Front Plant Sci. 2025 Jan 20;16:1541642. doi: 10.3389/fpls.2025.1541642. eCollection 2025.

NO ABSTRACT

PMID:39906500 | PMC:PMC11788399 | DOI:10.3389/fpls.2025.1541642

JBMR Plus. 2025 Jan 30;9(3):ziae173. doi: 10.1093/jbmrpl/ziae173. eCollection 2025 Mar.

ABSTRACT

Activating internal tandem duplications (ITD) in the juxtamembrane domain of receptor tyrosine kinase FLT3 occur frequently in patients with acute myeloid leukemia (AML). Constitutive active FLT3-ITD mutations induce aberrant signaling and promote leukemic cell transformation. Inactivation of the attenuating receptor protein tyrosine phosphatase CD45 (PTPRC) in FLT3-ITD mice resulted in the development of a severe hematopoietic phenotype with characteristics of AML. In addition, abnormal bone structures and ectopic bone formation were observed in these mice, suggesting a previously unknown role of FLT3 to control bone development and remodeling. While Ptprc knockout and Flt3-ITD mutant mice showed a largely normal bone microarchitecture, micro-CT analysis of femurs from Flt3-ITD Ptprc knockout mice revealed trabecularization of the cortical bone. This resulted in increased trabecular bone volume at the metaphysis, while the cortical bone at the diaphysis was thinner and less dense. In the metaphysis, severely reduced osteoclast and osteoblast numbers were observed. Reduced capacity of ex vivo differentiation of CD11b-positive bone marrow stem cells to mature osteoclast was accompanied by their abnormal morphology and reduced size. Transcriptome analysis revealed reduced expression of osteoclastogenic genes. Unexpectedly, cumulative resorption activity of osteoclasts was increased. Size and structure of resorption pits of differentiated osteoclasts remained similar to those observed in osteoclast cultures derived from control animals. Enhanced proliferation of cells in osteoclast cultures derived from FLT3-ITD-expressing mice was mediated by increased expression of STAT5 target genes. Transcriptome analysis of differentiated osteoclasts showed dysregulated signaling pathways influencing their differentiation as well as the coupling of bone resorption and formation. Taken together, inactivation of attenuating CD45 in mice expressing oncogenic FLT3-ITD resulted in marked abnormalities of the osteo-hematopoietic niche, which can be explained by aberrant STAT5 activation.

PMID:39906260 | PMC:PMC11788565 | DOI:10.1093/jbmrpl/ziae173

Hortic Res. 2024 Oct 23;12(2):uhae291. doi: 10.1093/hr/uhae291. eCollection 2025 Jan.

ABSTRACT

The large diversity of grapevine cultivars includes genotypes more tolerant to water deficit than others. Widely distributed cultivars, like Merlot, are more sensitive to water deprivation than local cultivars like Callet, which are more adapted to water deficit due to their Mediterranean origin. Despite their tolerance, adaptation to water deficit influenced by grafting in rootstocks like 110 Richter is key to facing drought in vineyards, defining the scion-rootstock relationship. To understand these differences, we explored transcriptomic, metabolic, hormonal and physiological responses under three levels of water deficit (mild, high, and extreme), using 110 Richter as the rootstock in both cultivars. Results revealed that sensitivity to abscisic acid (ABA) is essential for water deficit tolerance in the aerial part, guiding root responses. Callet/110 Richter activates more gene expression patterns in response to ABA, reducing water loss compared to Merlot/110 Richter in both aerial and root parts. This modulation in Callet/110 Richter involves regulating metabolic pathways to increase cell turgor, reducing photosynthesis, and producing molecules like polyphenols or flavonoids to respond to oxidative stress. In contrast, Merlot/110 Richter shows a lack of specific response, especially in the roots, indicating less resilience to water stress. Therefore, selecting genotypes more sensitive to ABA and their interaction with rootstocks is key for managing vineyards in future climate change scenarios.

PMID:39906169 | PMC:PMC11789524 | DOI:10.1093/hr/uhae291

Environ Microbiome. 2025 Feb 4;20(1):17. doi: 10.1186/s40793-025-00677-7.

