Biology subjects

li, h.

Publications and source records attributed to li, h..

6 recordsLinked to original sources

bioRxiv2026

Genome-wide analysis of the annexin gene family in alfalfa (Medicago sativa L.) and functional characterization of MsANN22 under drought stress

Annexins are a conserved family of calcium-dependent phospholipid-binding proteins that participate in diverse plant stress responses. However, the annexin gene family in Medicago sativa and the molecular mechanisms underlying annexin-mediated drought tolerance remain largely unexplored. In this study, 73 MsANN genes were identified in the alfalfa genome. Their phylogenetic relationships, synteny, conserved motifs, gene structures, and promoter cis-acting elements were systematically analyzed. Synteny analysis revealed 75 segmental/whole-genome duplication-associated gene pairs but no tandem duplications, indicating that large-scale duplication was the major driver of MsANN family expansion. The MsANN promoters contained ABA- and drought-responsive elements. Expression profiling identified MsANN22 as a strongly drought-responsive gene encoding a cytoplasm-localized protein. MsANN22 overexpression enhanced drought tolerance in both Arabidopsis thaliana and alfalfa: in A. thaliana, MsANN22 overexpression promoted seed germination under osmotic stress, whereas in alfalfa it enhanced antioxidant capacity, with superoxide dismutase and peroxidase activities reaching 1.38- and 1.70-fold those of wild-type plants, respectively. Consistently, MsANN22-overexpressing alfalfa accumulated approximately 20% less malondialdehyde than wild-type plants and exhibited reduced H2O2 and O2*- accumulation, as indicated by DAB and NBT staining. Yeast two-hybrid and luciferase complementation assays further supported physical interactions of MsANN22 with MsIAA and MsPR-10. These findings provide insight into the molecular mechanism by which MsANN22 mediates drought tolerance and offer a candidate gene for improving drought tolerance in alfalfa.

plant biology↗

bioRxiv2026

Widespread Recruitment of ParA-like NTPases into Prokaryotic Immunity reveals a diversity of anti-selfish element strategies

The SIMIBI subgroup within the GTPase class of P-loop NTPases, including ParA/MinD, is best known for chromosome segregation, cell division, and macromolecular localization. Its role in immunity remains largely unexplored relative to TRAFAC-subgroup GTPases and other NTPases. Using systematic sequence, structure, and comparative genomics analysis, we surveyed the ParA clade for roles in immunity. ParA underwent at least two major, independent transitions from core cellular functions to prokaryotic immunity, producing two large "conflict" branches with diverse, uncharacterized systems, plus smaller, restricted immune lineages arising sporadically outside these branches. Across 28 conflict systems, ParA couples to a wide range of partners, including nuclease, NADase, and peptidase effectors, novel sensor domains such as a variant HeH domain, and apoptosis-inducing modules reminiscent of eukaryotic programmed cell death; several systems are enriched in multicellular bacteria, and a subset was transferred to eukaryotes on multiple occasions. Newly characterized ParA partner domains, including a nucleotide cyclase, a TIM-barrel domain, START, and permuted FHA domains, further define new antiselfish-element systems independent of ParA. Together, these findings establish ParA as a recurrently coopted "fulcrum" NTPase in prokaryotic immunity, predicted to act as an interceptor of invasive nucleic acids, a multimerizing effector, and a switch regulating other immune effectors.

bioinformatics↗

bioRxiv2025

TRIO-AI: Hybrid temporal graph, ODE, and VAE modeling for high-resolution cellular trajectory inference in liver injury

Resolving dynamic cellular transitions at single-cell resolution is essential for understanding complex biological processes in development, disease, and regeneration. However, existing trajectory inference methods struggle to capture heterogeneous temporal dynamics, particularly for rare or transitional cell populations critical to injury and repair responses. Here, we present TRIO-AI, a hybrid computational framework that synergistically integrates three complementary approaches: Temporal Graph Neural Networks (Temporal GNN) for branching detection, Neural Ordinary Differential Equations (Neural ODEs) for continuous state flow modeling, and Time-Variational Autoencoders (Time-VAE) for density-based transitional state identification. We applied TRIO-AI to single-cell RNA sequencing data from mouse liver ischemia-reperfusion (IR) injury across multiple timepoints (days 0, 1, 3, and 5 post-injury), comprehensively characterizing major hepatic macrophage populations. TRIO-AI identified a distinct transitional macrophage population (MPs_3) that peaks at 48 hours post-injury and exhibits coordinated signatures for lipid handling (LRP1, LRP6, ABCA1, LDLR, SCARB1), efferocytosis (MARCO, MERTK, MSR1), and extracellular matrix engagement (ITGA9, ITGB1, SDC2). This population serves as a critical integrator of multicellular pro-reparative signals through APOE-LRP1 and FN1-ITGA9 signaling axes. Spatial transcriptomics validation confirmed MPs_3 localization to peri-necrotic borders with dramatic enrichment of APOE-LRP1 co-localization at 48 hours (19 pairs) compared to 24 hours (3 pairs). Comparative analysis against five state-of-the-art methods demonstrated TRIO-AIs superior performance in detecting transitional states, accurately reconstructing branching trajectories, and identifying off-path populations missed by conventional approaches. This framework provides a powerful platform for dissecting cellular dynamics in complex biological systems and reveals new insights into macrophage-mediated tissue repair mechanisms.

