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6,171 results for “mutant”
LC-HRMS study of Arabidopsis root metabolome in wild-type Col-0 and npr1 mutant upon in vitro inoculation with Streptomyces sp. AgN23.
<p>This archive compiles datasets related to studies of <em>Streptomyces</em> sp. AgN23 interaction with <em>Arabidopsis thaliana</em>. Ultra-high-performance liquid chromatography-high-resolution MS (UHPLC-HRMS) analyses were performed on a Q Exactive Plus quadrupole (Orbitrap) mass spectrometer, equipped with a heated electrospray probe (HESI II) coupled to a U-HPLC Ultimate 3000 RSLC system (Thermo Fisher Scientific, Hemel Hempstead, United Kigdom). For each biological sample, the RAW file obtained in ESI+ and ESI- mode were retrieved from the Xcalibur version 4.4 software and are deposited in separate sub-folders termed "RawPos" and "RawNeg". Each folder contains all the data relative to the cohort comprising "Blank" samples (n=13), Quality Check samples (pool of all samples from the cohort) "QC" (n=8), Control Col-0 plant samples "Col0CTRL" (n=6), Col-0 plant inoculated with AgN23 samples "Col0AgN23WT" (n=6), Control npr1 plant samples"NPR1CTRL" (n=6), npr1 plant inoculated with AgN23 samples "NPR1AgN23WT" (n=6). The files belonging to Negative mode bare the "neg" suffix and those belonging to Positive mode "pos" suffix, i.e. "Col0AgN23WT1_neg" and Col0AgN23WT1_pos". The details regarding samples preparation, analytic parameters and mass spectrometry, statistical treatment and visualization of the data will be made available in the publication relating to this archive. </p>
Kroll et al., 2024. Behavioural pharmacology predicts disrupted signalling pathways and candidate therapeutics from zebrafish mutants of Alzheimer's disease risk genes
<p>Data repository for</p> <p>François Kroll, Joshua Donnelly, Joshua Donnelly, Güliz Gürel Özcan, Eirinn Mackay, Jason Rihel</p> <div> <div><strong>Behavioural pharmacology predicts disrupted signalling pathways and candidate therapeutics from zebrafish mutants of Alzheimer’s disease risk genes</strong></div> <br> <div>eLife, 2024.</div> <br> <div><a href="https://doi.org/10.7554/eLife.96839.1">https://doi.org/10.7554/eLife.96839.1</a></div> <div> </div> <div>Code is found in the <a href="https://github.com/francoiskroll/ZFAD">GitHub repository</a>. Please see notes there.</div> </div> <p>___</p> <p>Contact:</p> <p>Twitter: @francois_kroll</p> <p>Email: francois@kroll.be</p>
Exploring the Molecular Pathways of the Activation Process on PPARγ Recurrent Bladder Cancer Mutants
<p>The intricate involvement of Peroxisome Proliferator-Activated Receptor Gamma (PPARγ) in vital processes such as glucose homeostasis and adipogenesis is well established. However, its multifaceted role in cancer, particularly in luminal bladder cancer, remains a subject of intense debate. In this context, PPARγ’s overexpression and activation have been implicated in tumorigenesis. Notably, specific gain-of-function mutations (M280I, I290M, and T475M) within PPARγ’s ligand-binding domain have been pinpointed in bladder cancer, correlating with receptor activation. Nonetheless, the underlying molecular pathways prompted by these mutations remain obscure. Here, we employed a dual-basin structure-based model (db SBM) to unveil the intricate conformational dynamics that underlie the transition between PPARγ’s inactive and active states. Additionally, we explored the effects of the M280I, I290M, and T475M mutations on this pivotal process. Our findings concur with existing literature, revealing heightened ligand-independent transcriptional activity in the I290M and T475M mutants compared to other variants. Importantly, both mutants displayed enhanced stabilization of the active state relative to the wild-type receptor, and the I290M mutation promoted a remarkably specific transition route, rendering it a prime candidate for further investigation. Electrostatic analysis pinpointed the pivotal role of residues K303 and E488 in the activation cascade of I290M. This insight was substantiated by biophysical assays, as disruption of the K303-E488 interaction curtailed the thermal stabilization characteristic of the I290M mutation. These findings designate K303 and E488 as potential targets for inhibitors aimed at modulating PPARγ activation, with promising implications for refining bladder cancer prognosis. In sum, our study highlights the remarkable predictive capabilities achieved through the integration of simulation and cheminformatics methods, validated by biochemical experiments, to gain deeper insights into molecular mechanisms of activation and identify target residues for protein modulation.</p>
