGK1 proteins. CircSTT3A-mediated serine metabolism was determined by UHPLC-QTRAP-MS system and ELISA kit. BC mouse model was used to assess the effects of circSTT3A/Hsp70/PGK1 on tumorigenesis and chemotherapy resistance in vivo. ResultsA novel hypoxia specific circSTT3A was significantly upregulated in clinical breast cancer tissues, and was related to the clinical stage and poor prognosis of BC patients. The hypoxia inducible factor 1 alpha (HIF1)-regulated circSTT3A has remarkable effect on mammosphere formation in breast cancer cells. Our work revealed that circSTT3A directly interacting with nucleotide-binding domain of heat shock protein 70 (HSP70) increases the ability of HSP70 to recruit phosphoglycerate kinase 1 (PGK1) via its substrate-binding domain, which reduces the ubiquitination of PGK1 and increases the stability of PGK1. The enhanced PGK1 catalyzes 1,3-diphosphoglycerate (1, 3-BPG) into 3-phosphoglycerate (3-PG) leading to 3-PG accumulation and increase of serine synthesis, thus to facilitate BCSC enrichment under hypoxic microenvironment. Loss of circSTT3A or PGK1 substantially induces suppression in tumor initiation and tumor growth, which dramatically increases tumor sensitivity to Doxorubicin treatment in mice. ConclusionsHypoxia induced circSTT3A/HSP70/PGK1 axis plays a critical role in maintaining BCSC properties and may be meaningful for treating patients with breast cancer.

cancer biology↗

bioRxiv2023

Learning the Language of Antibody Hypervariability

Protein language models (PLMs) based on machine learning have demon-strated impressive success in predicting protein structure and function. However, general-purpose ("foundational") PLMs have limited performance in predicting antibodies due to the latters hypervariable regions, which do not conform to the evolutionary conservation principles that such models rely on. In this study, we propose a new transfer learning framework called AbMAP, which fine-tunes foundational models for antibody-sequence inputs by supervising on antibody structure and binding specificity examples. Our feature representations accurately predict an antibodys 3D structure, mutational effects on antigen binding, and paratope identification. AbMAPs scalability paves the way for large-scale analyses of human antibody repertoires. AbMAP representations of immune repertoires reveal a remarkable overlap across individuals, overcoming the limitations of sequence analyses. Our findings provide compelling evidence for the hypothesis that antibody repertoires of individuals tend to converge towards comparable structural and functional coverage. We validate AbMAP for antibody optimization, applying it to optimize a set of antibodies that bind to a SARS-CoV-2 peptide and obtaining 82% hit-rate and upto 22-fold increase in binding affinity. We anticipate AbMAP will accelerate the efficient design and modeling of antibodies and expedite the discovery of antibody-based therapeutics. Availability:https://github.com/rs239/ablm

bioinformatics↗

bioRxiv2023

3D structural human interactome reveals proteome-wide perturbations by disease mutations

Human genome sequencing studies have identified numerous loci associated with complex diseases. However, translating human genetic and genomic findings to disease pathobiology and therapeutic discovery remains a major challenge at multiscale interactome network levels. Here, we present a deep-learning-based ensemble framework, termed PIONEER (Protein-protein InteractiOn iNtErfacE pRediction), that accurately predicts protein binding partner-specific interfaces for all known protein interactions in humans and seven other common model organisms, generating comprehensive structurally-informed protein interactomes. We demonstrate that PIONEER outperforms existing state-of-the-art methods. We further systematically validated PIONEER predictions experimentally through generating 2,395 mutations and testing their impact on 6,754 mutation-interaction pairs, confirming the high quality and validity of PIONEER predictions. We show that disease-associated mutations are enriched in PIONEER-predicted protein-protein interfaces after mapping mutations from [~]60,000 germline exomes and [~]36,000 somatic genomes. We identify 586 significant protein-protein interactions (PPIs) enriched with PIONEER-predicted interface somatic mutations (termed oncoPPIs) from pan-cancer analysis of [~]11,000 tumor whole-exomes across 33 cancer types. We show that PIONEER-predicted oncoPPIs are significantly associated with patient survival and drug responses from both cancer cell lines and patient-derived xenograft mouse models. We identify a landscape of PPI-perturbing tumor alleles upon ubiquitination by E3 ligases, and we experimentally validate the tumorigenic KEAP1-NRF2 interface mutation p.Thr80Lys in non-small cell lung cancer. We show that PIONEER-predicted PPI-perturbing alleles alter protein abundance and correlates with drug responses and patient survival in colon and uterine cancers as demonstrated by proteogenomic data from the National Cancer Institutes Clinical Proteomic Tumor Analysis Consortium. PIONEER, implemented as both a web server platform and a software package, identifies functional consequences of disease-associated alleles and offers a deep learning tool for precision medicine at multiscale interactome network levels.

bioinformatics↗

bioRxiv2023

Circulating exosomes from Alzheimer's disease suppress VE-cadherin expression and induce barrier dysfunction in recipient brain microvascular endothelial cell

