Biology subjects

Meng, W.

Publications and source records attributed to Meng, W..

At least 37 records · Page 2Linked to original sources

bioRxiv2025

SELECTION OF ANTI-NUCLEAR ANTIGEN (ANA) REACTIVE B CELLS IN SYSTEMIC LUPUS ERYTHEMATOSUS.

ObjectiveAutoreactive B cells that recognize nuclear antigens are normally present in healthy individuals and patients with systemic lupus erythematosus (SLE), yet their activation and the production of IgG autoantibodies is a hallmark of SLE. The selection process and regulation of these cells in patients with SLE has not been completely understood. To gain insights into tolerance checkpoints and the developmental trajectories of autoreactive clones, we studied the BCR sequences from thousands of anti-nuclear antigen binding (ANA)+ and ANA-B cells from patients with SLE. MethodsFrom a cohort of 13 patients with SLE, we identified and isolated ANA+ and ANA-B cells by flow cytometry using a method based on their binding to nuclear extracts. We sequenced B cell receptor (BCR) heavy chain variable regions and investigated the features of the IgH repertoire of ANA+ and ANA-B cells from naive, memory and age-associated B cells (ABCs), and from total plasmablasts. ResultsThe frequency of ANA+ B cells was similar in ABCs and naive B cells and higher in both than in memory B cells. We observed preferential usage of some VH (IGHV1-18, IGHV3-21, IGHV3-23|3-23D, IGHV4-34, IGHV4-39 and IGHV4-59) and VJ genes (IGHJ4 and IGHJ6) in B cells from these patients. ANA+ naive and ANA+ ABCs used different gene segments and have longer CDR3 sequences than ANA+ memory B cells and ANA-subsets. ANA+ ABCs and memory B cells have a lower frequency of somatic hypermutation (SHM) and less activation induced deaminase (AID) targeting to WRC hotspots compared with their ANA-counterparts. Patients with active disease have a lower frequency of SHM in ANA+ ABCs and memory B cells and in ANA-ABCs. ConclusionCompared to memory B cells, ABCs are enriched in autoreactivity. Our results suggest that there is an immune checkpoint that restricts the differentiation of ANA+ naive B cells into memory B cells and that ANA+ ABCs originate from ANA+ naive B cells. Lower frequencies of SHM in antigen experienced ANA+ B cells, and particularly ANA+ ABCs, suggest that these cells might be generated through an extrafollicular (EF) pathway, and that in patients with active SLE there is more EF activation.

immunology↗

bioRxiv2025

Systematic Identification of Microtubule Inner Proteins Reveals JPT2 as a Key Regulator of Lumen Microenvironment and Drug Sensitivity

Microtubules are primarily studied for the interactions of proteins that bind to their outer surfaces and ends, while the regulatory mechanisms within the microtubule lumen, particularly in singlet microtubules critical for essential cellular processes, remain largely unexplored. Our study provides the first systematic identification of key regulatory proteins within the single microtubule lumen. Using proximity-dependent biotin identification (Bio-ID) coupled with mass spectrometry, we identified candidate microtubule inner proteins (MIPs), including Jupiter microtubule-associated homolog 2 (JPT2). JPT2 binds directly to microtubules and specifically localizes within the lumen, where it modulates the luminal environment by inhibiting acetylase MEC17 and independently affects the binding and efficacy of Paclitaxel. Furthermore, our screening identified additional MIPs that influence cellular sensitivity to Paclitaxel, indicating a link between luminal regulation and drug responsiveness. These discoveries reveal JPT2s critical role in singlet microtubule regulation and suggest new therapeutic targets for enhancing cancer drug sensitivity.

cell biology↗

bioRxiv2024

Finding Salient Multi-Omic Interactomes Relevant to Multiple Biomedical Outcomes using Graph Ensemble Neural Networks