Mutant Harmonia axyridis raw sequencing data of CRISPR/Cas9 induced mutations in the genes laccase2 and scarlet
<p><em>Harmonia axyridis</em> (Pallas), commonly known as the Asian lady beetle, is a native insect species of Asia that has been intentionally introduced to various regions for biocontrol purposes. However, its widespread presence beyond its original release sites suggests a high degree of invasiveness. In this study, we utilized the CRISPR-Cas9 approach to achieve precise genome editing in <em>H. axyridis</em>. Specifically, we targeted two genes in <em>H. axyridis</em>, <em>laccase2</em> and <em>scarlet</em>, knockdown of which orthologs in other insects showed visible phenotypic changes. The knockout <em>laccase2</em> resulted in an early-detectable phenotype but also in lethality. However, we successfully established a viable and genetically stable mutant colony by disrupting the <em>scarlet </em>gene, resulting in beetles with white eyes. Our findings contribute to the expanding knowledge of genetic manipulation in <em>H. axyridis</em> and provide insights into its potential for future research and practical applications for biocontrol and invasive species management.</p>
ASO-mediated knockdown of GPNMB in mutant-GRN and Grn-deficient peripheral myeloid cells disrupts lysosomal function and immune responses
<p><strong>Background: </strong>Increases in GPNMB are detectable in FTD-<em>GRN</em> cerebrospinal fluid (CSF) and post-mortem brain, and brains of aged <em>Grn</em>-deficient mice. Although no upregulation of GPNMB is observed in the brains of young <em>Grn</em>-deficient mice, peripheral immune cells of these mice do exhibit this increase in GPNMB. Importantly, the functional significance of GPNMB upregulation in progranulin-deficient states is currently unknown. Given that GPNMB has been discussed as a potential therapeutic target in <em>GRN</em>-mediated neurodegeneration, it is vital for the field to determine what the normal function of GPNMB is in the immune system, and whether targeting GPNMB will elicit beneficial or deleterious effects.</p> <p><strong>Methods: </strong>The effects of GPNMB knock-down via antisense oligonucleotide (ASO) were assessed in peripheral blood mononuclear cells (PBMCs) from 25 neurologically healthy controls (NHCs) and age- and sex-matched FTD-<em>GRN </em>patients, as well as peritoneal macrophages (pMacs) from progranulin-deficient (<em>Grn</em><sup>-/-</sup>) and B6 mice. Lysosomal function, antigen presentation and MHC-II processing and recycling were assessed, as well as cytokine release and transcription.</p> <p><strong>Results: </strong>We demonstrate here that ASO-mediated knockdown of GPNMB increases lysosomal burden and cytokine secretion in FTD-GRN carrier and neurologically healthy controls (NHCs) monocytes. <span>ASO-mediated knockdown of GPNMB in <em>Grn</em>-deficient macrophages decreased lysosomal pan-cathepsin activity and protein degradation. In addition, </span>ASO-mediated knockdown of GPNMB increased MHC-II surface expression, which was driven by decreased MHC-II uptake and recycling, in macrophages from <em>Grn</em>-deficient females. Finally, ASO-mediated knockdown of GPNMB dysregulated IFN<span><span><span>g</span></span>-stimulated cytokine transcription and secretion by mouse macrophages due to the absence of regulatory actions of the GPNMB extracellular fragment (ECF). </span></p> <p><strong>Conclusions: </strong><span>Our data herein reveals that </span>GPNMB has a regulatory effect on multiple immune effector functions, including capping inflammation and immune responses in myeloid cells via secretion of its ECF. Therefore, in progranulin-deficient states, the drastic upregulation in GPNMB transcript and protein may represent a compensatory mechanism to preserve lysosomal function in myeloid cells. These novel findings indicate that targeted depletion in FTD-<em>GRN</em> would not be a rational therapeutic strategy because it is likely to dysregulate important immune cell effector functions.</p>
High-throughput phenotyping of salt-stress responses of the selected Arabidopsis hormone mutants
