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Liu, Y.

Publications and source records attributed to Liu, Y..

At least 1,279 records · Page 71Linked to original sources

Systematics of the fleshy-fruited Sonerileae (Melastomataceae)

With approximately 1080 species, Sonerileae is the second largest tribe in the Melastomataceae. Approximately 40% of Sonerileae species belong to fleshy-fruited genera (Catanthera, Heteroblemma, Kendrickia, Medinilla, Pachycentria, and Plethiandra). Relatively few species, especially of the fleshy-fruited taxa, have been sampled for phylogenetic study. Consequently, there is huge uncertainty resulting in many unanswered questions about their evolutionary history, including the monophyly of the largest genus, Medinilla. In this study, the phylogeny of the fleshy-fruited Sonerileae was reconstructed using 385 nuclear and 81 plastid protein-coding loci recovered from target capture. Our study revealed that the fleshy fruited Sonerileae are polyphyletic and belong to three lineages. Kendrickia is sister to an Afrotropical endemic clade. Heteroblemma and Catanthera belong to a second clade and are most closely related to some Phyllagathis and Driessenia species. Medinilla forms a third clade, and includes Pachycentria and Plethiandra. Within Medinilla, fifteen clades are identified and characterized. To make Medinilla monophyletic, the genus is redefined to include Pachycentria and Plethiandra. Major lineages identified within Medinilla lay the groundwork for an infrageneric classification system. Areas of the phylogenetic tree with high conflict or weak sampling are identified to aid further studies in the tribe.

plant biology↗

On Monitoring Brain Health from the Depths of Sleep: Feature Engineering and Machine Learning Insights for Digital Biomarker Development

BackgrounSingle-channel sleep electroencephalography (EEG) is a promising technology for creating cost-effective and widely accessible digital biomarkers for monitoring brain health. Sleep, notable for its numerous connections to brain health, is of particular interest in this context. Indeed, several of the best studied and widely recognized risk factors for neurodegenerative disease are also connected to aspects of sleep physiology, including biological sex, hypertension, diabetes, obesity/metabolic dysregulation, and immune system dysfunction. In this study, we utilize the unique signal characteristics of slow wave sleep (SWS) oscillatory events as features in machine learning models to predict underlying biological processes that are highly relevant to brain health. Our objective is to establish a foundation for algorithms capable of effectively monitoring physiological processes in sleep that directly and indirectly inform brain health using single-channel sleep EEG as a functional metric of brain activity. MethodsUtilizing data from the Cleveland Family Study, we analyzed 726 overnight polysomnography recordings to extract features from slow waves and adjacent oscillatory events. Advanced signal processing and machine learning techniques, including random forest models, were employed to engineer features and predict health-related outcomes such as age, cerebrovascular risk factors, endocrine functions, immune system activity, and sleep apnea. ResultsOur models demonstrated significant predictive capability for several outcomes, including age (R2 = 0.643, p < 0.001), and sex classification (area under the receiver operator characteristic (AUROC) curve = 0.808), diabetes and hypertension diagnosis (AUROC = 0.832 and 0.755, respectively). Significant predictions were also modeled for metabolic/endocrine functions (including blood concentrations of IGF-1, leptin, ghrelin, adiponectin, and glucose), and immune markers (including IL-6, TNF-alpha, and CRP). In addition, this approach provided successful predictions in regression modeling of BMI and both regression and classification of sleep apnea. DiscussionThis study demonstrates the potential of using features from oscillatory events in single-channel sleep EEG as digital biomarkers. These biomarkers can identify key health and demographic factors that both affect brain health and are indicative of core brain functions. By capturing the complex interactions of neural, metabolic, endocrine, and immune systems during sleep, our findings support the development of single-channel EEG as a practical tool for monitoring complex biological processes through metrics that originate in brain physiology. Future research should aim to refine these digital biomarkers for broader home-based applications that may utilize inexpensive "wearable" devices to provide a scalable and accessible tool for tracking brain health-related outcomes.

neuroscience↗

Dynamics of RNA localization to nuclear speckles are connected to splicing efficiency