ABSTRACT

Urban green areas provide multiple ecosystem services in cities, mitigating environmental risks and providing a healthier environment for humans. Even if urban ecology has become popular in the last decade, the soil environment with its microbiota, which sustains many other biodiversity layers, remains overlooked. Here, a comprehensive database of scientific papers published in the last 30 years investigating different aspects of soil microbial diversity was built and systematically reviewed. The aim was to identify the taxa, experimental methods and geographical areas that have been investigated, and to highlight gaps in knowledge and research prospects. Our results show that current knowledge on urban soil microbiota remains incomplete, mainly due to the lack of publications on functional aspects, and is biased, in terms of investigated taxa, with most studies focused on Prokaryotes, and geographic representativeness, with the interest focused on a few large cities in the Northern hemisphere. By coupling bibliometrics with statistical modelling we found that soil microbial traits such as biomass and respiration and omics techniques attract the interest of the scientific community while multi-taxa and time-course studies appeal more to the general public.

PMID:39905522 | DOI:10.1186/s40793-025-00677-7

BMC Genomics. 2025 Feb 4;26(1):106. doi: 10.1186/s12864-025-11308-3.

ABSTRACT

BACKGROUND: Chickpea (Cicer arietinum L.) ranks as the third most crucial grain legume worldwide. Fusarium wilt (Fusarium oxysporum f. sp. ciceri (Foc)) is a devastating fungal disease that prevents the maximum potential for chickpea production.

RESULTS: To identify genes and pathways involved in resistance to race 6 of Foc, this study utilized transcriptome sequencing of two chickpea cultivars: resistant (Ana) and susceptible (Hashem) to Foc race 6. Illumina sequencing of the root samples yielded 133.5 million raw reads, with about 90% of the clean reads mapped to the chickpea reference genome. The analysis revealed that 548 genes (332 upregulated and 216 downregulated) in the resistant genotype (Ana) and 1115 genes (595 upregulated and 520 downregulated) in the susceptible genotype (Hashem) were differentially expressed under Fusarium wilt (FW) disease stress caused by Foc race 6. The expression patterns of some differentially expressed genes (DEGs) were validated using quantitative real-time PCR. A total of 131 genes were exclusively upregulated under FW stress in the resistant cultivar, including several genes involved in sensing (e.g., CaNLR-RPM1, CaLYK5-RLK, CaPR5-RLK, CaLRR-RLK, and CaRLP-EIX2), signaling (e.g., CaPP7, CaEPS1, CaSTY13, and CaPR-1), transcription regulation (e.g., CaMYBs, CaGLK, CaERFs, CaZAT11-like, and CaNAC6) and cell wall integrity (e.g., CaPGI2-like, CaEXLs, CaCSLD and CaCYP73A100-like).

CONCLUSIONS: The achieved results could provide insights into the molecular mechanism underlying resistance to FW and could be valuable for breeding programs aimed at developing FW-resistant chickpea varieties.

PMID:39905311 | DOI:10.1186/s12864-025-11308-3

Genet Sel Evol. 2025 Feb 4;57(1):3. doi: 10.1186/s12711-025-00951-9.

ABSTRACT

BACKGROUND: Milk production traits are complex and influenced by many genetic and environmental factors. Although extensive research has been performed for these traits, with many associations unveiled thus far, due to their crucial economic importance, complex genetic architecture, and the fact that causal variants in cattle are still scarce, there is a need for a better understanding of their genetic background. In this study, we aimed to identify new candidate loci associated with milk production traits in German Holstein cattle, the most important dairy breed in Germany and worldwide. For that purpose, 180,217 cattle were imputed to the sequence level and large-scale genome-wide association study (GWAS) followed by fine-mapping and evolutionary and functional annotation were carried out to identify and prioritize new association signals.

RESULTS: Using the imputed sequence data of a large cattle dataset, we identified 50,876 significant variants, confirming many known and identifying previously unreported candidate variants for milk (MY), fat (FY), and protein yield (PY). Genome-wide significant signals were fine-mapped with the Bayesian approach that determines the credible variant sets and generates the probability of causality for each signal. The variants with the highest probabilities of being causal were further classified using external information about the function and evolution, making the prioritization for subsequent validation experiments easier. The top potential causal variants determined with fine-mapping explained a large percentage of genetic variance compared to random ones; 178 variants explained 11.5%, 104 explained 7.7%, and 68 variants explained 3.9% of the variance for MY, FY, and PY, respectively, demonstrating the potential for causality.

CONCLUSIONS: Our findings proved the power of large samples and sequence-based GWAS in detecting new association signals. In order to fully exploit the power of GWAS, one should aim at very large samples combined with whole-genome sequence data. These can also come with both computational and time burdens, as presented in our study. Although milk production traits in cattle are comprehensively investigated, the genetic background of these traits is still not fully understood, with the potential for many new associations to be revealed, as shown. With constantly growing sample sizes, we expect more insights into the genetic architecture of milk production traits in the future.

