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Biology subjects

ZHANG, H.

Publications and source records attributed to ZHANG, H..

11 recordsLinked to original sources

A Multi-modal LLM-Knowledge Fusion Framework for Predicting Single-cell Genetic Perturbation Effects

Understanding cellular responses to genetic perturbations is fundamental for drug discovery, yet experimental approaches face significant limitations in coverage and cost that prevent comprehensive mapping of cellular behavior. This has motivated the development of virtual cells--computational models that learn the relationship between cell state and function to predict the consequences of perturbations across diverse contexts. However, current computational methods suffer from limited accuracy in complex genetic interactions, poor biological interpretability, and inadequate generalization to unseen genes, severely constraining virtual cell capabilities. We present scPert, a multi-modal framework based on Transformer architecture that integrates large language model embeddings with structured biological knowledge to predict single-cell transcriptomic responses to genetic perturbations. Through hierarchical fusion of knowledge graph representations, contextual embeddings from foundation models, and gene-specific encodings, scPert achieves significant performance improvements in both single-gene and combinatorial perturbations over existing methods. In cancer-relevant applications, scPert demonstrates the capability to reveal p53 pathway dynamics and immune checkpoint regulatory mechanisms. Systematic evaluation on 42 cancer dependency genes demonstrates scPerts ability to identify critical potential therapeutic targets. Our framework establishes a powerful computational foundation for virtual cell construction and accelerates drug target discovery.

bioinformatics↗

Fusarium oxysporum f. sp. vasinfectum race 4 (Fov4) FNP1, a unique non-ribosomal peptide synthetase gene, plays an important role in fungal development and cotton Fusarium wilt pathogenesis

Fusarium wilt, caused by Fusarium oxysporum f. sp. vasinfectum (Fov), is one of the most destructive early-season cotton diseases worldwide. The recent emergence of the highly virulent Fov race 4 (Fov4) and its aggressiveness have raised significant concerns for the U.S. cotton industry. Unlike predominant Fov races in US cotton production, which require root-knot nematodes to cause damage, Fov4 is known to infect cotton independent of nematodes. However, molecular mechanisms of Fov4 virulence in cotton are not clearly understood. Secondary metabolites are often identified as the culprits in pathogen virulence toward plant hosts. To investigate these factors in Fov4, we analyzed the genomes of Fov1 and Fov4 using Fungal antiSMASH and identified a Fov4-specific nonribosomal peptide synthetase (NRPS) gene FNP1. To investigate its function, we generated FNP1 knock-out mutant using CRISPR-Cas9 approach. Growth assays revealed that the mutants exhibit significantly attenuated hyphal production on media containing cotton roots as the sole carbon source, increased sensitivity to cell stress agents, as well as lagged spore germination. Furthermore, the mutant exhibited defect in cotton root rot virulence and significant decrease in Fusaric acid production. Microscopic observation of GFP-labeled FNP1 deletion mutant showed impeded infection progression in cotton roots compared to the wild type (WT), which further explained the impeded virulence in FNP1 mutant. Gene complementation restored the observed defects, confirming that FNP1 is critical for Fov4 virulence, hyphal development, Fusaric acid production, and stress responses. HighlightsComparative genomic analysis between Fov1 and Fov4 identified FNP1 as a gene specific to Fov4. CRISPR/Cas9 system was employed in Fov4 to generate gene deletion mutants and GFP labeling. FNP1 plays a critical role in Fov4 hyphal development, virulence, fusaric acid production, and stress responses. This study is the first report to identify and functionally characterize a virulence gene in Fusarium oxysporum f. sp. vasinfectum (Fov) race 4 (Fov4) in cotton wilt pathogenesis.

