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Wang, J.

Publications and source records attributed to Wang, J..

At least 829 records · Page 46Linked to original sources

Dissecting dynamic gene regulatory network using transformer-based temporal causality analysis

The AI Virtual Cell (AIVC) framework promises to revolutionize biological research through high-fidelity simulations of cellular behaviors and responses to perturbations. Central to realizing this vision is the ability to model cell differentiation dynamics, which requires accurate inference of gene regulatory network (GRN) that govern cell fate decisions. However, existing computational approaches rely on static GRN models that fail to capture the dynamic changes of regulatory relationships during differentiation, limiting their utility for simulating developmental processes and predicting perturbation outcomes. Here, we present CellProphet, an interpretable AI model that infers dynamic GRN by integrating temporal causality with transformer self-attention mechanism. CellProphet captures time-lagged dependencies between transcription factor (TF) expression and target gene activation while providing interpretable regulatory weights, enabling both accurate prediction and mechanistic insight. When benchmarked against nine state-of-the-art methods across seven differentiation datasets, CellProphet achieves superior performance in all evaluation metrics. Applied to mouse embryonic stem cell differentiation, CellProphet identifies both well-known and potentially novel TFs with substantially high sensitivity and successfully reconstructs dynamic regulatory relations validated through multi-modal epigenomic data. In mouse hematopoietic differentiation, CellProphet accurately predicts cell fate transitions and gene expression changes following in silico perturbation of key TFs Gata1 and Spi1, demonstrating its capability for virtual experimentation. These results establish CellProphet as a foundational tool for the AIVC framework, enabling researchers to decode the dynamic regulatory logic of differentiation, accelerate discovery of key regulatory factors, and design targeted cellular interventions for widespread applications.

bioinformatics↗

Targeting FGFR4 Abrogates HNF1A-driven Metastasis in Pancreatic Ductal Adenocarcinoma

PurposeWe previously identified an oncogenic role for the transcription factor HNF1A in pancreatic ductal adenocarcinoma (PDAC). However, the role of HNF1A in the metastatic progression of PDAC remains unknown and targeting modalities for HNF1A -dependent phenotypes have yet to be identified. Experimental DesignTranswell chambers were used to assess the effects of HNF1A and FGFR4 modulation on the migration and invasion of ATCC and patient-derived PDAC cells in vitro. An intrasplenic injection xenograft model was used to evaluate the impact of HNF1A knockdown and overexpression on metastatic tumor burden. Single-cell RNA sequencing, tissue microarray (TMA) data, and UMAP spatial profiling were used to identify FGFR4 as an HNF1A target gene upregulated in metastatic cells. RNAi and two FGFR4 inhibiting modalities (H3B-6527 and U3- 1784) were utilized to demonstrate the efficacy of FGFR4 inhibiting agents at reducing HNF1A- driven metastasis. ResultsKnockdown of HNF1A significantly decreases and HNF1A overexpression significantly increases PDAC cell migration and invasion. In vivo studies show that HNF1A knockdown significantly abrogates metastasis, while overexpression significantly promotes metastasis. Single-cell RNAseq shows that FGFR4 is upregulated in metastatic PDAC cells and staining for HNF1A and FGFR4 in a PDAC TMA reveals significant correlation between HNF1A and FGFR4 in PDAC patients. Further, knockdown and inhibition of FGFR4 significantly decreases HNF1A- mediated cell migration and invasion, and blocks HNF1A-driven metastasis in vivo. ConclusionsThese findings demonstrate that HNF1A drives PDAC metastasis via upregulation of FGFR4, and FGFR4 inhibition is a potential mechanism to target metastasis in PDAC patients. Translational RelevancePancreatic ductal adenocarcinoma (PDAC) is one of the most lethal malignancies, made even more devastating when metastases overwhelm major organs. The vast majority of PDAC patients either present with metastases or will relapse with recurrent metastatic PDAC after primary tumor resection. Unfortunately, toxic and largely ineffective chemotherapies are currently the only approved treatment options for these patients and therefore there exists a critical and unmet clinical need for targeted therapies against pro-metastatic pathways in PDAC. In the current study, we identify HNF1A as an oncogenic transcription factor that drives metastasis in PDAC, and it does so through upregulation of the receptor tyrosine kinase FGFR4. Importantly, FGFR4 is a targetable vulnerability and treatment with an FGFR4 blocking antibody reduces HNF1A-driven metastasis. These findings suggest that FGFR4 inhibitors could be an efficacious treatment for PDAC patients for the prevention or delay of metastatic tumor development.