Although multi-omics integration relevant to patient outcome is typically characterized by an analyte interactome, current multi-omic integration methods either (1) model outcome without directly including associations between analytes, (2) model the interactome without directly evaluating the saliency of the model in the context of outcome, or (3) model outcome in a high-dimensional parameter space not suitable for small sample sizes (which are common in multi-omics studies). We introduce Graph Ensemble Neural Network (GENN), a methodology that learns the interactome most predictive of outcome in a low-dimensional parameter space built on complementary attributes for all possible analyte associations (metafeatures). We show that GENN is robust to noise in measurements using a theoretical model, outperforms the predictive performance of existing methods when evaluated on Tegafur drug response in NCI-60 cancer cell line data, and uncovers potentially novel multi-omic mechanisms driving total serum IgE levels in pediatric asthma and patient survival in glioblastomas.

bioinformatics↗

bioRxiv2024

Dynamic p21-dependency during quiescence arrest unveiled by a rapid p21 depletion system

Stress- or developmentally-induced signals can trigger G0/G1 cell cycle arrest through the upregulation of p21, a key inhibitor that halts proliferation. While p21 is widely recognized as essential for establishing this arrest, its degradation is generally assumed to be a prerequisite for the exit from arrest and cell cycle re-entry. Using a rapid p21 degradation system that allows for both endogenous p21 tracking and controlled depletion, we uncovered an extended role for p21 during the exit from G0/G1 arrest. Our results showed that removal of the arrest inducing signals did not lead to an immediate decline of p21 during the exit process; instead, p21 levels continued to maintain for a period before its gradual down-regulation. Importantly, premature depletion of p21 during this process weakened the capacity of cell cycle re-entry, particularly in cells with high levels of pre-existent p21. We found that during the release from arrest, cells with high levels of pre-existent p21 but a premature p21 depletion exhibited reduced capacity to restore KRAS/ERK activity, and supplementing KRAS/ERK activity rescued the failure of cell cycle re-entry in these cells. These findings reveal a previously unappreciated function for p21 during the exit from G0/G1 arrest, aside and distinct from its role in initiating the arrest. This new paradigm extends across multiple cell lines and stress-induced arrest contexts, offering a new framework for understanding p21 function in response to anticancer therapies and in development.

cell biology↗

bioRxiv2024

Urinary Proteome Characterization of Stroke-Prone Spontaneously Hypertensive Rats

BackgroundHypertension is a multifactorial, complex disease related to genetic and environmental factors and has become the most serious public health problem. This study aimed to explore the changes of hypertension based on urinary proteome. MethodsThe stroke-prone spontaneously hypertensive rats (SHRSPs) model was used to examined urinary proteome changes during hypertension development. Urine proteome at months 1, 4, 8, 10, 12, and 14 was profiled using liquid chromatography coupled with tandem mass spectrometry (LC-MS/MS). Considered the degree of disease progression may differ, each rat was compared before and after hypertension developed to screen for differential proteins. ResultsThe differential proteins in each rat can be enriched into some important biological processes and pathways associated with hypertension, such as regulation of systemic arterial blood pressure by renin-angiotensin, renin-angiotensin signaling, response to glucocorticoid and glucocorticoid receptor signaling, calcium transport I, aldosterone adipocyte signaling pathway, apelin adipocyte signaling pathway and oxidative stress response. The biological processes and pathways enriched at the same time point in the progression of hypertension differed significantly among different rat individuals. ConclusionsThis study showed that the changes of hypertension can be reflected in urine proteins. The urine proteomics has the potential to be used to study the mechanisms of hypertension, discovery new drug targets, and provide personalized antihypertensive treatment strategies.

molecular biology↗

bioRxiv2024

Fresh Human Retinal scRNA-seq Atlas Reveals a Novel Cone Subtype and Cellular Diversity