<p>This data was collected using Hight Throughput Phenotyping machine (psi.cz) purchased by KAUST in January 2018. The plants were germinated and grown under 12/12 light/dark light regime, 22C, 60% humidity for two weeks. After two weeks, half of the plants were exposed to approximately 100 mM NaCl (protocol described in Awlia et al., 2016, Frontiers in Plant Sci, <a href="https://doi.org/10.3389/fpls.2016.01414">https://doi.org/10.3389/fpls.2016.01414</a>). The rosettes of the plants were subsequently phenotyped using the Thermal Camera, RGB, and Chlorophyll Fluorescence camera (in this order). Chlorophyll fluorescence was measured after 15 minutes of dark adaptation using the "LightCurve2" protocol. </p> <p>The description of the traits is available in the notebook available at <a href="https://github.com/mmjulkowska/PSI_notebook">https://github.com/mmjulkowska/PSI_notebook</a> </p>
Engineering the plant intracellular immune receptor Sr50 to restore recognition of the AvrSr50 escape mutant
<p>The datasets for '<strong>Engineering the plant intracellular immune receptor Sr50 to restore recognition of the AvrSr50 escape mutant</strong><strong>'</strong>.</p> <p> </p> <p><strong>All_docking_models.zip</strong>: molecular docking models used to derive the initial structural hypothesis (Model I, Alternative models I and II). </p> <p><strong>Zdock1.AF2.zip</strong>: includes refined, relaxed structures of Model I. </p> <p><strong>Zdock5.AF2.zip</strong>: includes refined, relaxed structures of Alternative model II. </p> <p><strong>Zdock15.AF2.zip</strong>: includes refined, relaxed structures of Alternative moel I.</p> <p><strong>Model_II.zip</strong>: includes ColabDock outputs used as Model II.</p> <p><strong>Model_III.zip</strong>: includes ColabDock outputs used as Model III.</p> <p><strong>Model_IV.zip</strong>: includes ColabFold outputs used as Model IV.</p> <p><strong>Sr50*.AF.zip</strong>: predicted structures by ColabFold for the indicated pairs of the receptors and effectors. </p> <p> </p> <p>To read more about the workflow, please refer to https://github.com/s-kyungyong/Sr50-AvrSr50</p>
chr11 of the HoxBDel(i9-13):Ins(CBS5-10)/Del mutant genome used in Lopez-Delisle et al.
<p>Both alleles of chr11 of the HoxBDel(i9-13):Ins(CBS5-10)/Del mutant genome used in Lopez-Delisle et al..</p> <p>HoxBDel is a deletion of bases 96193822 to 96368393 included.<br></p> <p>HoxBDel(i9-13):Ins(CBS5-10) is composed of: a deletion of 96193812 to 96193909 included, deletion of 96197562 to 96264972 included, the insertion in place of 96266339 to 96266430 of a cassette of 3122bp containing 6 CBS binding sites (see below) and a deletion of 96368384 to 96368391 included. The cassette is composed of 96198511 to 96199030, followed by 96223753 to 96223991, followed by a 'G', followed by 96223992 to 96224032, followed by a 'T', followed by 96224033 to 96224272, followed by 96234852 to 96235371, followed by 96240168 to 96240687, followed by 96255914 to 96256433, followed by 96261499 to 96262018.</p> <p>The fasta files were built from chr11 of mm10 (http://hgdownload.soe.ucsc.edu/goldenPath/mm10/chromosomes/chr11.fa.gz).</p>
Chemical analyses and insect interactions of an easO mutant of Metarhizium brunneum
<p>Several fungi, including the plant root symbiont and insect pathogen <i>Metarhizium brunneum</i>, produce lysergic acid amides via a branch of the ergot alkaloid pathway. Lysergic acid amides include important pharmaceuticals and pharmaceutical lead compounds and have potential ecological significance, making knowledge of their biosynthesis relevant. Many steps in the biosynthesis of lysergic acid amides have been determined, but terminal steps in the synthesis of lysergic acid α-hydroxyethylamide (LAH)––by far the most abundant lysergic acid amide in <i>M. brunneum</i>––are unknown. Ergot alkaloid synthesis (<i>eas</i>) genes are clustered in the genomes of fungi that produce these compounds, and the <i>eas</i> clusters of LAH producers contain two uncharacterized genes (<i>easO</i> and <i>easP</i>) not found in fungi that do not produce LAH. Knockout of <i>easO</i> via a CRISPR-Cas9 approach eliminated LAH and resulted in accumulation of alternate lysergic acid amides lysergyl-alanine and ergonovine. Despite the elimination of LAH, the total concentration of lysergic acid derivatives was not affected significantly by the mutation. Complementation with a wild-type allele of <i>easO</i> restored the ability to synthesize LAH. Substrate feeding studies indicated that neither lysergyl-alanine nor ergonovine were substrates for the product of <i>easO</i> (EasO). EasO had structural similarity to Baeyer-Villiger monooxygenases (BVMOs), and labeling studies with deuterated alanine supported a role for a BVMO in LAH biosynthesis. The <i>easO</i> knockout had reduced virulence to larvae of the insect <i>Galleria mellonella</i>, indicating that LAH contributes to virulence of <i>M. brunneum</i> on insects and that LAH has biological activities different from ergonovine and lysergyl-alanine.</p>