cancer biology↗

Spatial transcriptomics reveals heterogeneous cell-cell interactions among brain regions in a cuprizone model consistent with multiple sclerosis lesions

The cuprizone (CPZ) model is widely used for modeling demyelination in multiple sclerosis (MS) and for testing potential remyelination therapies. We integrated single-cell and spatial transcriptomics (ST) to fine map the spatial cellular and molecular responses during de and remyelination. ST revealed global demyelination and neuroinflammation in the brain beyond the corpus callosum, with region-specific differences. We identified oligodendroglia and microglia as two major cell types with significant transcriptomic changes in the model. Ligand receptor pairing analyses predicted growth factor and phagocytic pathway enrichment during demyelination, which is consistent with changes in MS lesions. During remyelination, while mature oligodendrocytes nearly reversed their phenotype back to the control state, microglia remained associated with the demyelination phenotype. Finally, astrocytes in the CPZ model had the greatest preservation of disease-associated modules to MS lesions, while the MOL, OPC, and microglia showed moderate to low preservation, which overall suggested that the CPZ model had moderate translatability to chronically active MS lesions.

neuroscience↗

scBSP: A fast and accurate tool for identifying spatially variable features from high-resolution spatial omics data

Emerging spatial omics technologies empower comprehensive exploration of biological systems from multi-omics perspectives in their native tissue location in two and three- dimensional space. However, sparse sequencing capacity and growing spatial resolution in spatial omics present significant computational challenges in identifying biologically meaningful molecules that exhibit variable spatial distributions across different omics. We introduce scBSP, an open-source, versatile, and user-friendly package for identifying spatially variable features in high-resolution spatial omics data. scBSP leverages sparse matrix operation to significantly increase computational efficiency in both computational time and memory usage. In diverse spatial sequencing data and simulations, scBSP consistently and rapidly identifies spatially variable genes and spatially variable peaks across various sequencing techniques and spatial resolutions, handling two- and three-dimensional data with up to millions of cells. It can process high-definition spatial transcriptomics data for 19,950 genes across 181,367 spots within 10 seconds on a typical desktop computer, making it the fastest tool available for handling such high-resolution, sparse spatial omics data while maintaining high accuracy. In a case study of kidney disease using 10x Xenium data, scBSP identified spatially variable genes representative of critical pathological mechanisms associated with histology.

bioinformatics↗

Leopard Cats Occupied Human Settlements in China for 3,500 years before the Arrival of Domestic cats in 600-900 CE around the Tang Dynasty

The earliest cats in human settlements in China were not domestic cats (Felis catus), but native leopard cats (Prionailurus bengalensis). To trace when and how domestic cats arrived in East Asia, we analyzed 22 feline bones from 14 sites across China spanning 5,000 years. Nuclear and mitochondrial genomes revealed that leopard cats began occupying anthropogenic scenes around 5,400 years ago and last appeared in 150 CE. Following several centuries gap of archeological feline remains, the first known domestic cat (706-883 CE) in China was identified in Shaanxi during the Tang Dynasty. Genomic analysis suggested a white or partially white coat and a link to a contemporaneous domestic cat from Kazakhstan, indicating a likely dispersal route via the Silk Road. The two felids once independently occupied ancient anthropogenic environments in China but followed divergent paths and reached different destinations in human-animal interactions.

evolutionary biology↗

How Does Sampling Affect the AI Prediction Accuracy of Peptides' Physicochemical Properties?