BackgroundCurrent human retina studies predominantly utilize post-mortem tissue, and the sample accessibility constraints make the characterization of the living human retina at single-cell resolution a challenge. Although single-nucleus RNA-seq expands the utility of frozen samples, it provides a nuclear-centric view, potentially missing key cytoplasmic information and transient biological processes. Thus, it is important to generate resources directly from living human retinal tissue to complement existing datasets. MethodsWe profiled 106,829 single cells from nine unfrozen human retina samples. Living samples were collected withinLJ10LJmin of therapeutic enucleation and four postmortem samples were collected within 6LJh. After standardized dissociation, single-cell transcriptomes were generated using 10x Genomics 3 RNA-seq and applied scVI to generate batch-corrected integrated atlas. Major cell types and subtypes were annotated through iterative Leiden clustering, canonical markers. Subsequent analyses included differential expression comparisons between cell states and regulon activity profiling to further characterize cellular identities and regulatory networks. Transcriptional dynamics were assessed using RNA velocity, and cell-cell signaling pathways were inferred with CellChat. Key findings were validated in independent samples from two additional donors (four samples) using the identical workflow. ResultsWe contribute to establishing a reference for retinal cell type proportions and cellular states. Our analysis revealed ELF1-mlCone, a distinct cluster of mlCone photoreceptors identified by distinct transcriptional features. The presence and transcriptional features of this cluster were validated in independent samples. Additionally, by comparing living and post-mortem samples, our study highlights differences in transcriptional dynamics: living tissue preserved coherent RNA velocity streams, enabling clear dynamic state transitions, while post-mortem tissue exhibited disorganized patterns. These findings suggest that using living tissue can improve the capture of active cellular states and transitions. ConclusionsOur atlas provides a single-cell reference contrasting living versus early post-mortem human retina, integrating cell type composition, transcriptional diversity, and functional insights. It may serve as a useful resource for retinal research and for understanding aspects of human retinal biology, particularly given its inclusion of living tissue and diverse pathological states.

bioinformatics↗

bioRxiv2024

Exploring the effect of capsaicin on gene expression and chemotherapy sensitization in gastric cancer cells

PurposeCapsaicin has previously been demonstrated to exhibit anti-tumor effect in various cancer type. However, the effect of capsaicin on gene expression and its potential mechanism on chemotherapy sensitization were still uncertain. MethodHuman AGS gastric cancer cell line was treated with different concentrations of capsaicin, 5-fluorouracil and oxaliplatin. Cell viability was assessed using cell viability assay. High throughput RNA sequencing was used to screen differentially expressed genes triggered by capsaicin in AGS cells. qPCR and Western blotting were used to detect the expression of mRNAs and proteins induced by capsaicin. ResultCapsaicin could significantly inhibit cell viability at a dose-depend manner in AGS gastric cancer cell line. Through high-throughput RNA sequencing, genes regulating DNA repair, DNA replication and chromosome assemble pathways were analyzed to be down-regulated by capsaicin. qPCR and western blot assay demonstrated that capsaicin could inhibit expression of the key enzymes (FEN1, LIG1 and PARP1) which play critical roles in DNA damage response and chemotherapy resistance. In vitro assay demonstrated that capsaicin could significantly induce chemo-sensitivity of 5-FU and Oxaliplatin at low dose. ConclusionCapsaicin could inhibit DNA repair pathway, which might contribute to cell growth inhibition and improvement of chemotherapy sensitization. These results revealed a novel function of capsaicin in DNA damage repair and provided new potential targets in cancer therapy.

cancer biology↗

bioRxiv2024

Cholinergic signaling differentially regulates song premotor circuits to stabilize songs in songbirds

Cholinergic modulation plays an important role in motor skill performance, including vocal control. In songbirds, song motor nucleus RA simultaneously receives inputs from song nuclei HVC and LMAN, and then its projection neurons (RAPNs) generate song motor control output. Using electrophysiological and pharmacological methods, we found that cholinergic signaling can enhance song stability by reducing HVC-RAPN excitatory synaptic transmission in adult male zebra finches, mediated by mAChRs. Although nAChRs are not effective overall, cholinergic signaling can also decrease LMAN-RAPN excitatory synaptic transmission induced by electrical stimulation via nAChRs, suggesting the potential role of cholinergic regulation in song behavior through LMAN-RA pathway. On the contrary, in adult female zebra finches, only LMAN-RAPN synaptic transmission was reduced by cholinergic signaling via mAChRs. The role of differential cholinergic regulation of song premotor circuits in songbirds singing provides insights into the neural control mechanism of motor skill performance.