pathology↗

Proterozoic Tectonic Drivers Underpin Flavobacterial Diversification

Flavobacteria are keystone taxa in global carbon cycling, degrading complex glycans in marine and terrestrial ecosystems. In both environments, polysaccharides constitute a major fraction of organic matter but differ in origin: marine glycans primarily derive from micro- and macroalgae, while terrestrial counterparts originate from land plants. Flavobacteria deploy distinct suites of carbohydrate-active enzymes (CAZymes) tailored to these habitat-specific substrates, yet the evolutionary drivers of their diversification remain unresolved. Two competing hypotheses exist: one posits glycan specialization as the primary driver of divergence, while the other implicates extrinsic geological factors in shaping their evolution. By integrating mitochondrial- and plastid-based molecular clocks with eukaryotic fossil calibrations, we infer that flavobacteria emerged between 2.15 and 1.98 billion years ago (Gya), shortly after the Great Oxidation Event (GOE; 2.4-2.32 Gya). Subsequent diversification involved three independent marine-to-non-marine transitions during the Proterozoic Eon (1.98-1.70 Gya, 1.72-1.40 Gya, and 1.28-1.14 Gya), temporally aligned with the formation and the fragmentation of the Columbia supercontinent and preceded the evolution of the major glycan contributors in both marine and non-marine niches. This temporal mismatch disfavors the glycan specialization hypothesis, instead implicating tectonic-driven habitat shifts as the primary driver of lineage diversification. Non-marine flavobacteria exhibited higher turnover but lower net diversification rates than marine counterparts, reflecting the challenges of adapting to fragmented non-marine niches. Genome erosion and deleterious mutation accumulation further constrained reverse transitions, locking lineages into non-marine habitats. Our findings highlight Proterozoic tectonics, rather than substrate-specific CAZyme innovation, as the catalyst for flavobacterias evolutionary success across Earths carbon-rich biomes.

evolutionary biology↗

Suppression of piriform cortex alters brain-wide dynamics and alleviates seizures in temporal lobe epilepsy

BackgroundTemporal lobe epilepsy (TLE) involves aberrant changes in the brain at molecular, cellular and circuitry levels, leading to recurrent seizures. Approximately one-third of patients develop drug resistance. Circuit-based interventions show promise for alleviating the drug-resistant seizures. This study explored the efficacy of chemogenetic stimulation on specific neuronal populations in piriform cortical microcircuits in a mouse TLE model. ObjectiveThe anterior piriform cortex (APC) is a limbic area closely associated with TLE but is understudied. Our previous study demonstrated that in the APC, parvalbumin-expressing (PV+) interneurons provide strong inhibition and help maintain excitation-inhibition balance. Here, we examined whether and how APCPV neurons can ameliorate seizure symptoms in TLE. MethodsWe used a chronic intrahippocampal kainic acid (IHKA) mouse model that develops hippocampal pathology and spontaneous recurrent seizures (SRSs). APCPV neurons were chemogenetically activated, and local field potentials were recorded longitudinally from multiple regions. Seizure metrics, spectral power and functional connectivity were compared between APCPV-activated and control samples. ResultsLoss of PV+ synapses emerged in the APC during epileptogenesis. Selective activation of APCPV neurons reduced the frequency and duration of hippocampal SRSs and modified long-range dynamics, with region- and frequency-specific changes in interictal band power and functional connectivity. ConclusionAPCPV chemogenetic activation exerts a robust anti-seizure effect and identifies the APC as a promising cortical node for seizure network control. The associated spectral and connectivity signatures suggest that targeted modulation of APC microcircuits can rebalance distributed seizure networks and lower seizure recurrence.

neuroscience↗

Post-translational regulation of Platelet-derived growth factor receptor β is critical for fracture repair in aged mice

Increased protein ubiquitination was observed in fracture callus and particularly in aged mice. Treatment of proteasome inhibitor enhanced fracture repair in young and mice by increasing the number of mesenchymal progenitor cells (MPCs). However, the protein targets of proteasome inhibitor are still not known. Ub-proteomics identifies the top ub-proteins in MPCs and osteoblasts. Among them, PDGFR{beta} plays important roles both in osteogenesis and angiogenesis, which were reduced in callus of aged mice. We examine the dramatic decrease of PDGFR{beta} protein level, increased Ub-PDGFR{beta}, but mild decrease of mRNA in callus of aged mice, suggesting dys-regulated protein modification is the major cause of decreased PDGFR{beta} level. Decreased PDGFR{beta} results in the failure of PDGF-BB enhanced MPCs proliferation and fracture repair in aged mice. Co-treatment with proteasome inhibitor rescues the ability of PDGF-BB on MPC proliferation and fracture repair. Our findings not only discover the protein target of proteasome inhibitor in MPCs, but importantly connect the compromised effect of PDGF treatment on diseases with PDGFR{beta} proteasomal degradation. We open a new avenue for the treatment of fracture repair in elderly with the combination of PDGF-BB and proteasome inhibitor.

cell biology↗

Senescent cells impair fracture repair through elevating ubiquitin-proteasome system activity in aged mice.