Accurate AI prediction of peptide physicochemical properties is essential for advancing peptide-based biomedicine, biotechnology, and bioengineering. However, the performance of predictive AI models is significantly affected by the representativeness of the training data, which depends on the sample size and sampling methods employed. This study addresses the challenge of determining the optimal sample size and sampling methods to enhance the predictive accuracy and generalization capacity of AI models for estimating the aggregation propensity, hydrophilicity, and isoelectric point of tetrapeptides. Four sampling methods were evaluated: Latin Hypercube Sampling (LHS), Uniform Design Sampling (UDS), Simple Random Sampling (SRS), and Probability-Proportional-to-Size Sampling (PPS), across sample sizes ranging from 100 to 20,000. A sample size of approximately 12,000 (7.5% of the total tetrapeptide dataset) marks a key threshold for stable and consistent model performance. This study provides valuable insights into the interplay between sample size, sampling strategies, and model performance, offering a foundational framework for optimizing data collection and AI model training for the prediction of peptides physicochemical properties, especially for prediction in the complete sequence space of longer peptides with more than four amino acids.

bioinformatics↗

Ku suppresses RNA-mediated innate immune responses in human cells to accommodate primate-specific Alu expansion.

Ku70 and Ku80 form Ku, a ring-shaped protein that initiates the non-homologous end-joining (NHEJ) DNA repair pathway.1 Specifically, Ku binds to double-stranded DNA (dsDNA) ends and recruits other NHEJ factors (e.g., DNA-PKcs and LIG4). While Ku binds to double-stranded RNA (dsRNA)2 and traps mutated-DNA-PKcs on ribosomal RNA in vivo,3,4 the physiological significance of Ku-dsRNA interactions in otherwise wild-type cells remains elusive. Intriguingly, while dispensable for murine development,5,6 Ku is essential in human cells.7 Despite similar genome sizes, human cells express [~]100-fold more Ku than mouse cells, implying functions beyond NHEJ, possibly through a dose-sensitive interaction with dsRNA, which is [~]100 times weaker than with dsDNA.2,8 While investigating the essentiality of Ku in human cells, we found that depletion of Ku - unlike LIG4 - induces profound interferon (IFN) and NF-kB responses reliant on the dsRNA-sensor MDA5/RIG-I and adaptor MAVS. Prolonged Ku-degradation also activates other dsRNA-sensors, e.g. PKR that suppresses protein translation, and OAS/RNaseL that cleaves rRNAs and eventually induces growth arrest and cell death. MAVS, RIG-I, or MDA5 knockouts suppressed IFN signaling and, together with PKR knockouts, partially rescued Ku-depleted human cells. Ku-irCLIP analyses revealed that Ku binds to diverse dsRNA, predominantly stem-loops in primate-specific Alu elements9 at anti-sense orientation in introns and 3-UTRs. Ku expression rose sharply in higher primates tightly correlating with Alu-expansion (r = 0.94/0.95). Together, our study identified a vital role of Ku in accommodating Alu-expansion in primates by mitigating a dsRNA-induced innate immune response, explaining the rise of Ku levels and its essentiality in human cells.

genetics↗

Nipah virus matrix protein utilizes cortical actin to stabilize the virus assembly sites and promote budding

Several families of enveloped viruses assemble and bud from the host cell plasma membranes (PM), including paramyxoviruses. Nipah virus (NiV) is a deadly zoonotic paramyxovirus causing yearly outbreaks in Southeast Asia with >75% mortality. NiV encodes matrix proteins (M) that drive assembly and budding. NiV-M forms dimers and interacts with membrane lipids in the host cells PM for budding. Using single-molecule localization microscopy and single-particle tracking, we show that the host F-actin maintains the nanoscale organization of NiV assembly sites at the PM. This F-actin-dependent integrity of NiV assembly sites is observed at the membrane retention stage after the assembly process is complete, rather than during the recruitment of NiV-M molecules to these sites. NiV-M interacts with actin via its C-terminal domain. We also show that the actin-branching factor, Arp2/3 complex, promotes virus-like-particle production. Meanwhile, inhibiting Arp2/3 disfavors the PM retention of NiV assembly sites and NiV-M-mediated generation of membrane protrusions, but does not affect the assembly rate. This suggests that Arp2/3-nucleated actin polymerization and branching are critical for maintaining NiV-M assembly sites at the PM, allowing it to facilitate membrane protrusion generation for virus budding. Our findings support the following model: NiV-M interacts with F-actin through its C-terminus to remain at the host PM after assembly completion. This F-actin-dependent retention is promoted by the Arp2/3-driven actin branching and polymerization, which also drives the formation of NiV-M-induced membrane protrusions necessary for virus budding. SignificanceNipah virus (NiV) is a deadly paramyxovirus capable of animal-animal and animal-human transmissions. To produce a NiV particle, the NiV matrix protein (M) must create an assembly site by binding to the surface of an infected cell and pushing the cell membrane outward for virus budding. To do so, the NiV matrix protein must co-opt or overcome an actin network underneath the cell membrane. We provide single-molecule evidence that M interacts with the actin cytoskeleton for membrane retention but not recruitment of M to existing assembly sites. This process is promoted by the Arp2/3-driven actin branching and polymerization. Our findings suggest the role of actin remodeling in NiV budding and identify a druggable site at the C-terminus of NiV-M.