neuroscience↗

bioRxiv2024

CAMSAP3 Forms Dimers via its lapha-helix Domain that Directly Stabilize Non-centrosomal Microtubule Minus Ends

Microtubules are vital components of the cytoskeleton. Their plus ends are dynamic and respond to changes in cell morphology, while the minus ends are stable and serve a crucial role in microtubule seeding and maintaining spatial organization. In mammalian cells, the calmodulin-regulated spectrin-associated proteins (CAMSAPs), play a key role in directly regulating the dynamics of non-centrosomal microtubules minus ends. However, the molecular mechanisms are not yet fully understood. Our study reveals that CAMSAP3 forms dimers through its C-terminal -helix; this dimerization not only enhances the microtubule-binding affinity of the CKK domain but also enables the CKK domain to regulate the dynamics of microtubules. Furthermore, CAMSAP3 also specializes in decorating at the minus end of microtubules through the combined action of the microtubule-binding domain (MBD) and the C-terminal -helix, thereby achieving dynamic regulation of the minus ends of microtubules. These findings are crucial for advancing our understanding and treatment of diseases associated with non-centrosomal microtubules. SignificanceOur study reveals the molecular mechanism of how CAMSAP3, a key regulator of non-centrosomal microtubule dynamics, directly regulates the dynamics of non-centrosomal microtubule minus ends through CKK domain. CAMSAP3 forms dimers through its C-terminal -helix, which enhances the CKK domain of CAMSAP3 binding to microtubule minus ends and confers stability of them. This finding is not limited to CAMSAP3, but can also be applied to the understanding of the regulation of non-centrosomal microtubule minus end stability by CAMSAP family proteins. Our findings deepen our comprehension of cellular structure and function, offering insights into the role of microtubules in cellular integrity and disease. This study fills a significant knowledge gap and lays the foundation for future research into the complex balance of microtubule dynamics required for cellular health and disease prevention.

cell biology↗

bioRxiv2024

MARK2 regulates Golgi apparatus reorientation by phosphorylation of CAMSAP2 in directional cell migration

The reorientation of the Golgi apparatus is crucial for cell migration and is regulated by multi-polarity signals. A number of non-centrosomal microtubules anchor at the surface of the Golgi apparatus and play a vital role in the Golgi reorientation, but how the Golgi are regulated by polarity signals remains unclear. Calmodulin-regulated spectrin-associated protein 2 (CAMSAP2) is a protein that anchors microtubules to the Golgi, a cellular organelle. Our research indicates that CAMSAP2 is dynamically localized at the Golgi during its reorientation processing. Further research shows that CAMSAP2 is potentially regulated by a polarity signaling molecule called MARK2, which interacts with CAMSAP2. We used mass spectrometry to find that MARK2 phosphorylates CAMSAP2 at serine 835, which affects its interaction with the Golgi associated protein USO1 but not with CG-NAP or CLASPs. This interaction is critical for anchoring microtubules to the Golgi during cell migration, altering microtubule polarity distribution, and aiding Golgi reorientation. Our study reveals an important signaling pathway in Golgi reorientation during cell migration, which can provide insights for research in cancer cell migration, immune response, and targeted drug development.

cell biology↗

bioRxiv2024

YAP promotes chromosomal instability by transcriptionally activating AJUBA through its super enhancer in breast cancer