Nuclear speckles, a type of membraneless nuclear organelle in higher eukaryotic cells, play a vital role in gene expression regulation. Using the reverse transcription-based RNA-binding protein binding sites sequencing (ARTR-seq) method, we study human transcripts associated with nuclear speckles. We identify three gene groups whose transcripts demonstrate different speckle localization properties and dynamics: stably enriched in nuclear speckles, transiently enriched in speckles at the pre-mRNA stage, and not enriched in speckles. Specifically, we find that stably-enriched transcripts contain inefficiently spliced introns. We show that nuclear speckles specifically facilitate splicing of speckle-enriched transcripts. We further reveal RNA sequence features contributing to transcript speckle localization, underscoring a tight interplay between genome organization, RNA cis-elements, and transcript speckle enrichment, and connecting transcript speckle localization with splicing efficiency. Finally, we show that speckles can act as hubs for the regulated retention of introns during cellular stress. Collectively, our data highlight a role of nuclear speckles in both co- and post-transcriptional splicing regulation. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=189 SRC="FIGDIR/small/581881v1_ufig1.gif" ALT="Figure 1"> View larger version (53K): org.highwire.dtl.DTLVardef@1a55b13org.highwire.dtl.DTLVardef@fe50baorg.highwire.dtl.DTLVardef@6610fborg.highwire.dtl.DTLVardef@e4df5b_HPS_FORMAT_FIGEXP M_FIG GRAPHICAL ABSTRACT C_FIG

cell biology↗

Timescales and genetic linkage explain the variable impact of defense systems on horizontal gene transfer

Prokaryotes have evolved a wide repertoire of defense systems to prevent invasion by mobile genetic elements (MGE). However, because MGE are vehicles for the exchange of beneficial accessory genes, defense systems could consequently impede rapid adaptation in microbial populations. Here, we study how defense systems impact horizontal gene transfer (HGT) in the short and long terms. By combining comparative genomics and phylogeny-aware statistical methods, we quantified the association between the presence of 7 widespread defense systems and the abundance of MGE in the genomes of 196 bacterial and 1 archaeal species. We also calculated the differences in the rates of gene gain and loss between lineages that possess and lack each defense system. Our results show that the impact of defense systems on HGT is highly taxon- and system-dependent. CRISPR-Cas stands out as the defense system that most often associates with a decrease in the number of MGE and reduced gene acquisition. Timescale analysis reveals that defense systems must persist in a lineage for a relatively long time to exert an appreciable negative impact on HGT. In contrast, at short evolutionary times, defense systems, MGE, and gene gain rates tend to be positively correlated. Based on these results and given the high turnover rates experienced by defense systems, we propose that the inhibitory effect of most defense systems on HGT is masked by recent co-transfer events involving MGE.

microbiology↗

A generative model of the connectome with dynamic axon growth

Connectome generative models, otherwise known as generative network models, provide insight into the wiring principles underpinning brain network organization. While these models can approximate numerous statistical properties of empirical networks, they typically fail to explicitly characterize an important contributor to brain organization - axonal growth. Emulating the chemoaffinity guided axonal growth, we provide a novel generative model in which axons dynamically steer the direction of propagation based on distance-dependent chemoattractive forces acting on their growth cones. This simple dynamic growth mechanism, despite being solely geometry-dependent, is shown to generate axonal fiber bundles with brain-like geometry and features of complex network architecture consistent with the human brain, including lognormally distributed connectivity weights, scale-free nodal degrees, small-worldness, and modularity. We demonstrate that our model parameters can be fitted to individual connectomes, enabling connectome dimensionality reduction and comparison of parameters between groups. Our work offers an opportunity to bridge studies of axon guidance and connectome development, providing new avenues for understanding neural development from a computational perspective. Author SummaryGenerative models of the human connectome provide insight into principles driving brain network development. However, current models do not capture axonal outgrowth, which is crucial to the formation of neural circuits. We develop a novel generative connectome model featuring dynamic axonal outgrowth, revealing the contribution of microscopic axonal guidance to the network topology and axonal geometry of macroscopic connectomes. Simple axonal outgrowth rules representing continuous chemoaffinity gradients are shown to generate complex, brain-like topologies and realistic axonal fascicle architectures. Our model is sufficiently sensitive to capture subtle interindividual differences in axonal outgrowth between healthy adults. Our results are significant because they reveal core principles that may give rise to both complex brain networks and brain-like axonal bundles, unifying neurogenesis across scales.

neuroscience↗

Fair molecular feature selection unveils universally tumor lineage-informative methylation sites in colorectal cancer