PMID:39905301 | DOI:10.1186/s12711-025-00951-9

Nat Genet. 2025 Feb 4. doi: 10.1038/s41588-025-02078-5. Online ahead of print.

ABSTRACT

Cell division drives somatic evolution but is challenging to quantify. We developed a framework to count cell divisions with DNA replication-related mutations in polyguanine homopolymers. Analyzing 505 samples from 37 patients, we studied the milestones of colorectal cancer evolution. Primary tumors diversify at ~250 divisions from the founder cell, while distant metastasis divergence occurs significantly later, at ~500 divisions. Notably, distant but not lymph node metastases originate from primary tumor regions that have undergone surplus divisions, tying subclonal expansion to metastatic capacity. Then, we analyzed a cohort of 73 multifocal lung cancers and showed that the cell division burden of the tumors' common ancestor distinguishes independent primary tumors from intrapulmonary metastases and correlates with patient survival. In lung cancer too, metastatic capacity is tied to more extensive proliferation. The cell division history of human cancers is easily accessible using our simple framework and contains valuable biological and clinical information.

PMID:39905260 | DOI:10.1038/s41588-025-02078-5

Nat Immunol. 2025 Feb 4. doi: 10.1038/s41590-024-02075-6. Online ahead of print.

ABSTRACT

Regulatory T (Treg) cells are a specialized CD4+ T cell lineage with essential anti-inflammatory functions. Analysis of Treg cell adaptations to non-lymphoid tissues that enable their specialized immunosuppressive and tissue-supportive functions raises questions about the underlying mechanisms of these adaptations and whether they represent stable differentiation or reversible activation states. Here, we characterize distinct colonic effector Treg cell transcriptional programs. Attenuated T cell receptor (TCR) signaling and acquisition of substantial TCR-independent functionality seems to facilitate the terminal differentiation of a population of colonic effector Treg cells that are distinguished by stable expression of the immunomodulatory cytokine IL-10. Functional studies show that this subset of effector Treg cells, but not their expression of IL-10, is indispensable for colonic health. These findings identify core features of the terminal differentiation of effector Treg cells in non-lymphoid tissues and their function.

PMID:39905200 | DOI:10.1038/s41590-024-02075-6

Nat Rev Gastroenterol Hepatol. 2025 Feb 4. doi: 10.1038/s41575-025-01039-x. Online ahead of print.

NO ABSTRACT

PMID:39905174 | DOI:10.1038/s41575-025-01039-x

Nat Commun. 2025 Feb 4;16(1):1346. doi: 10.1038/s41467-025-56590-7.

ABSTRACT

Cell signaling plays a critical role in neurodevelopment, regulating cellular behavior and fate. While multimodal single-cell sequencing technologies are rapidly advancing, scalable and flexible profiling of cell signaling states alongside other molecular modalities remains challenging. Here we present Phospho-seq, an integrated approach that aims to quantify cytoplasmic and nuclear proteins, including those with post-translational modifications, and to connect their activity with cis-regulatory elements and transcriptional targets. We utilize a simplified benchtop antibody conjugation method to create large custom neuro-focused antibody panels for simultaneous protein and scATAC-seq profiling on whole cells, alongside both experimental and computational strategies to incorporate transcriptomic measurements. We apply our workflow to cell lines, induced pluripotent stem cells, and months-old retinal and brain organoids to demonstrate its broad applicability. We show that Phospho-seq can provide insights into cellular states and trajectories, shed light on gene regulatory relationships, and help explore the causes and effects of diverse cell signaling in neurodevelopment.

PMID:39905064 | DOI:10.1038/s41467-025-56590-7

Nat Commun. 2025 Feb 4;16(1):1347. doi: 10.1038/s41467-025-56646-8.

ABSTRACT

Ion suppression is a major problem in mass spectrometry (MS)-based metabolomics; it can dramatically decrease measurement accuracy, precision, and sensitivity. Here we report a method, the IROA TruQuant Workflow, that uses a stable isotope-labeled internal standard (IROA-IS) library plus companion algorithms to: 1) measure and correct for ion suppression, and 2) perform Dual MSTUS normalization of MS metabolomic data. We evaluate the method across ion chromatography (IC), hydrophilic interaction liquid chromatography (HILIC), and reversed-phase liquid chromatography (RPLC)-MS systems in both positive and negative ionization modes, with clean and unclean ion sources, and across different biological matrices. Across the broad range of conditions tested, all detected metabolites exhibit ion suppression ranging from 1% to >90% and coefficients of variation ranging from 1% to 20%, but the Workflow and companion algorithms are highly effective at nulling out that suppression and error. To demonstrate a routine application of the Workflow, we employ the Workflow to study ovarian cancer cell response to the enzyme-drug L-asparaginase (ASNase). The IROA-normalized data reveal significant alterations in peptide metabolism, which have not been reported previously. Overall, the Workflow corrects ion suppression across diverse analytical conditions and produces robust normalization of non-targeted metabolomic data.