microbiology↗

Estimating the effect of tissue- and blood-derived cell reference matrices on deconvolving bulk transcriptomic datasets

BackgroundCell deconvolution is a method used to characterize the composition of the mixed cell population in bulk transcriptomic datasets. Tissue- and blood-derived cell reference matrices (CRMs) are typically used, but their impact on deconvolution has yet to be evaluated. MethodsRecursive feature elimination and random forest methods were applied to build tissue- and blood-derived CRMs using single-cell RNA sequencing (scRNA-seq) datasets of inflammatory bowel disease (IBD) which comprises two subtypes (Crohns disease (CD) and ulcerative colitis (UC)). Combining with three published blood-derived CRMs (IRIS, LM22, and ImmunoStates), public bulk transcriptomes datasets and simulated datasets generated from scRNA-Seq were used to evaluate the deconvolution performance by goodness-of-fit and cell fractions correlation. Additionally, two infliximab-treated bulk datasets were used to compare the treatment-related cell types revealed by tissue- and blood-derived CRMs. Lung adenocarcinoma (LUAD) single-cell and TCGA bulk transcriptomic datasets were also used for evaluation. ResultsFor CD and UC tissue bulk datasets, tissue-derived CRMs showed better deconvolution goodness-of-fit scores compared to blood-derived CRMs. Meanwhile, tissue-derived CRMs represented more accurate cellular proportion estimates for most cell types, such as immune and stromal cells in tissue pseudobulk datasets. They also revealed more treatment-related cell types. Additionally, CRMs derived from the scRNA-seq datasets from CD and UC colon samples had similar performance. In contrast, CRMs derived from CD ileum scRNA-seq dataset had better performance in the ileum bulk datasets. All CRMs yielded consistent deconvolution performance when deconvolving blood bulk transcriptomics. The similar results have also been shown using LUAD datasets. ConclusionsOur results emphasize the importance of selecting appropriate CRMs for cell deconvolution, particularly in bulk tissue transcriptomes in immunology and oncology. Such considerations can be extended to encompass other disease implications. AbbVie Disclosure statementAll authors are current employees of AbbVie. The design, study conduct, and financial support for this research were provided by AbbVie. AbbVie participated in the interpretation of data, review, and approval of the publication. Key PointsO_LITissue-derived CRMs showed higher goodness-of-fit compared to blood-derived CRMs for deconvolving bulk tissue transcriptomics. C_LIO_LIAll CRMs yield consistent goodness-of-fit for deconvolving bulk blood transcriptomics. C_LIO_LITissue-derived CRMs represent more accurate cellular proportion estimates and reveal more treatment-related cell types, and the specific tissue type is relevant to the deconvolution performance. C_LI

bioinformatics↗

YTHDF3 promotes the progression of gastric cancer by activating Wnt/β-catenin signaling pathway via targeting NEK7

Gastric cancer (GC) is a widespread and deadly malignancy among global digestive tract tumors, alarmingly ranked the fifth most common cancer in terms of incidence and mortality. This study used immunohistochemistry and RT-qPCR to reveal a significant upregulation of YTHDF3 expression in GC tissues compared with that of adjacent normal tissues. This increased expression of YTHDF3 was closely associated with the incidence of lymph node metastasis and the progression to more advanced TNM stages. In vitro experiments demonstrated that YTHDF3 was crucial in promoting the aggressive characteristics of GC cells by enhancing their ability to proliferate, migrate, and invade, while simultaneously inhibiting apoptosis. The role of YTHDF3 in the progression of GC was further confirmed using the BALB/c nude mice subcutaneous tumor model, which showed a slowed tumor growth after YTHDF3 knockdown. This study further confirmed through Co-IF RIP-qPCR, western blotting, and rescue studies that YTHDF3 promotes GC progression by targeting NEK7 to regulate the Wnt/{beta}-catenin signaling pathway. In conclusion, our pivotal findings highlight the YTHDF3/NEK7/Wnt/{beta}-catenin axis as a promising and accessible therapeutic target for the development of new treatments aimed at improving clinical outcome of patients with GC.