BackgroundBlood-brain barrier (BBB) breakdown is a component of the progression and pathology of Alzheimers disease (AD). BBB dysfunction is primarily caused by reduced or disorganized tight junction or adherens junction proteins of brain microvascular endothelial cell (BMEC). While there is growing evidence of tight junction disruption in BMECs in AD, the functional role of adherens junctions during BBB dysfunction in AD remains unknown. Exosomes secreted from senescent cells have unique characteristics and contribute to modulating the phenotype of recipient cells. However, it remains unknown if and how these exosomes cause BMEC dysfunction in AD. ObjectivesThis study aimed to investigate the potential roles of AD circulating exosomes and their RNA cargos in brain endothelial dysfunction in AD. MethodsWe isolated exosomes from sera of five cases of AD compared with age- and sex-matched cognitively normal controls using size-exclusion chromatography technology. We validated the qualities and particle sizes of isolated exosomes with nanoparticle tracking analysis and atomic force microscopy. We measured the biomechanical natures of the endothelial barrier of BMECs, the lateral binding forces between live BMECs, using fluidic force miscopy. We visualized the paracellular expressions of the key adherens junction protein VE-cadherin in BMEC cultures and a 3D BBB model that employs primary human BMECs and pericytes with immunostaining and evaluated them using confocal microscopy. We also examined the VE-cadherin signal in brain tissues from five cases of AD and five age- and sex-matched cognitively normal controls. ResultsWe found that circulating exosomes from AD patients suppress the paracellular expression levels of VE-cadherin and impair the barrier function of recipient BMECs. Immunostaining analysis showed that AD circulating exosomes damage VE-cadherin integrity in a 3D model of microvascular tubule formation. We found that circulating exosomes in AD weaken the BBB depending on the RNA cargos. In parallel, we observed that microvascular VE-cadherin expression is diminished in AD brains compared to normal controls. ConclusionUsing in vitro and ex vivo models, our study illustrates that circulating exosomes from AD patients play a significant role in mediating the damage effect on adherens junction of recipient BMEC of the BBB in an exosomal RNA-dependent manner. This suggests a novel mechanism of peripheral senescent exosomes for AD risk.

neuroscience↗

bioRxiv2023

A deep population reference panel of tandem repeat variation

Tandem repeats (TRs) represent one of the largest sources of genetic variation in humans and are implicated in a range of phenotypes. Here we present a deep characterization of TR variation based on high coverage whole genome sequencing from 3,550 diverse individuals from the 1000 Genomes Project and H3Africa cohorts. We develop a method, EnsembleTR, to integrate genotypes from four separate methods resulting in high-quality genotypes at more than 1.7 million TR loci. Our catalog reveals novel sequence features influencing TR heterozygosity, identifies population-specific trinucleotide expansions, and finds hundreds of novel eQTL signals. Finally, we generate a phased haplotype panel which can be used to impute most TRs from nearby single nucleotide polymorphisms (SNPs) with high accuracy. Overall, the TR genotypes and reference haplotype panel generated here will serve as valuable resources for future genome-wide and population-wide studies of TRs and their role in human phenotypes.

genomics↗

bioRxiv2023

A MAP kinase cascade broadly regulates development and virulence of Sclerotinia sclerotiorum and can be targeted by HIGS for disease control

Sclerotinia sclerotiorum causes white mold or stem rot in a broad range of economically important plants, bringing significant yield losses worldwide. Host-induced gene silencing (HIGS) has been showing promising effects in controlling many fungal pathogens, including S. sclerotiorum. However, molecular genetic understanding of signaling pathways involved in its development and pathogenicity is needed to provide effective host-induced gene silencing (HIGS) targets for disease control. Here, by employing a forward genetic screen, we characterized an evolutionarily conserved mitogen-activated protein kinase (MAPK) cascade in S. sclerotiorum, consisting of SsSte50-SsSte11-SsSte7-Smk1, controlling mycelial growth, sclerotia development, compound appressoria formation, virulence, and hyphal fusion. Moreover, disruption of the putative downstream transcription factor SsSte12 led to normal sclerotia but aberrant appressoria formation and host penetration defects, suggestive of diverged regulation downstream of the MAPK cascade. Most importantly, targeting of SsSte50 using host-expressed HIGS double stranded RNA resulted in largely reduced virulence of S. sclerotiorum on Nicotiana benthamiana leaves. Therefore, this MAPK signaling cascade is generally needed for its growth, development, and pathogenesis, and is an ideal HIGS target for mitigating economic damages caused by S. sclerotiorum infection.

microbiology↗

bioRxiv2023

Structure of human NaV1.6 channel reveals Na+ selectivity and pore blockade by 4,9-anhydro-tetrodotoxin