In the era of precision medicine, performing comparative analysis over diverse patient populations is a fundamental step towards tailoring healthcare interventions. However, the critical aspect of equitably selecting molecular features across multiple patients is often overlooked. To address this challenge, we introduce FALAFL (FAir muLti-sAmple Feature seLection), an algorithmic approach based on combinatorial optimization. FALAFL is designed to bridge the gap between molecular feature selection and algorithmic fairness, ensuring a fair selection of molecular features from all patient samples in a cohort. We have applied FALAFL to the problem of selecting lineage-informative CpG sites within a cohort of colorectal cancer patients subjected to low read coverage single-cell methylation sequencing. Our results demonstrate that FALAFL can rapidly and robustly determine the optimal set of CpG sites, which are each well covered by cells across the vast majority of the patients, while ensuring that in each patient a high proportion of these sites have good read coverage. An analysis of the FALAFL-selected sites reveals that their tumor lineage-informativeness exhibits a strong correlation across a spectrum of diverse patient profiles. Furthermore, these universally lineage-informative sites are highly enriched in the inter CpG island regions. FALAFL integrates equity considerations into the molecular feature selection from single-cell sequencing data obtained from a patient cohort. We hope that it will help propel equitable healthcare data science practices and contribute to the advancement of our understanding of complex diseases.

bioinformatics↗

NSD2 is a requisite subunit of the AR/FOXA1 neo-enhanceosome in promoting prostate tumorigenesis

The androgen receptor (AR) is a ligand-responsive transcription factor that binds at enhancers to drive terminal differentiation of the prostatic luminal epithelia. By contrast, in tumors originating from these cells, AR chromatin occupancy is extensively reprogrammed to drive hyper-proliferative, metastatic, or therapy-resistant phenotypes, the molecular mechanisms of which remain poorly understood. Here, we show that the tumor-specific enhancer circuitry of AR is critically reliant on the activity of Nuclear Receptor Binding SET Domain Protein 2 (NSD2), a histone 3 lysine 36 di-methyltransferase. NSD2 expression is abnormally gained in prostate cancer cells and its functional inhibition impairs AR trans-activation potential through partial off-loading from over 40,000 genomic sites, which is greater than 65% of the AR tumor cistrome. The NSD2-dependent AR sites distinctly harbor a chimeric AR-half motif juxtaposed to a FOXA1 element. Similar chimeric motifs of AR are absent at the NSD2-independent AR enhancers and instead contain the canonical palindromic motifs. Meta-analyses of AR cistromes from patient tumors uncovered chimeric AR motifs to exclusively participate in tumor-specific enhancer circuitries, with a minimal role in the physiological activity of AR. Accordingly, NSD2 inactivation attenuated hallmark cancer phenotypes that were fully reinstated upon exogenous NSD2 re-expression. Inactivation of NSD2 also engendered increased dependency on its paralog NSD1, which independently maintained AR and MYC hyper-transcriptional programs in cancer cells. Concordantly, a dual NSD1/2 PROTAC degrader, called LLC0150, was preferentially cytotoxic in AR-dependent prostate cancer as well as NSD2-altered hematologic malignancies. Altogether, we identify NSD2 as a novel subunit of the AR neo-enhanceosome that wires prostate cancer gene expression programs, positioning NSD1/2 as viable paralog co-targets in advanced prostate cancer.

cancer biology↗

MICROCOSM FABRICATION PLATFORM FOR LIVE MICROSCOPY OF PLANT-SOIL SYSTEMS

Biological processes in soil pores are critical to crop nutrition and productivity, but live observations of these processes at that scale have been difficult to accomplish. To address this challenge, we have developed new techniques for the fabrication of microcosms dedicated to live imaging of the rhizosphere which incorporate the ability to control water content in transparent soil. Chambers were assembled using poly(dimethyl siloxane) (PDMS) parts fabricated by injection moulding and subsequently joined to glass slides. The control of liquid fluxes in the microcosm was achieved by syringes passing through the PDMS parts or through custom made PDMS sponges. We then tested various low refractive index materials for the fabrication of transparent soils and carried out live microscopy using Fluorescence Light Sheet microscopy. The proposed fabrication techniques are modular and enabled the construction of a wide range of experimental systems, including split chamber systems for the control of water content in soil, heterogeneous distribution of water content, monitoring of dye tracers, and live observation of plant roots. Using the techniques, we show how plant roots increase water infiltration through increased permeability of dry soil layers. This study therefore establishes that material property control and microfabrication in model rhizosphere systems can greatly enhance our understanding of plant-soil interactions.