cancer biology↗

Single-Cell Genomics Elucidates Molecular Variations and Regulatory Mechanisms in Circulating Immune Cells

The human peripheral blood displays diverse molecular characteristics across populations, understanding the drivers and underlying mechanisms of which remains challenging. Here, we introduce the Chinese Immune Multi-Omics Atlas (CIMA), elucidating sex-, age-, and genetic-related molecular variations by analyzing multi-omics data from 428 adults with over 10 million immune cells. CIMA generated an enhancer-driven gene regulatory network, identifying 237 high-quality regulons and revealing cell type-specific regulatory mechanisms. Additionally, 11,521 lead cis-expression quantitative trait loci (eQTLs) and 46,339 chromatin accessibility QTLs (caQTLs) were identified at cell type level. CIMA also uncovered pleiotropic associations among immune-related disease risk loci, eQTLs, and caQTLs in a cell type-specific manner. Lastly, a novel cell language model, CIMA-CLM, was developed to predict chromatin accessibility and noncoding variant effects using chromatin sequences and gene expressions. This work represents a population-scale multi-omics resource of human immune cells, providing a valuable reference for future investigation of immune-related diseases.

immunology↗

Avoidance of fratricide and improved efficacy of CD33-MSLN CAR-iNK cells in treating acute myeloid leukemia

Acute myeloid leukemia (AML) patients are often older, which brings challenges of endurance and persistent efficacy of autologous CAR-T cell therapies. Allogenic CAR-NK cell therapies may offer reduced toxicities and enhanced anti-leukemic potential against AML. In this study, we designed a novel CD33-mesothelin loop CAR (Loop CAR) and evaluated its anti-tumor efficacy in human umbilical cord blood-derived NK (UCB-NK) cells and human pluripotent stem cell-derived NK (hPSC-iNK) cells. The Loop CAR exhibited superior cytotoxicity against dual-antigen-positive tumor cell lines and primary AML cells. To further avoid fratricide caused by endogenous CD33 expression in NK cells, we established a hPSC-derived cell line via knockout of CD33 gene (CD33KO) and engineered Loop CAR. Rather than enforced expression of exogenous CD16, we generated abundant mature CD33KO-Loop CAR-iNK cells highly expressing endogenous CD16 via an organoid induction approach. This innovative strategy effectively mitigated NK cell fratricide and significantly enhanced CD33 and mesothelin-mediated specific cytotoxicity. Moreover, the CD33KO-Loop CAR-iNK cells demonstrated superior tumor-killing activity in AML xenograft mice and significantly prolonged survival. hPSC-derived CD33KO-Loop CAR-iNK cells possess unique advantages and translational potential for treating AML.

cancer biology↗

Engineered CRO-CD7 CAR-NK cells derived from pluripotent stem cells avoid fratricide and efficiently suppress human T-cell malignancies