The sodium channel NaV1.6 is widely expressed in neurons of the central and peripheral nervous systems, which plays a critical role in regulating neuronal excitability. Dysfunction of NaV1.6 has been linked to epileptic encephalopathy, intellectual disability and movement disorders. Here we present cryo-EM structures of human NaV1.6/{beta}1/{beta}2 alone and complexed with a guanidinium neurotoxin 4,9-anhydro-tetrodotoxin (4,9-ah-TTX), revealing molecular mechanism of NaV1.6 inhibition by the blocker. In the apo-form structure, two potential Na+ binding sites were revealed in the selectivity filter, suggesting a possible mechanism for Na+ selectivity and conductance. In the 4,9-ah-TTX-bound structure, 4,9-ah-TTX binds to a pocket similar to the tetrodotoxin (TTX) binding site, which occupies the Na+ binding sites and completely blocks the channel. Molecular dynamics simulation results show that subtle conformational differences in the selectivity filter affect the affinity of TTX analogues. Taken together, our results provide important insights into NaV1.6 structure, ion conductance, and inhibition.

biophysics↗

bioRxiv2023

Updated phylogeny and protein structure predictions revise the hypothesis on the origin of MADS-box transcription factors in land plants

MADS-box transcription factors (TFs) are broadly present in eukaryotes. Varying by domain architecture, MADS-box TFs in land plants are categorized into Type I (M-type) and Type II (MIKC-type). For about twenty years, Type I and II genes were considered orthologous to the SRF and MEF2 genes in animals, respectively, presumably originating from a duplication before the divergence of eukaryotes. Here, we exploited the increasing eukaryotic MADS-box sequences and reassessed their evolution. While supporting the ancient duplication giving rise to SRF- and MEF2-types, we found that Type I and II genes originated from the MEF2-type genes through another duplication in the most recent common ancestor (MRCA) of land plants. Protein structures predicted by AlphaFold2 and OmegaFold support our phylogenetic analyses, with plant Type I and II TFs resembling the MEF2-type structure, rather than SRFs. We hypothesize that the ancestral SRF-type TFs got lost in the MRCA of Archaeplastida (the kingdom Plantae sensu lato). The retained MEF2-type TFs acquired a Keratin-like domain and became MIKC-type upon the evolution of Streptophyta. Subsequently in the MRCA of land plants, M-type TFs evolved from a duplicated MIKC-type precursor through loss of the Keratin-like domain, leading to the Type I clade. Both Type I and II TFs largely expanded and functionally differentiated in concert with the increasing complexity of land plant body architecture. We attribute the adaptation to the terrestrial environment partly to the divergence among MEF2-type MADS-box genes and the repetitive recruitment of these originally stress-responsive TFs into developmental programs, especially those underlying reproduction.

plant biology↗

bioRxiv2023

Identification of common sequence motifs shared exclusively among selectively packed exosomal pathogenic microRNAs during rickettsial infections

We previously reported that microRNA (miR)23a and miR30b are selectively sorted into rickettsia-infected, endothelial cell-derived exosomes (R-ECExos). Yet, the mechanism remains unknown. The number of cases of spotted fever rickettsioses has been increasing in recent years, and infections with these bacteria cause life-threatening diseases by targeting brain and lung tissues. Therefore, the aim of the present study is to continue to dissect the molecular mechanism underlying R-ECExos-induced barrier dysfunction of normal recipient microvascular endothelial cells (MECs), depending on their exosomal RNA cargos. Rickettsiae are transmitted to human hosts by the bite of an infected tick into the skin. In the present study we demonstrate that treatment with R-ECExos, which were derived from spotted fever group R parkeri infected human dermal MECs, induced disruptions of the paracellular adherens junctional protein VE-cadherin and breached the paracellular barrier function in recipient pulmonary MECs (PMECs) in an exosomal RNA-dependent manner. Similarly, we did not detect different levels of miRs in parent dermal MECs following rickettsial infections. However, we demonstrated that the microvasculopathy-relevant miR23a-27a-24 cluster and miR30b are selectively enriched in R-ECExos. Bioinformatic analysis revealed that common sequence motifs are shared exclusively among the exosomal, selectively-enriched miR23a cluster and miR30b at different levels. Taken together, these data warrant further functional identification and characterization of a single, bipartition, or tripartition among ACA, UCA, and CAG motifs that guide recognition of microvasculopathy-relevant miR23a-27a-24 and miR30b, and subsequently results in their selective enrichments in R-ECExos.

molecular biology↗

bioRxiv2023

Leafhopper transmits soybean stay-green associated virus to legume plants

A novel geminivirus, soybean stay-green associated virus (SoSGV), was previously shown to cause soybean delayed senescence and is associated with the incidences of soybean stay-green syndrome. The transmission methods of SoSGV were not yet understood. We captured insects belonging to 24 distinct species in a soybean field with the SoSGV outbreak and detected the presence of SoSGV only in leafhoppers and bean bugs (Riptortus pedestris). Caged feeding experiments using captured leafhoppers and bean bugs from soybean fields showed that leafhoppers, but not bean bugs, are vectors transmitting SoSGV. The common brown leafhopper (Orosius orientalis) is identified as the dominant leafhopper species and can establish colonies feeding on soybean plants in experimental conditions. An investigation of SoSGV defective DNA revealed that soybean genomic DNA could be inserted into the SoSGV genome, while sequences from wild soybean, red bean, and cowpea were also identified. We further showed that the common brown leafhopper could transmit SoSGV to wild soybean and red bean plants, emphasizing the vector role of the leafhopper in the transmission of SoSGV in the field.

microbiology↗