PMID:39905052 | DOI:10.1038/s41467-025-56646-8

Nat Commun. 2025 Feb 4;16(1):1356. doi: 10.1038/s41467-025-56533-2.

ABSTRACT

Pluripotent stem cells provide a scalable approach to analyse molecular regulation of cell differentiation across developmental lineages. Here, we engineer barcoded induced pluripotent stem cells to generate an atlas of multilineage differentiation from pluripotency, encompassing an eight-day time course with modulation of WNT, BMP, and VEGF signalling pathways. Annotation of in vitro cell types with reference to in vivo development reveals diverse mesendoderm lineage cell types including lateral plate and paraxial mesoderm, neural crest, and primitive gut. Interrogation of temporal and signalling-specific gene expression in this atlas, evaluated against cell type-specific gene expression in human complex trait data highlights the WNT-inhibitor gene TMEM88 as a regulator of mesendodermal lineages influencing cardiovascular and anthropometric traits. Genetic TMEM88 loss of function models show impaired differentiation of endodermal and mesodermal derivatives in vitro and dysregulated arterial blood pressure in vivo. Together, this study provides an atlas of multilineage stem cell differentiation and analysis pipelines to dissect genetic determinants of mammalian developmental physiology.

PMID:39904980 | DOI:10.1038/s41467-025-56533-2

Nat Commun. 2025 Feb 4;16(1):1094. doi: 10.1038/s41467-024-55085-1.

ABSTRACT

UDP-GlcNAc serves as a building block for glycosaminoglycan (GAG) chains in cartilage proteoglycans and simultaneously acts as a substrate for O-GlcNAcylation. Here, we show that transporters for UDP-GlcNAc to the endoplasmic reticulum (ER) and Golgi are significantly downregulated in osteoarthritic cartilage, leading to increased cytosolic UDP-GlcNAc and O-GlcNAcylation in chondrocytes. Mechanistically, upregulated O-GlcNAcylation governs the senescence-associated secretory phenotype (SASP) by stabilizing GATA4 via O-GlcNAcylation at S406, which compromises its degradation by p62-mediated selective autophagy. Elevated O-GlcNAcylation in the superficial layer of osteoarthritic cartilage coincides with increased GATA4 levels. The topical deletion of Gata4 in this cartilage layer ameliorates post-traumatic osteoarthritis (OA) in mice while inhibiting O-GlcNAc transferase mitigates OA by decreasing GATA4 levels. Excessive glucosamine-induced O-GlcNAcylation stabilizes GATA4 in chondrocytes and exacerbates post-traumatic OA in mice. Our findings elucidate the role of UDP-GlcNAc compartmentalization in regulating secretory pathways associated with chronic joint inflammation, providing a senostatic strategy for the treatment of OA.

PMID:39904978 | DOI:10.1038/s41467-024-55085-1

Open Biol. 2025 Feb;15(2):240291. doi: 10.1098/rsob.240291. Epub 2025 Feb 5.

ABSTRACT

Peroxisomes are essential organelles involved in critical metabolic processes in animals such as fatty acid oxidation, ether phospholipid production and reactive oxygen species detoxification. We have generated transgenic Drosophila melanogaster models expressing fluorescent reporters for the selective autophagy of peroxisomes, a process known as pexophagy. We show that these reporters are colocalized with a peroxisomal marker and that they can reflect pexophagy induction by iron chelation and inhibition by depletion of the core autophagy protein Atg5. Using light sheet microscopy, we have been able to obtain a global overview of pexophagy levels across the entire organism at different stages of development. Tissue-specific control of pexophagy is exemplified by areas of peroxisome abundance but minimal pexophagy, observed in clusters of oenocytes surrounded by epithelial cells where pexophagy is much more evident. Enhancement of pexophagy was achieved by feeding flies with the iron chelator deferiprone, in line with past results using mammalian cells. Specific drivers were used to visualize pexophagy in neurons, and to demonstrate that specific depletion in the larval central nervous system of Hsc70-5, the Drosophila homologue of the chaperone HSPA9/mortalin, led to a substantial elevation in pexophagy.