Data from: Selective sets of mRNAs localize to extracellular paramural bodies in the rice glup6 mutant line
The transport of rice glutelin storage proteins to the storage vacuoles requires Rab5 and its cognate guanine nucleotide exchange factor (Rab5-GEF). Loss of function of these membrane vesicular trafficking factors results in the initial secretion of storage proteins and later their partial engulfment by the plasma membrane to form an extracellular paramural body (PMB); an aborted endosome complex. Here we show that in the Rab5-GEF mutant glup6 line, glutelin RNAs are specifically mis-localized from their normal location on the cisternal-ER to the protein body-ER and also apparently translocated to the PMBs. We substantiated the association of mRNAs with this aborted endosome complex by RNA-seq of PMBs purified by flow cytometry. Two PMB-associated RNA groups are readily resolved: those that are specifically enriched in this aborted complex and those that are highly expressed in the cytoplasm. Examination of the PMB-enriched RNAs indicates that they were not a random sampling of the glup6 transcriptome but, instead, encompassed only a few functional mRNA classes. Although specific autophagy is also an alternative mechanism, these studies support the view that RNA localization may co-opt membrane vesicular trafficking and that many RNAs, which share function or intracellular location, are co-transported in developing rice seeds.
Cell size, chlorophyll fluorescence and cadmium bioaccumulation between wild-type and mutant strains of Chlamydomonas reinhardtii upon exposure to cadmium
<p>Heavy metal contamination presents a constant threat to biological systems. Simultaneously, heavy metals have become one of the major contaminants in the aquatic ecosystem. In this regard, the investigation of heavy metal-tolerance genes in algae is relevant. <i>Chlamydomonas reinhardtii</i> is a unicellular green alga, and an excellent model organism used in heavy metal studies. In <i>C. reinhardtii</i>, a novel gene designated as Cia7, was hypothesized to play a role in heavy metal homeostasis due to CIA7's conserved cysteine-residue motif. This study compared two strains of <i>C. reinhardtii</i>, cc4425, the wild-type possessing the functional CIA7 protein and cc5013, the mutant strain possessing the disrupted cia7- gene. The hypothesis was that the expression of Cia7 contributes to an increased cadmium (Cd)-tolerance in <i>C. reinhardtii</i>. The Cd-tolerance would be described by physiological markers of microalgae health, and by intracellular accumulation of the metal. Methods: The objectives of this study were (1) to compare chlorophyll fluorescence and cell size in cc4425 and cc5013 exposed to Cd<sup>2+</sup>, and (2) to compare Cd<sup>2+</sup> bioaccumulation in cc4425 and cc5013 strains in different growth media. Flow cytometry, and inductively coupled plasma optical emission spectrometry (ICP-OES) analysis were performed. Results: There was no significant statistical difference in Cd<sup>2+</sup> bioaccumulation between the two strains, cc4425 and cc5013, regardless of growth media. However, a statistically significant difference in Cd<sup>2+</sup> bioaccumulation (p<0.0001) was determined between the media (with acetate and without acetate). The cia7- mutant, cc5013 was found to be more susceptible to a Cd<sup>2+</sup>-induced decrease in chlorophyll fluorescence and had a reduced cell size compared to cc4425, the wild-type strain. Conclusions: These observed differences between the strains suggest that CIA7's biological activity could play a direct or indirect role in increasing Cd tolerance in <i>C. reinhardtii</i>.</p>
FIGURE 2 in The structure of the cataract causing P23T mutant of human gamma-D crystallin
FIGURE 2. Ampelisca dingaal sp. nov., holotype, female, 7.1 mm, AM P75520, Cobia Hole, Lizard Island, Great Barrier Reef.