Chromosomal instability (CIN) has been proven to be a fundamental property of cancer and a key underlying mechanism of tumorigenesis and progression. Still, relatively few studies have revealed the mechanism of this process. In this research, we identified the core Hippo component, YAP, played a crucial role in CIN formation in breast cancer. Using public ChIP-seq data and bioinformatic analysis, we found YAP could transcriptionally induce spindle assembly checkpoint, AJUBA, via TEAD, then activate AJUBA-AURKA signaling. Abolish AJUBA-AURKA axis could reverse YAP-induced CIN formation and aberrant mitosis. Mechanically, YAP/TEAD complex could accumulate to the super enhancer region of AJUBA, thus significantly induced its expression, and subsequently promoted AURKA auto-phosphorylating. These findings revealed a novel cross-talk between Hippo and AJUBA-AURKA signaling, and provided a new insight in CIN formation in breast cancer.

cancer biology↗

bioRxiv2023

Exploring information exchange between Thesium chinense and its host Prunella vulgaris through joint transcriptomic and metabolomic analysis

Background: Thesium chinense known as "plant antibiotic" is a facultative root hemi-parasitic herb while Prunella vulgaris can serve as its host. However, the molecular mechanisms underlying the communication between T. chinense and its host remained largely unexplored. The aim of this study was to provide a comprehensive view of transferred metabolites and mobile mRNAs between T. chinense and P. vulgaris. Results: The wide-target metabolomic and transcriptomic analysis identified 5 transferred metabolites and 668 mobile genes between T. chinense and P. vulgaris, as well as haustoria formation related 56 metabolites and 189 genes. Furthermore, we inferred a regulatory network that might be involved in haustoria formation, and 18 genes promoting haustoria formation and 1 gene inhibiting it were identified as a consequence. There were 4 metabolites (ethylsalicylate, eriodictyol-7-O-glucoside, aromadendrin-7-O-glucoside and pruvuloside B) that are transferred from P. vulgaris to T. chinense, whereas 2-ethylpyrazine was transferred from T. chinense to P. vulgaris. Conclusions: These results suggested that there was an extensive exchange of information with P. vulgaris including transferred metabolites and mobile mRNAs, which might facilitate the haustoria formation and parasition of T. chinense. Author summaryT. chinense known as "plant antibiotic" is a facultative root hemi-parasitic herb while P. vulgaris can serve as its host. Currently, the information exchange between T. chinense and its host remained unknown, and a comprehensive view of transferred metabolites and mobile mRNAs between T. chinense and its host is critical so that appropriate chemical and genetic improvement can be used to facilitate haustoria formation and successful parasitism. Here, we employ the conjoint wide-target metabolomic and transcriptomic analysis to explore the information exchange between T. chinense and P. vulgaris. We identified 5 transferred metabolites and 668 mobile genes between T. chinense and P. vulgaris, as well as haustoria formation related 56 metabolites and 189 genes. Our study provides new insights into the complex interplay between parasite and host during parasitism.

plant biology↗

bioRxiv2023

METTL16 Controls Kaposi's Sarcoma-Associated Herpesvirus Replication by Regulating S-Adenosylmethionine Cycle

Oncogenic Kaposis sarcoma-associated herpesvirus (KSHV) consists of latent and lytic replication phases, both of which are important for the development of KSHV- related cancers. As one of the most abundant RNA modifications, N6-methyladenosine (m6A) and its related complexes regulate KSHV life cycle. However, the role of METTL16, a new RNA methyltransferase, in KSHV life cycle remains unknown. In this study, we have identified a suppressive role of METTL16 in KSHV lytic replication. METTL16 knockdown increased while METTL16 overexpression reduced KSHV lytic replication. METTL16 binding to and writing of m6A on MAT2A transcript are essential for its splicing, maturation and expression. As a rate-limiting enzyme in the methionine- S-adenosylmethionine (SAM) cycle, MAT2A catalyzes the conversion of L-methionine to SAM required for the transmethylation of protein, DNA and RNA, transamination of polyamines, and transsulfuration of cystathionine. Consequently, knockdown or chemical inhibition of MAT2A reduced intracellular SAM level and enhanced KSHV lytic replication. In contrast, SAM treatment was sufficient to inhibit KSHV lytic replication and reverse the effect of the enhanced KSHV lytic program caused by METTL16 or MAT2A knockdown. Mechanistically, METTL16 or MAT2A knockdown increased while SAM treatment decreased the intracellular reactive oxygen species level by altering glutathione level, which is essential for efficient KSHV lytic replication. These findings demonstrate that METTL16 suppresses KSHV lytic replication by modulating the SAM cycle to maintain intracellular SAM level and redox homeostasis, thus illustrating the linkage of KSHV life cycle with specific m6A modifications, and cellular metabolic and oxidative conditions.