PMID:39904371 | DOI:10.1098/rsob.240291

Immunity. 2025 Jan 31:S1074-7613(25)00032-9. doi: 10.1016/j.immuni.2025.01.007. Online ahead of print.

ABSTRACT

Activation of the NLRP3 inflammasome has been implicated in the pathogenesis of Alzheimer's disease (AD) via the release of IL-1β and ASC specks. However, whether NLRP3 is involved in pathways beyond this remained unknown. Here, we found that Aβ deposition in vivo directly triggered NLRP3 activation in APP/PS1 mice, which model many features of AD. Loss of NLRP3 increased glutamine- and glutamate-related metabolism and increased expression of microglial Slc1a3, which was associated with enhanced mitochondrial and metabolic activity. The generation of α-ketoglutarate during this process impacted cellular function, including increased clearance of Aβ peptides as well as epigenetic and gene transcription changes. This pathway was conserved between murine and human cells. Critically, we could mimic this effect pharmacologically using NLRP3-specific inhibitors, but only with chronic NLRP3 inhibition. Together, these data demonstrate an additional role for NLRP3, where it can modulate mitochondrial and metabolic function, with important downstream consequences for the progression of AD.

PMID:39904338 | DOI:10.1016/j.immuni.2025.01.007

PLoS Pathog. 2025 Feb 4;21(2):e1012813. doi: 10.1371/journal.ppat.1012813. eCollection 2025 Feb.

ABSTRACT

The var multigene family encodes Plasmodium falciparum erythrocyte membrane protein 1 (PfEMP1), central to host-parasite interactions. Genome structure studies have identified three major groups of var genes by specific upstream sequences (upsA, B, or C). Var with these ups groups have different chromosomal locations, transcriptional directions, and associations with disease severity. Here we explore temporal and spatial diversity of a region of var genes encoding the DBLα domain of PfEMP1 in Africa. By applying a novel ups classification algorithm (cUps) to publicly-available DBLα sequence datasets, we categorised DBLα according to association with the three ups groups, thereby avoiding the need to sequence complete genes. Data from deep sequencing of DBLα types in a local population in northern Ghana surveyed seven times from 2012 to 2017 found variants with rare-to-moderate-to-extreme frequencies, and the common variants were temporally stable in this local endemic area. Furthermore, we observed that every isolate repertoire, whether mono- or multiclonal, comprised DBLα types occurring with these frequency ranges implying a common genome structure. When comparing African countries of Ghana, Gabon, Malawi, and Uganda, we report that some DBLα types were consistently found at high frequencies in multiple African countries while others were common only at the country level. The implication of these local and pan-Africa population patterns is discussed in terms of advantage to the parasite with regards to within-host adaptation and resilience to malaria control.

PMID:39903780 | DOI:10.1371/journal.ppat.1012813

Melanoma Res. 2025 Feb 4. doi: 10.1097/CMR.0000000000001025. Online ahead of print.

ABSTRACT

While the association between chronic lymphocytic leukemia (CLL) and a higher incidence of melanoma is well documented, the diagnosis of concurrent high-risk chronic myelomonocytic leukemia (CMML) and metastatic melanoma (MM) has not previously been described. Moreover, the treatment of MM and CMML differ greatly in the mechanism of action of their corresponding antineoplastic therapies: treatment of MM frequently involves immune checkpoint inhibitors (ICI), while patients with CMML receive myelosuppressive agents. Simultaneous management of these malignancies can be nuanced due to the potential impact of one treatment's constituents on the activity of the other and the broad and nonoverlapping array of potential adverse effects of these agents. Here, we describe the clinical course of a patient who was diagnosed with concurrent MM and CMML and our approach to the challenging balance of delivering ICI concurrently with the hypomethylating agent azacitidine and the BCL-2 inhibitor venetoclax.

PMID:39903257 | DOI:10.1097/CMR.0000000000001025

J Virol. 2025 Feb 4:e0141324. doi: 10.1128/jvi.01413-24. Online ahead of print.