bioengineering↗

Canonical AREs are tumor suppressive regulatory elements in the prostate

The androgen receptor (AR) is the central determinant of prostate tissue identity and differentiation, controlling normal, growth-suppressive prostate-specific gene expression1. It is also a key driver of prostate tumorigenesis, becoming "hijacked" to drive oncogenic transcription2-5. However, the regulatory elements determining the execution of the growth suppressive AR transcriptional program, and whether this can be reactivated in prostate cancer (PCa) cells remains unclear. Canonical androgen response element (ARE) motifs are the classic DNA binding element for AR6. Here, we used a genome-wide strategy to modulate regulatory elements containing AREs to define distinct AR transcriptional programs. We find that activation of these AREs is specifically associated with differentiation and growth suppressive transcription, and this can be reactivated to cause death in AR+ PCa cells. In contrast, repression of AREs is well tolerated by PCa cells, but deleterious to normal prostate cells. Finally, gene expression signatures driven by ARE activity are associated with improved prognosis and luminal phenotypes in human PCa patients. This study demonstrates that canonical AREs are responsible for a normal, growth-suppressive, lineage-specific transcriptional program, that this can be reengaged in PCa cells for potential therapeutic benefit, and genes controlled by this mechanism are clinically relevant in human PCa patients.

cancer biology↗

Proteomic Analysis of Urine from Youths Indulging in Gaming

Video game addiction manifests as an escalating enthusiasm and uncontrolled use of digital games, yet there are no objective indicators for gaming addiction. This study employed mass spectrometry proteomics to analyze the proteomic differences in the urine of adolescents addicted to gaming compared to those who do not play video games. The study included 10 adolescents addicted to gaming and 9 non-gaming adolescents as a control group. The results showed that there were 125 significantly different proteins between the two groups. Among these, 11 proteins have been reported to change in the body after the intake of psychotropic drugs and are associated with addiction: Calmodulin, ATP synthase subunit alpha, ATP synthase subunit beta, Acid ceramidase, Tomoregulin-2, Calcitonin, Apolipoprotein E, Glyceraldehyde-3-phosphate dehydrogenase, Heat shock protein beta-1, CD63 antigen, Ephrin type-B receptor 4, Tomoregulin-2. Additionally, several proteins were found to interact with pathways related to addiction: Dickkopf-related protein 3, Nicastrin, Leucine-rich repeat neuronal protein 4, Cerebellin-4. Enriched biological pathways discovered include those related to nitric oxide synthase, amphetamine addiction, and numerous calcium ion pathways, all of which are associated with addiction. Moreover, through the analysis of differentially expressed proteins, we speculated about some proteins not yet fully studied, which might play a significant role in the mechanisms of addiction: Protein kinase C and casein kinase substrate in neurons protein, Cysteine-rich motor neuron 1 protein, Bone morphogenetic protein receptor type-2, Immunoglobulin superfamily member 8. In the analysis of urinary proteins in adolescents addicted to online gaming, we identified several proteins that have previously been reported in studies of drug addiction.

molecular biology↗

Exploring the repository of de novo designed bifunctional antimicrobial peptides through deep learning

Antimicrobial peptides (AMPs) are attractive candidates to combat antibiotic resistance for their capability to target bio-membranes and restrict a wide range of pathogens. It is a daunting challenge to discover novel AMPs due to their sparse distributions in a vast peptide universe, especially for peptides that demonstrate potencies for both bacterial membranes and viral envelopes. Here we establish a de novo AMP design framework by bridging a deep generative module and a graph-encoding activity regressor. The generative module learns hidden grammars of AMP features and produces candidates sequentially pass antimicrobial predictor and antiviral classifiers. We discover 16 bifunctional AMPs and experimentally validated their abilities to inhibit a spectrum of pathogens in vitro and in animal models. Notably, P076 is a highly potent bactericide with the minimal inhibitory concentration of 0.21 M against multidrug-resistant A. baumannii, while P002 broadly inhibits five enveloped viruses. Our study provides feasible means to uncover sequences that simultaneously encode antimicrobial and antiviral activities, thus bolstering the function spectra of AMPs to combat a wide range of drug-resistant infections.