Senescent cells accumulate in multiple tissues with aging. Depletion of senescent cells benefits the aging related disease, such as aging bone fracture. However, the molecular mechanisms by which senescent cells regulate their neighboring bone cells are still not well-known. We reported that proteasome inhibitor enhanced fracture repair in aged mice. Senescent cells are major source of chronic inflammatory cytokines, which in turn induced protein ubiquitination. We reported that PDGFR{beta} was one of the highly ubiquitinated proteins in mesenchymal progenitors (MPCs) and TGF{beta} was the most increased SASP. In the current study, we found TGF{beta} induced PDGFR{beta} ubiquitination and proteasomal degradation through its E3 ligases. TGF{beta} neutralizing antibody blocked the inhibited callus derived MPC growth and increased Ub-PDGFR{beta} by senescent cells, which could be further prevented PDGFR{beta} inhibitor. These findings suggested senescent cells derived TGF{beta} impaired fracture repair in aged mice through elevating ubiquitination of PDGFR{beta}. The discovery of TGF{beta}-PDGFR{beta} pathway triggered by senescent cells opens avenues for optimizing treatment strategies for aging related disease by combination with the ligand of PDGFR{beta}.

cell biology↗

Rapid Directed Molecular Evolution of Fluorescent Proteins in Mammalian Cells

In vivo imaging of model organisms is heavily reliant on fluorescent proteins with high intracellular brightness. Here we describe a practical method for rapid optimization of fluorescent proteins via directed molecular evolution in cultured mammalian cells. Using this method, we were able to perform screening of large gene libraries containing up to 2{middle dot}107 independent random genes of fluorescent proteins expressed in HEK cells completing one iteration directed evolution in a course of [~]8 days. We employed this approach to develop a set of green and near-infrared fluorescent proteins with enhanced intracellular brightness. The developed near-infrared fluorescent proteins demonstrated high performance for fluorescent labeling of neurons in culture and in vivo in model organisms such as C.elegans, Drosophila, zebrafish, and mice. Spectral properties of the optimized near-infrared fluorescent proteins enabled crosstalk-free multicolor imaging in combination with common green and red fluorescent proteins, as well as dual-color near-infrared fluorescence imaging. The described method has a great potential to be adopted by protein engineers due to its simplicity and practicality. We also believe that the new enhanced fluorescent proteins will find wide application for in vivo multicolor imaging of small model organisms.

molecular biology↗

Snowball Earths, population bottlenecks, and the evolution of marine photosynthetic bacteria

Prochlorococcus are the most abundant photosynthetic organisms in the modern ocean. A massive DNA loss event occurred in their early evolutionary history, leading to highly reduced genomes in nearly all lineages, as well as enhanced efficiency in both nutrient uptake and light absorption. The environmental landscape that shaped this ancient genome reduction, however, remained unknown. Through careful molecular clock analyses, we established that this Prochlorococcus genome reduction occurred during the Neoproterozoic Snowball Earth climate catastrophe. The lethally low temperature and exceedingly dim light during the Snowball Earth event would have inhibited Prochlorococcus growth and proliferation and caused severe population bottlenecks. These bottlenecks are recorded as an excess of deleterious mutations that accumulated across genomic regions in the descendant lineages. Prochlorococcus adaptation to extreme environmental conditions during Snowball Earth intervals can be inferred by tracing the evolutionary paths of genes that encode key metabolic potential. This metabolic potential includes modified lipopolysaccharide structure, strengthened peptidoglycan biosynthesis, the replacement of a sophisticated circadian clock with an hourglass-like mechanism that resets daily for dim light adaption, and the adoption of ammonia diffusion as an efficient membrane transporter-independent mode of nitrogen acquisition. In this way, the Neoproterozoic Snowball Earth event altered the physiological characters of Prochlorococcus, shaping their ecologically vital role as the most abundant primary producers in the modern oceans.

microbiology↗

Simultaneously monitoring aquatic and terrestrial biodiversity using riverine water eDNA: seasonal variation of monitoring effectiveness