ABSTRACT

Type III interferons (IFNs) primarily act on epithelial cells and protect against virus infection of the mucosa, whereas type I IFNs act more systemically. To date, it has been unknown which epithelial subtypes in the upper airways, the primary site for initial infection for most respiratory viruses, primarily rely on type III IFN or type I IFNs for antiviral protection. To address this question, we performed a single-cell transcriptomics analysis of the epithelial IFN-mediated response focusing on the upper airways of mice. This work identified nine distinct cell types derived from the olfactory epithelium and thirteen distinct cell types from the respiratory epithelium. Interestingly, type I IFNs induced a stronger antiviral transcriptional response than type III IFN in respiratory epithelial cells, whereas in olfactory epithelial cells, including sustentacular (SUS) and Bowman's gland cells (BGC), type III IFN was more dominant compared to type I IFN. SUS and BGC, which provide structural support and maintain the integrity of olfactory sensory neurons, were highly susceptible to infection with a mouse-adapted variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2 MA20) but were protected against infection if the animals were prophylactically treated with type III IFN. These findings demonstrate a high degree of cell type heterogeneity in terms of interferon-mediated antiviral responses and reveal a potent role for type III IFNs in protecting the olfactory epithelium.IMPORTANCESARS-CoV-2 infects SUS and BGC in the olfactory epithelium, causing an impairment of structural support and integrity of olfactory sensory neurons that can result in severe olfactory dysfunctions. We observed an unexpected compartmentalization of the IFN-mediated transcriptional response within the airway epithelium, and we found that olfactory epithelial cells preferentially respond to type III IFN, which resulted in robust antiviral protection of SUS and BGC. Given the proximity of the olfactory epithelium to the central nervous system, we hypothesize that evolution favored a type III IFN-biased antiviral immune response in this tissue to limit inflammatory responses in the brain. Cell type-specific antiviral responses in the upper airways, triggered by the different types of IFNs, should be investigated in more detail and carefully taken into consideration during the development of IFN-based antivirals for clinical use.

PMID:39902863 | DOI:10.1128/jvi.01413-24

Front Cell Infect Microbiol. 2025 Jan 20;14:1502339. doi: 10.3389/fcimb.2024.1502339. eCollection 2024.

ABSTRACT

Conserved histone methyltransferases of the DOT1 family are involved in replication regulation, cell cycle progression, stage differentiation, and gene regulation in trypanosomatids. However, the specific functions of these enzymes depend on the host evasion strategies of the parasites. In this study, we investigated the role of DOT1B in Leishmania mexicana, focusing on life cycle progression and infectivity. In contrast to Trypanosoma brucei, in which DOT1B is essential for the differentiation of mammal-infective bloodstream forms to insect procyclic forms, L. mexicana DOT1B (LmxDOT1B) is not critical for the differentiation of promastigotes to amastigotes in vitro. Additionally, there are no significant differences in the ability to infect or differentiate in macrophages or sand fly vectors between the LmxDOT1B-depleted and control strains. These findings highlight the divergence of the function of DOT1B in these related parasites, suggesting genus-specific adaptations in the use of histone modifications for life cycle progression and host adaptation processes.

PMID:39902184 | PMC:PMC11788152 | DOI:10.3389/fcimb.2024.1502339

Front Immunol. 2025 Jan 20;15:1439434. doi: 10.3389/fimmu.2024.1439434. eCollection 2024.

ABSTRACT

Multi-cellular biological systems, including the immune system, are highly complex, dynamic, and adaptable. Systems biologists aim to understand such complexity at a quantitative level. However, these ambitious efforts are often limited by access to a variety of high-density intra-, extra- and multi-cellular measurements resolved in time and space and across a variety of perturbations. The advent of automation, OMICs and single-cell technologies now allows high dimensional multi-modal data acquisition from the same biological samples multiplexed at scale (multi-OMICs). As a result, systems biologists -theoretically- have access to more data than ever. However, the mathematical frameworks and computational tools needed to analyze and interpret such data are often still nascent, limiting the biological insights that can be obtained without years of computational method development and validation. More pressingly, much of the data sits in silos in formats that are incomprehensible to other scientists or machines limiting its value to the vaster scientific community, especially the computational biologists tasked with analyzing these vast amounts of data in more nuanced ways. With the rapid development and increasing interest in using artificial intelligence (AI) for the life sciences, improving how biologic data is organized and shared is more pressing than ever for scientific progress. Here, we outline a practical approach to multi-modal data management and FAIR sharing, which are in line with the latest US and EU funders' data sharing policies. This framework can help extend the longevity and utility of data by allowing facile use and reuse, accelerating scientific discovery in the biomedical sciences.

PMID:39902035 | PMC:PMC11788310 | DOI:10.3389/fimmu.2024.1439434