microbiology↗

Ubiquitin-mediated stabilization of SlPsbS regulates low night temperature tolerance in tomatoes

Non-photochemical quenching (NPQ) plays a fundamental role in safely operating photosynthesis under low night temperatures (LNT). PsbS protein is essential for the rapid induction of NPQ, and its stability is often affected by adverse environmental conditions. However, the regulatory mechanism for the stability of PsbS or chloroplast proteins remains to be fully characterized. We showed that LNT decreased NPQ levels and SlPsbS protein abundance in tomato leaves. COP9 signalosome subunit 5A (SlCSN5A) facilitated SlPsbS ubiquitination and degradation in the cytosol. Further, tomato chloroplast vesiculation (SlCV) was activated by LNT. Under LNT, SlCV targeted the chloroplasts and induced the formation of CV-containing vesicles (CCVs) containing SlPsbS, which were exported from the chloroplasts. Subsequently, SlCV and SlPsbS contact SlCSN5A in the cytosol and are ubiquitinated and degraded. Genetic evidence demonstrated that overexpression of SlCV aggravated SlPsbS protein degradation, whereas silencing of SlCSN5 and SlCV delayed LNT-induced NPQ reduction and SlPsbS protein turnover. This study provides evidence that CSN5A is associated with chloroplast proteins, and reveals a ubiquitin-dependent degradation pathway of chloroplast proteins co-mediated by CV and CSN5A, thereby providing new insights into the regulation of chloroplast protein stability under stress conditions.

plant biology↗

A comprehensive personal omics clinical interpreter based on genomic and transcriptomic profiles

Advances in precision medicine rely on the accurate identification and analysis of molecular alterations for personalized diagnostic, prognostic, and therapeutic decision-making. A critical obstacle is the integration of heterogeneous interpretations of clinically actionable alterations from various knowledgebases. Here, we present the Personal Omics Interpreter (POI), a web-based application engineered to aggregate and interpret therapeutic options, including targeted, immunological, and chemotherapeutic agents, by leveraging personal genomic and transcriptomic profiles. POI employs the Precision Medicine Knowledgebase (PreMedKB), an updated harmonized resource we previously reported, to annotate the clinically actionable somatic variants. It further incorporates a predictive algorithm to broaden therapeutic options according to established gene-gene interactions and offers insights into phenotypic responses of chemotherapeutic agents through phasing germline diplotypes. Validated against three cohort datasets encompassing over 22,000 cancer patients, POI demonstrates consistently high matching rates (94.7 [~] 95.6%) between patients and suggested therapies, highlighting its potential in supporting precision-driven informed treatment strategies.

genomics↗

Unraveling the Role of Urea Hydrolysis in Salt Stress Response during Seed Germination and Seedling Growth in Arabidopsis thaliana

Urea is intensively utilized as a nitrogen fertilizer in agriculture, originating either from root uptake or from catabolism of arginine by arginase. Despite its extensive use, the underlying physiological mechanisms of urea, particularly its adverse effects on seed germination and seedling growth under salt stress remains unclear. In this study, we demonstrate that salt stress induces excessive hydrolysis of arginine-derived urea, leading to an increase in cytoplasmic pH within seed radical cells, which, in turn, triggers salt-induced inhibition of seed germination (SISG) and hampers seedling growth. Our findings challenge the long-held belief that ammonium accumulation and toxicity are the primary causes of SISG, offering a novel perspective on the mechanism underlying these processes. This study provides significant insights into the physiological impact of urea hydrolysis under salt stress, contributing to a better understanding of SISG.

plant biology↗

Personalized composite scaffolds for accelerated cell- and growth factor-free craniofacial bone regeneration