Environmental DNA (eDNA) metabarcoding for biodiversity monitoring is a critical technical advance. Both aquatic and terrestrial biodiversity information can be detected in riverine water eDNA. However, it remains unverified whether riverine water eDNA can be used to simultaneously monitor aquatic and terrestrial biodiversity. Our specific objective was to assess the effectiveness of monitoring aquatic and riparian biodiversity using riverine water eDNA. We proposed that the monitoring effectiveness (the proportion of aquatic and terrestrial biodiversity information detected by riverine water eDNA samples) could be approximated by the transportation effectiveness of land-to-river and upstream-to-downstream biodiversity information flow. We conducted a case study in a watershed on the Qinghai-Tibet Plateau and estimated the effectiveness of using riverine water eDNA to monitor aquatic and riparian biodiversity based on comparing the operational taxonomic units (OTUs) and species assemblages of three taxonomic communities detected in riverine water eDNA samples and riparian soil eDNA samples in spring, summer, and autumn. The aquatic and riparian biodiversity of a watershed on the Qinghai-Tibet Plateau could be simultaneously effectively monitored using riverine water eDNA on summer or autumn rainy days. Monitoring bacterial communities was more efficient than monitoring eukaryotic communities. On summer rainy days, 43%-76% of riparian species could be detected in water eDNA samples, 92%-99% of upstream species could be detected in a 1-km downstream eDNA sample, and more than 50% of dead bioinformation (i.e., the bioinformation labeling the biological material without life activity and fertility) could be monitored 4-6 km downstream for eukaryotes and 13-19 km for bacteria. We encourage more studies on the monitoring effectiveness for each taxonomic community in other watersheds with different environmental conditions. We believe that in future ecological research, conservation and management, we could efficiently monitor and assess the aquatic and terrestrial biodiversity by simply using riverine water eDNA samples.

ecology↗

Introducing undergraduate students to reverse genetics in the laboratory: a case study of a project-oriented learning (POL) system in Taishan Medical University, China

Biochemistry and molecular biology have become increasingly reliant on experimental experience, because they are difficult subjects to understand from a theoretical approach. The Innovation and Entrepreneurship Training Program was established by the China Ministry of Education to foster the scientific interests and experiences of undergraduate students. Here, we reported on an innovative project-oriented learning (POL) system directed by Taishan Medical University (Named Shandong First Medical University & Shandong Academy of Sciences since February 2019) China, which fused innovative project with biochemical course concepts. This study takes reverse genetics, which is considered to be difficult to understand through course-only learning, as an example. To help undergraduate students understand the principle of reverse genetics, the project involved producing hepatitis C virus in vitro. Furthermore, to give them a comprehensive scientific experience based on their knowledge from textbook, extensive mentorship was provided through the project, including theoretical guidance and technical support for experiments. Assessment showed a comprehensive improvement after participating in these programs. In conclusion, this POL system was a good model that enabled undergraduates to learn more during courses. It also provided a chance to experience hands-on sciences, which might motivate them to pursue a career in science.View Full Text

scientific communication and education↗

Different obesity phenotypes correlated with the PI3K-AKT signaling pathway in tree shrews

ObjectiveTo identify the meaningful co-expressed gene network in mRNA extracted from adipose tissue representing different obesity phenotypes in a new tree shrew model. Furthermore, to locate the potential drug target based on analyzing the possible pathways and hub genes responsible for obesity.\n\nMethodsTen tree shrews were selected from F1 populations and divided into 3 groups based on their Lees index for mRNA sequencing. We identified clusters of highly correlated genes (modules) by weighted gene co-expression network analysis (WGCNA).\n\nResultsThree modules were strongly correlated with not less than one obesity phenotype (associations ranging from -0.94 to 0.85, P < 0.01). The ribosome, lysosome and ubiquitin-mediated proteolysis pathways were the most enriched pathways of the blue (including 481 genes), brown (389 genes) and turquoise (1781 genes) modules, respectively. The hub genes were determined, including UBA52 in the blue module, AKT1 in the brown module and LRRK2 in the turquoise module.\n\nConclusionsWe characterized different obesity phenotypes in tree shrews for the first time. The most represented gene AKT1 indicated the vital role of the PI3K-AKT pathway through interactions with downstream pathways and differentially expressed genes (DEGs). The work will help provide new insight into the prevention and treatment strategies of obesity.

genetics↗