FIGURE 3 in The structure of the cataract causing P23T mutant of human gamma-D crystallin
FIGURE 3. Ampelisca dingaal sp. nov., holotype, female, 7.1 mm, AM P75520, Cobia Hole, Lizard Island, Great Barrier Reef.
FIGURE 1 in The structure of the cataract causing P23T mutant of human gamma-D crystallin
FIGURE 1. Ampelisca dimboola Lowry & Poore, 1985, female, 11.8 mm, AM P75275, Reef front, Fantome Island, Great Barrier Reef.
FIGURE 5 in The structure of the cataract causing P23T mutant of human gamma-D crystallin
FIGURE 5. Ampelisca jiigurru sp. nov., holotype, female, 7.1 mm, AM P75274, Mrs Watsons Bay, Lizard Island, Great Barrier Reef.
FIGURE 4 in The structure of the cataract causing P23T mutant of human gamma-D crystallin
FIGURE 4. Ampelisca jiigurru sp. nov., holotype, female, 7.1 mm, AM P75274, Mrs Watsons Bay, Lizard Island, Great Barrier Reef, paratype, male, 5.7 mm, AM P71034, near North Point, Lizard Island, Great Barrier Reef.
Mass spectrometry of natively decorated doublet microtubule from Tetrahymena thermophila WT and mutants
<p>Cilia are thin microtubule-based protrusions of eukaryotic cells. The swimming of ciliated protists and sperm cells is propelled by the beating of cilia. Cilia propagate the flow of mucus in the trachea and protect the human body from viral infections. The main force generators of ciliary beating are the outer dynein arms (ODAs) which attach to the doublet microtubules. The bending of cilia is driven by the ODAs' conformational changes caused by ATP hydrolysis. Here, we report the native ODA complex structure attaching to the doublet microtubule by cryo-electron microscopy and mass spectrometry. The structure reveals how the ODA complex is attached to the doublet microtubule via the docking complex in its native state. Combined with coarse-grained molecular dynamics simulations, we present a model of how the attachment of the ODA to the doublet microtubule induces remodeling and activation of the ODA complex.</p>
Single-nucleus Transcriptomics of IDH1- and TP53-mutant Glioma Stem Cells Displays Diversified Commitment on Highly Invasive Cancer Progenitors
<p><strong>Fig. S1</strong>. <strong>Marker genes for Seurat clusters.</strong> (<strong>A</strong>) distribution of marker genes for cluster 0 on the 2D-UMAP space. (<strong>B</strong>) distribution of marker genes for cluster 1 on the 2D-UMAP space. (<strong>C</strong>) distribution of marker genes for cluster 2 on the 2D-UMAP space. (<strong>D</strong>) distribution of marker genes for cluster 3 on the 2D-UMAP space. (<strong>E</strong>) distribution of marker genes for cluster 4 on the 2D-UMAP space. (<strong>F</strong>) distribution of marker genes for cluster 5 on the 2D-UMAP space. (<strong>G</strong>) Stuck violin plot of marker gene expression for Seurat clusters (bottom panel) and their annotation (right side panel). The violin shape displays the number of the cells expressing a gene, the continuous color panel defines median expression value of a gene from the absence of expression (white) to high expression (dark blue).</p> <p><strong>Fig. S2</strong>. <strong>Expression of genes marking cell malignization.</strong> (<strong>A</strong>) expression of collagens in Surat clusters (bottom panel) (<strong>B</strong>) expression of genes linked to Migration and ECM in Surat clusters (bottom panel) (<strong>C</strong>) expression of genes classified as Proto-oncogenes in Surat clusters (bottom panel). The violin shape displays the number of the cells expressing a gene, the violin color defines the Seurat cluster. Gene expression displayed in log-transformed normalized expression values.</p> <p><strong>Fig. S3</strong>. <strong>Expression of genes involved in proliferation and survival of cancer cells.