BackgroundT cell malignancies are highly aggressive hematological tumors with limited effective treatment options. CAR-NK cell therapy targeting CD7 has emerged as a promising approach for treating T-cell malignancies. However, conventional CAR-NK cell therapy faces the challenges of cell fratricide due to CD7 expression on both malignant cells and normal NK cells. Additionally, engineering CARs into human tissue-derived NK cells demonstrates heterogeneity, low transduction efficiency, and high manufacturing costs. MethodsThe human pluripotent stem cells (hPSCs) were genetically modified by knocking out the CD7 gene and introducing the CD7 CAR expression cassette to generate CD7 KO-CD7 CAR-hPSCs. These modified hPSCs were subsequently differentiated into CD7 KO-CD7 CAR-iNK cells using an efficient organoid induction method. The cytotoxicity of CD7 KO-CD7 CAR-iNK cells against CD7+ tumor cells was evaluated. Furthermore, we overexpressed the CXCR4 gene in CD7 KO-CD7 CAR-hPSCs and derived CXCR4-expressing CD7 KO-CD7 CAR-iNK (CRO-CD7 CAR-iNK) cells. The dynamics of CRO-CD7 CAR-iNK cells in vivo were tracked, and their therapeutic efficacy was assessed using human T-cell acute lymphoblastic leukemia (T-ALL) xenograft models. ResultsThe CD7 KO-CD7 CAR-iNK cells derived from CD7 KO-CD7 CAR-hPSCs effectively avoided fratricide, demonstrated normal expansion, and exhibited potent and specific anti-tumor activity against CD7+ T-cell tumor cell lines and primary T-ALL cells. CXCR4 overexpression in CRO-CD7 CAR-iNK cells improved their homing capacity and extended their persistence in vivo. The CRO-CD7 CAR iNK cells significantly suppressed tumor growth and prolonged the survival of T-ALL tumor-bearing mice. ConclusionsOur study provides a reliable strategy for the large-scale generation of fratricide-resistant CD7 CAR-iNK cells with robust anti-tumor effects from hPSCs, offering a promising cell product to treat T-cell malignancy.

cancer biology↗

Impact of cross-validation designs on cattle behavior prediction using machine learning and deep learning models with tri-axial accelerometer data

1Assessing cattle behaviors provides insights into animal health, welfare, and productivity to support on-farm management decisions. Wearable accelerometers offer an alternative approach to traditional human evaluation, providing a more objective and efficient method for predicting cattle behavior. Random cross-validation (CV) is commonly used to evaluate behavior prediction by splitting data into training and testing sets, but it can yield inflated results when records from the same animal are included in both sets. Block CV splits data by block effects, offering a more realistic evaluation but remains underexplored for predicting multi-class imbalanced cattle behavior. Additionally, deep learning (DL) models have not been fully explored for behavior prediction compared to machine learning (ML) models. The objectives of this study were to examine the impact of CV designs on multi-class imbalanced cattle behavior prediction and to compare the performance of ML and DL models. Three ML and two DL models were used to predict the four behaviors of six beef cows from a public tri-axial accelerometer dataset, with model performance evaluated using both hold-out and leave-cow-out CV designs representing random and block CV, respectively. In hold-out CV, ML models achieved accuracies of 0.94 to 0.96 and F1 scores of 0.93 to 0.95, while DL models achieved accuracies of 0.9 to 0.92 and F1 scores of 0.89 to 0.91. In the leave-cow-out CV, ML models obtained accuracies of 0.72 to 0.82 and F1 scores of 0.64 to 0.82, whereas DL models obtained accuracies of 0.76 to 0.82 and F1 scores of 0.64 to 0.76. Generally, ML models outperformed DL models in the hold-out CV, but the multi-layer perceptron DL model demonstrated comparable or superior performance in the leave-cow-out CV. All models performed better with hold-out CV than leave-cow-out CV. Our results suggest that CV designs can affect behavior prediction performance. While a random CV produces seemingly good predictions, these results can be artificially inflated by the data partition. A block CV that strategically partitions data could be a more appropriate design.

animal behavior and cognition↗

SpatialFormer: Universal Spatial Representation Learning from Subcellular Molecular to Multicellular Landscapes

Spatial transcriptomics quantifies gene expression within its spatial context, significantly advancing biomedical research. Understanding gene spatial expression and the organization of multicellular systems is vital for disease diagnosis and studying biological processes. However, existing models often struggle to integrate gene expression data with cellular spatial information effectively. In this study, we introduce SpatialFormer, a hybrid framework combining convolutional networks and transformers to learn single-cell multimodal and multi-scale information in the niche context, including expression data and subcellular gene spatial distribution. Pre-trained on 300 million cell pairs from 12 million spatially resolved single cells across 62 Xenium slides, SpatialFormer merges gene spatial expression profiles with cell niche information via the pair-wise training strategy. Our findings demonstrate that SpatialFormer distills biological signals across various tasks, including single-cell batch correction, cell-type annotation, co-localization detection, and identifying gene pairs that are critical for the immune cell-cell interactions involved in the regulation of lung fibrosis. These advancements enhance our understanding of cellular dynamics and offer new pathways for applications in biomedical research.