microbiology↗

bioRxiv2023

In vivo Ontogeny of human forebrain neural progenitor cell grafts in adult rats: an immunohistological study

A thorough understanding of the cell behaviors of the human neural grafts is fundamental to exploit them to achieve cell therapy for recovering brain functions. Here by using immunohistological staining, we trace the cell fate of the intrastriatal human neural progenitor cell (NPC) grafts up to 9 months in adult rats, with multiple examining time points to provide a unified working time frame for future transplantation study. Lots of Nestin+/Sox2+ human cells continuously migrate along the white matter tracts into distal brain parenchyma even long time after transplantation, providing a potential for curing diffuse brain damage. Further analysis reveals a significant heterogeneity of the long-term sustained neural stem cells (NSC)/NPCs that progressing throughout different stages, mimicking the neural development of human forebrain. More importantly, the initial GFAP expression in human grafts marks the NSC progression instead of terminal astrocyte differentiation. The distally migrating human cells continuously show the capability to produce new neurons, albeit at a low efficiency in the intact brain. Further investigations in neural disease models are needed. Such study would benefit neural cell therapy with regarding to the optimization of the transplantation strategy and choosing of acting mode by neural grafts (e.g. via cell replacement or ex vivo gene therapy).

cell biology↗

bioRxiv2023

HERC5-catalyzed ISGylation potentiates cGAS-mediated innate immunity

The key cytosolic DNA sensor cyclic GMP-AMP (cGAMP) synthetase (cGAS) is essential to elicit anti-infection innate immunity whereas aberrant activation of cGAS by endogenous DNA promotes severe autoimmune diseases, thus the activity of cGAS must be strictly regulated to maintain immune homeostasis. Here we report that the E3 ISG15-protein ligase HERC5 interacts with and catalyzes the cGAS ISGylation robustly, whereas the deconjugating enzyme USP18 removes the ISG15 conjugation of cGAS. The interaction of cGAS and HERC5 depends on the cGAS N-terminal domain and the RRC1-4 and HECT domain of HERC5. Mass spectrometry reveals that the Lys21,187,219,458 are the potential ISGylation sites in human cGAS. Deficiency of ISG15 or the E1 ubiquitin-activating enzyme UBA7 greatly attenuate the downstream gene expression induced by cGAS-STING axis and the antiviral ability in mouse and human cells. Collectively, our study uncovered an important role of the HERC5-facilitated cGAS ISGylaion in promoting antiviral defense.

immunology↗

bioRxiv2022

N6-methyladenosine (m6A) and reader protein YTHDF2 enhance innate immune response by mediating DUSP1 mRNA degradation and activating mitogen-activated protein kinases during bacterial and viral infections