</strong> (<strong>A</strong>) Genes involved in Wnt-pathway in Surat clusters (bottom panel). (<strong>B</strong>) Genes involved in Akt-pathway in Surat clusters (bottom panel). (<strong>C</strong>) Genes inducing resistance to cancer therapeutics in Surat clusters (bottom panel). The violin shape displays the number of the cells expressing a gene, the violin color defines the Seurat cluster. Gene expression displayed in log-transformed normalized expression values.\</p> <p><strong>Fig. S4</strong>. <strong>Expression of genes marking CSC profile.</strong> (<strong>A</strong>) Ion channel genes in Surat clusters (bottom panel). (<strong>B</strong>) Antioncogenes in Surat clusters (bottom panel). <strong>C</strong>. Stem-cell genes in Surat clusters (bottom panel). (<strong>D</strong>) Antiapoptotic genes in Surat clusters (bottom panel). The violin shape displays the number of the cells expressing a gene, the violin color defines the Seurat cluster. Gene expression displayed in log-transformed normalized expression values.</p> <p><strong>Fig. S5</strong>. <strong>Genes differentially expressed between UMAP clusters</strong>. (<strong>A</strong>) Heatmap for wt-GSCs. (<strong>B</strong>) Heatmap for mt-GSCs. Upper colour panel in the heatmap designates Seurat clusters. Gene expression is indicated by continuous colour panel starting from the most downregulated (blue) to the most upregulated (red).</p> <p><strong>Fig. S6</strong>. <strong>Marker genes defying cell annotations</strong>. (<strong>A</strong>) Stack violin plot displays marker gene expression in wt-GSC clusters. (<strong>B</strong>) Stack violin plot displays marker gene expression in mt-GSC clusters. Genes grouped by cell annotations (side description) and UMAP clusters (down column bar). The violin shape displays the number of the cells expressing a gene, the continuous color panel defines median expression value of a gene from the absence of expression (white) to high expression (dark blue).</p> <p><strong>Fig. S7</strong>. <strong>Differentially expressed proliferation and adhesion pathways comparing mutant samples to wild type.</strong> (<strong>A</strong>) ERBB signalling pathway. (<strong>B</strong>) Wnt signalling pathway. (<strong>C</strong>) Genes linked to Focal adhesion. (<strong>D</strong>) Genes classified as Cell adhesion molecules. Red rectangles display upregulated genes (proteins), green rectangles define downregulated genes (proteins). Pictures obtained by KEGG pathview.</p> <p><strong>Table S1. Glioma genotyping primers</strong></p> <p><strong>Table S2. Smart-seq2 Primers</strong></p>
RNA sequencing of PET127 mutants overexpressed using the galactose inducible promoter
<p>In Saccharomyces cerevisiae, <em>PET127</em> is a mitochondrial RNA exonuclease known to interact with the mitochondrial RNA polymerase <em>RPO41</em>. The nature of the interaction between <em>PET127</em> and <em>RPO41</em> is unclear. Here, we overexpressed different <em>PET127</em> mutants for five hours utilizing the galactose inducible promoter on high-copy plasmids, collected samples, and performed RNA sequencing to understand the mitochondrial RNA landscape in each condition. The mutants tested were <em>PET127</em> lacking the nuclease activity (<em>pet127-nd</em>) and two truncated forms of <i>PET127</i>: either lacking the <em>RPO41</em> binding region (<i>pet127∆(48-215</i>)), or only containing the <i>RPO41</i> binding region (<em>pet127(1-215)</em>).</p>
Starting Coordinates for DNA Polymerase III* WT and Mutants
<p>Included are the starting coordinates and parameters for both MD and QM/MM simulations of DNA Polymerase III* of <em>E. coli</em>. The mutants studied were ß-L82E/L82'E and ß-L82D/L82'D. Systems studied include one with shorter DNA and the other with longer DNA.</p>
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.