Approaches to regenerating bone often rely on the integration of biomaterials and biological signals in the form of cells or cytokines. However, from a translational point of view, these approaches face challenges due to the sourcing and quality of the biologic, unpredictable immune responses, complex regulatory paths, and high costs. We describe a simple manufacturing process and a material-centric 3D-printed composite scaffold system (CSS) that offers distinct advantages for clinical translation. The CSS comprises a 3D-printed porous polydiolcitrate-hydroxyapatite composite elastomer infused with a polydiolcitrate-graphene oxide hydrogel composite. Using a continuous liquid interface production 3D printer, we fabricate a precise porous ceramic scaffold with 60% hydroxyapatite content resembling natural bone. The resulting scaffold integrates with a thermoresponsive hydrogel composite, customizable in situ to fit the defect. This hybrid phasic porous CSS mimics the bone microenvironment (inorganic and organic) while allowing independent control of each material phase (rigid and soft). The CSS stimulates osteogenic differentiation in vitro and in vivo. Moreover, it promotes M2 polarization and blood vessel ingrowth, which are crucial for supporting bone formation. Our comprehensive micro-CT analysis revealed that within 4 weeks in a critical-size defect model, the CSS accelerated ECM deposition (8-fold) and mineralized osteoid (69-fold) compared to the untreated. Our material-centric approach delivers impressive osteogenic properties and streamlined manufacturing advantages, potentially expediting clinical application for bone reconstruction surgeries.

bioengineering↗

Large-pore connexin hemichannels function as molecule transporters independently of ion conduction

Connexin hemichannels were identified as the first members of the eukaryotic large-pore channel family that mediate permeation of both atomic ions and small molecules between the intracellular and extracellular environments. The conventional view is that their pore is a large passive conduit through which both ions and molecules diffuse in a similar manner. In stark contrast to this notion, we demonstrate that the permeation of ions and of molecules in connexin hemichannels can be uncoupled and differentially regulated. We find that human connexin mutations that produce pathologies and were previously thought to be loss-of-function mutations due to the lack of ionic currents are still capable of mediating the passive transport of molecules with kinetics close to those of wild-type channels. This molecular transport displays saturability in the micromolar range, selectivity, and competitive inhibition, properties that are tuned by specific interactions between the permeating molecules and the N-terminal domain that lies within the pore -- a general feature of large-pore channels. We propose that connexin hemichannels and, likely, other large-pore channels, are hybrid channel/transporter-like proteins that might switch between these two modes to promote selective ion conduction or autocrine/paracrine molecular signaling in health and disease processes.

biophysics↗

Integrative phylogenetic analysis of the genus Episoriculus (Mammalia: Eulipotyphla: Soricidae)

Shrews in the genus Episoriculus are among the least-known mammals in China, where representatives occur mainly in the Himalayan and Hengduan mountains. We sequence one mitochondrial and three nuclear genes from 77 individuals referable to this genus, collect morphometric data for five shape and 11 skull measurements from 56 specimens, and use museum collections and GenBank sequences to analyze phylogenetic relationships between this and related genera in an integrated molecular and morphometric approach. Whereas historically anywhere from two to eight species have been recognized in this genus, we conclude that six (E. baileyi, E. caudatus, E. leucops, E. macrurus, E. sacratus, E. soluensis) are valid. We dissent from recent systematic reviews of this genus and regard E. sacratus to be a valid taxon, E. umbrinus to be a subspecies of E. caudatus, and transfer E. fumidus to Pseudosoriculus. Our record of E. soluensis is the first for China, and expands the previously recognized distribution of this taxon from Nepal and NE India into the adjacent Yadong and Nyalam counties. One further undescribed Episoriculus taxon may exist in Tibet.

zoology↗

Developmental emergence of quiescent-like neural progenitor cells in the zebrafish embryonic brain

The mature brain is made up of differentiated neurons and glial cells that are produced by embryonic neural stem and progenitor cells (collectively called neural stem cells (NSCs)) during brain development. In contrast, adult NSCs generate only a limited number of neuronal and glial cell types. Moreover, in contrast to embryonic NSCs, adult NSCs spend most of their time in a non-dividing resting phase called quiescence. In the adult brain, the quiescent NSCs are activated at a low frequency to divide and produce new cells to replace lost or damaged mature cells. Previous studies have demonstrated that about halfway through mammalian brain development, a subset of the embryonic NSCs population slows down their division rate and slowly transition into adult quiescent NSCs (qNSCs). However, the molecular mechanisms that underlie the emergence of the pre-adult SCs remain largely unknown. Here, we explored single-cell transcriptomes from several embryonic stages of zebrafish development in order to determine at what developmental stage transcriptional signatures typical of adult quiescent NSCs first emerge. We identified a subpopulation of embryonic NSCs with a distinct transcriptional profile from other embryonic NSCs. This population shares transcriptional similarities with adult qNSCs including genes known to maintain quiescence. We propose that this population constitute slower cycling embryonic NSCs that may transition into the adult qNSCs of the adult zebrafish brain.

developmental biology↗