bioinformatics↗

Harnessing landscape genomics to evaluate genomic vulnerability and future climate resilience in an East Asia perennial

In this era of rapid climate change, understanding the adaptive potential of organisms is imperative for buffering biodiversity loss. Genomic forecasting provides invaluable insights into population vulnerability and adaptive potential under diverse climatic conditions, thereby facilitating management interventions, bolstering population resilience, and shaping germplasm conservation strategies tailored to specific species. Here we integrated population genomics and landscape genomics approaches, leveraging single-nucleotide polymorphisms obtained through whole-genome resequencing of 43 Rheum palmatum complex populations, to pinpoint adaptive variation and its significance in the context of future climates, delineate seed zones, and establish guidelines for ex situ germplasm conservation to capture the majority of existing adaptive diversity. Our analysis unveiled that the species complex comprised two distinct genetic clusters, exhibiting differential climate adaptation and genomic vulnerabilities across its distribution range. We also determined that the species range could be subdivided into three distinct seed zones, with varying sample requirements per seed zone corresponding to differed conservation efforts. Overall, our findings provide a genome-wide perspective on climate adaptation and valuable insights into germplasm conservation strategies aimed at enhancing population resilience in future climates, serving as a blueprint for restoration plans of other vulnerable species.

evolutionary biology↗

Perinatal circadian desynchronization disrupts sleep and prefrontal cortex function in adult offspring

Sleep and circadian (daily) rhythms impact nearly all aspects of physiology and are critical for optimal organismal function. Disruption of the clock can lead to significant metabolic disorders, neuropsychiatric illness, and cognitive dysfunction. Our lab has previously shown that environmental circadian desynchronization (ECD) in adults alters the anatomical structure and neurophysiological function of prefrontal cortex (PFC) neurons, PFC mediated behaviors, as well as sleep quality. As the PFC undergoes significant development in utero and early life, and maternal disturbances during this period can have significant long-term ramifications, we hypothesized that disrupting the circadian environment of dams during the perinatal period would alter sleep and PFC function in adult offspring. Using a mouse model of ECD we investigated how perinatal ECD (pECD) modulates sleep quality in adult offspring. We also determined how pECD impacts PFC neural function in adult offspring using ex vivo patch-clamp electrophysiology, exploring how pECD alters synaptic function and action potential dynamics. We found that male pECD mice trended toward increased total sleep during the inactive (light) period with shorter sleep bouts during the active (dark) period. pECD did not change sleep behavior in female mice. Independent of time of day, pECD altered post-synaptic dynamics of excitatory neurotransmitter release onto plPFC pyramidal neurons. There was also a loss of time-of-day effects on cell endogenous properties in male pECD mice. Thus, pECD clearly alters sleep behavior and PFC function in male mice. However, female mice appear protected against the effects of pECD in these measures. Together, these experiments form the foundation for future studies to understand the lifelong neurobehavioral impact of pECD.

neuroscience↗

The RNA-binding protein RSRC2 promotes mitotic fidelity by interacting with the lncRNA C1QTNF1-AS1

Mitotic fidelity depends on proper chromosome alignment at the spindle equator, a process known as chromosome congression, driven by well-established protein networks. Whereas RNA-binding proteins and noncoding RNAs have been implicated in cell division, their interplay during this process remains unknown. Here, we discover that RSRC2, an arginine/serine-rich RNA-binding protein, plays an essential role in cell division by interacting with the long non-coding RNA C1QTNF1-AS1. The loss of either RSRC2 or C1QTNF1-AS1 results in defects in chromosome congression and mitotic progression. We show that RSRC2 interacts with distinct sets of proteins involved in splicing and centrosome biogenesis, contributing to the fidelity of cell division through two different mechanisms: one linked to the splicing of mitotic regulators and the other by localising to mitotic centrosomes for which the interaction with the C1QTNF1-AS1 RNA is required. Our study uncovers RSRC2 as a new regulator of cell division and illustrates how RNA-protein complexes promote error-free mitosis.

cell biology↗