bioinformatics↗

bioRxiv2021

ANXA2 enhances virus replication through negatively regulating cGAS-STING and RLRs2 mediated signal pathway

Host nucleic acid receptors can recognize the viral DNA or RNA upon virus infection, which further triggers multiple signal pathways to promote the translocation of the interferon regulatory factor 3 (IRF3) into nucleus and produce type I interferon (IFN), leading to the host antiviral response. Here, we report a novel negative regulator Annexin A2 (ANXA2) that regulates type I IFN production through multiple mechanisms. Ectopic expression of ANXA2 inhibited the production of type I IFN induced by DNA- and RNA viruses and enhanced virus replication, while knockout of ANXA2 expression enhanced the production of type I IFN and inhibited virus replication. Mechanistically, ANXA2 not only disrupted MDA5 recruiting MAVS, but also inhibited the interaction between MAVS and TRAF3 upon RNA virus infection. In addition, ANXA2 impacted the translocation of STING from endoplasmic reticulum to Golgi apparatus upon DNA virus infection. Interestingly, ANXA2 also inhibited IRF3 phosphorylation and nuclear translocation through competing with TANK-binds kinase 1 (TBK1) and inhibitor-{kappa}B kinase {varepsilon} (IKK{varepsilon}) for binding to IRF3. Anxa2 deficiency in vivo increased the production of type I IFN, which resulted in suppression of encephalomyocarditis virus (EMCV) replication. Our findings reveal that ANXA2, as a negative regulator of type I IFN production, plays an important role in regulating the host antiviral responses. Author summaryAnnexin is a family of evolutionarily conserved multi-gene proteins, which are widely distributed in various tissues and cells of plants and animals. These proteins can reversibly bind to phospholipid membranes and to calcium ions (Ca2+). To date, several studies have confirmed that some members of the Annexin family regulate the antiviral innate immune response. Until now, regulation of the production of type I IFN by ANXA2 is not reported. In this study, ANXA2 were found to strongly inhibit the production of type I IFN, leading to increased virus replication while knockout of ANXA2 expression inhibited virus replication by increasing the amount of IFN. Compared with wild-type littermates, ANXA2 deficiency mice produced more type I IFN to inhibit virus replication. Our results provide methanistic insights into the novel role of ANXA2 in the antiviral innate immune responses.

immunology↗

bioRxiv2021

Grp78 alleviates sodium iodate-induced retinal cell injury in vivo and in vitro

ObjectiveGlucose-regulated protein 78 (Grp78) has been regarded as a main member of the endoplasmic reticulum proteins, Grp78 could protect cells from apoptosis under stress conditions. However, whether Grp78 could protect retinal pigment epithelium (RPE) cells from oxidative injury and then protect retinas from morphological changes and functional abnormalities remain undetermined. Here, we try to explore the effect of Grp78 on retinal cell injury induced by sodium iodate in vivo and in vitro. MethodsTo investigate whether Grp78 has a protective effect on RPE injury in vitro, human retinal pigment epithelium (ARPE-19) cells were treated with sodium iodate. The cell proliferation, morphology, apoptosis and ROS production assays were detected. In vivo, We established sodium iodate-induced retinal injury model in mice by intravenous injection of sodium iodate into tail vein. After that, we examined the morphology and function of retina in mice by fundus photography, OCT and ERG. Finally, we removed the retina of mice for histological examination. ResultsGrp78 significantly inhibited sodium iodate-induced reactive oxygen species (ROS), and decreased apoptosis of RPE in vitro. Furthermore, Grp78 significantly decreased the apoptosis of retinal cells in vivo, resulting in the inhibition of morphological changes of retina, and improving the function of retina. The underlying mechanisms included inhibited caspase3 and Nos, and increased expression of Bcl2, thereby protecting RPE from SI-induced ROS and apoptosis. ConclusionGrp78 could reduce the injury of retinal cells induced by sodium iodate in vitro and in vivo. These findings suggested Grp78 may become a new therapeutic target for retinal injury in clinical practice.

molecular biology↗

bioRxiv2020

Controlled-release urea combined with potassium chloride improved the soil fertility and growth of Italian ryegrass

A field experiment with a split-plot design was conducted to study the effect of nitrogen fertilizer type combined with different potassium fertilizer rates on the soil fertility and growth of Italian ryegrass. The main plots were assigned to controlled-release urea (CRU) and common urea, while low, moderate and high potassium chloride (KCl) rates (150, 300 and 450 kg ha-1, respectively) were assigned to the subplots. The results showed compared with the common urea, the CRU significantly increased the SPAD value, plant height, leaf area, and photosynthetic index. Moreover, the dry and fresh yields of the CRU increased by 10.9-25.3% and 11.8-17.7%, respectively. At the same time, compared with the KCl150 and KCl450 treatments, the KCl300 treatment resulted in better plant growth. Overall, the CRUxKCl300 maximized the soil inorganic nitrogen and different soil potassium forms. The root length, volume, surface area, average diameter, tips and branches were also improved, and there was a significant NxK interaction effect on the tips. Our analysis corroborated the CRU combined with 300 kg ha-1 KCl fertilization enhances crop growth by improving leaf photosynthesis, soil fertility, and yield and should be recommended as the best fertilizer ratio for Italian ryegrass production.

plant biology↗