Mitogen-activated protein kinases (MAPKs) play critical roles in the induction of numerous cytokines, chemokines, and inflammatory mediators that mobilize the immune system to counter pathogenic infections. Dual-specificity phosphatase-1 (DUSP1) is a member of dual-specificity phosphatases, which inactivates MAPKs through a negative feedback mechanism. Here we report that in response to viral and bacterial infections, not only DUSP1 transcript but also its N6-methyladenosine (m6A) level rapidly increase together with the m6A reader protein YTHDF2, resulting in enhanced YTHDF2-mediated DUSP1 transcript degradation. Knockdown of DUSP1 promotes p38 and JNK phosphorylation and activation, thus increasing the expression of innate immune response genes including IL1{beta}, CSF3, TGM2 and SRC. Similarly, knockdown of m6A eraser ALKBH5 increases DUSP1 transcript m6A level resulting in accelerated transcript degradation, activation of p38 and JNK, and enhanced expression of IL1{beta}, CSF3, TGM2 and SRC. These results demonstrate that m6A and reader protein YTHDF2 orchestrate optimal innate immune response during viral and bacterial infections by downregulating the expression of a negative regulator DUSP1 of the p38 and JNK pathways that are central to innate immune response against pathogenic infections. IMPORTANCEInnate immunity is central for controlling pathogenic infections and maintaining the homeostasis of the host. In this study, we have revealed a novel mechanism regulating innate immune response during viral and bacterial infections. We have found that N6-methyladenosine (m6A) and the reader protein YTHDF2 regulate dual-specificity phosphatase-1, a negative regulator of mitogen-activated protein kinases p38 and JNK, to maximize innate immune response during viral and bacterial infections. These results provide novel insights into the mechanism regulating innate immunity, which could help the development of novel approaches for controlling pathogenic infections.

microbiology↗

bioRxiv2022

Changes of urinary proteome in an ApoE-/- mouse model of atherosclerosis

Cardiovascular disease is currently the leading cause of death worldwide. Atherosclerosis is an important pathological basis of cardiovascular disease, and its early diagnosis is of great significance. Urine is more conducive in the accumulation and response of changes in the physiological state of the body and is not regulated by homeostasis mechanisms, so it is a good source of biomarkers in the early stage of disease. In this study, ApoE-/- mice were fed with a high-fat diet for 5 months. Urine samples from the experimental group and control group, which were C57BL/6 mice fed a normal diet, were collected at seven time points. Proteomic analysis was used for internalcontrol and intergroup control. Internal control results showed a significant difference in the urinary proteome before and after a 1-week high-fat diet, and several differential proteins have been reported to be associated with atherosclerosis or for use as candidate biomarkers. The results of the intergroup control indicated that the biological process enriched by the GO analysis of the differential proteins corresponded to the progression of atherosclerosis. Differences in chemical modifications of urinary proteins have also been reported to be associated with the disease. This study demonstrates that urinary proteomics has the potential to monitor changes in the body sensitively and provides the possibility of identifying early biomarkers of atherosclerosis.

biochemistry↗

bioRxiv2022

A dataset of 5 million city trees: species clustering and climate effects in urban forests

Sustainable cities depend on urban forests. City trees improve our health, clean the air, store CO2, and cool local temperatures. Comparatively less is known about urban forests as ecosystems, particularly their spatial composition, nativity statuses, biodiversity, and tree health. Here, we assembled and standardized a new dataset of N=5,132,890 trees from 63 of the largest US cities with detailed information on location, health, nativity status, and species. We further designed new tools to analyze the ecosystem structure of urban forests, including spatial clustering and abundance of native trees, and validate these tools in comparison to past methods. We show that city trees are significantly clustered by species in 93% of cities, potentially increasing pest vulnerability (even in cities with biodiverse urban forests). Further, non-native species significantly homogenize urban forests across cities, while native trees comprise 0.44%-85.6% (median=45.6%) of city tree populations. Native trees are less frequent in drier cities, and indeed climate significantly shapes both nativity and biodiversity in urban forests. Parks are more biodiverse than urban settings. Compared to past work which focused primarily on canopy cover and species richness, we show the importance of analyzing spatial composition and nativity statuses in urban forests (and we created new datasets and tools to do so). This dataset could be analyzed in combination with citizen-science datasets on bird, insect, or plant biodiversity; social and demographic data; or data on the physical environment. Urban forests offer a rare opportunity to intentionally design biodiverse, heterogenous, rich ecosystems.

ecology↗