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Biology subjects

Cao, E. Y.

Publications and source records attributed to Cao, E. Y..

7 recordsLinked to original sources

Isoform-level discovery, quantification and fusion analysis from single-cell and spatial long-read RNA-seq data with Bambu-Clump

Single cell and spatial transcriptomics have dramatically changed how we can profile RNA from heterogenous biological samples. Combining single cell and spatial profiling with long read RNA-Seq promises to enable the discovery and quantification of individual RNA isoforms at the single-cell level. However, highly multiplexed data such as from a single cell experiment only generates a limited number of reads for each cell, constituting a major challenge for transcript discovery and quantification with existing approaches that usually have limited power for samples with low sequencing depth. Here we present Bambu-Clump, a computational method that performs transcript discovery and quantification from single cell and spatial long read RNA-Seq data using information from both each cell and the cell cluster. Using this approach, Bambu-Clump provides the most accurate transcript discovery compared to other existing methods, and improves transcript quantification compared to methods that rely on estimates derived from single cells. We apply Bambu-Clump to identify fusion transcripts in single-cells, compare 5 and 3 selection protocols, and identify novel isoform cell-type markers in spatial mouse brain data. Together, Bambu-Clump provides an easy-to-use, efficient, and accurate method for analysing individual isoform expression for single cells and cell clusters across multiple datasets and replicates from long read RNA-Seq.

bioinformatics↗

The commensal protist Tritrichomonas musculus exhibits a dynamic life cycle that induces B cell-modulated remodeling of the gut microbiota

Commensal protists and gut bacterial communities exhibit complex relationships, mediated at least in part through host immunity. To improve our understanding of this tripartite interplay, we investigated community and functional dynamics between the murine protist Tritrichomonas musculus (T. mu) and intestinal bacteria in healthy and B cell-deficient mice. We identified dramatic, protist-driven remodeling of resident microbiome growth and activities, in parallel with T. mu functional changes, accelerated in the absence of B cells. Metatranscriptomic data revealed nutrient-based competition between bacteria and the protist. Single cell transcriptomics identified distinct T. mu life stages, providing new evidence for trichomonad sexual replication and the formation of pseudocysts. Unique cell states were validated in situ through microscopy and flow cytometry. Our results reveal complex microbial dynamics during the establishment of a commensal protist in the gut, and provide valuable datasets to drive future mechanistic studies.

microbiology↗

The protozoan commensal Tritrichomonas musculis is a natural adjuvant for mucosal IgA.

Immunoglobulin(Ig) A antibodies are the most abundant antibodies supporting mucosal immune homeostasis and host-microbiota interactions. Driven by gut commensal microbes, IgA-secreting plasma cells (PC) differentiate through T cell-dependent (Td) or T cell independent (Ti) mechanisms. While commensal bacteria within the microbiota are known for their ability to promote IgA, the role of non-bacterial commensal microbes on the induction of IgA remains elusive. Here, we demonstrate that permanent colonization with the protozoan commensal Tritrichomonas musculis (T.mu) promotes T-cell dependent, IgA class-switch recombination and intestinal accumulation of IgA-secreting PC. T.mu colonization specifically drives the expansion of T follicular helper cells and a unique ICOS+ non-Tfh cell population, accompanied by an increase in germinal center B cells. Blockade of ICOS:ICOSL co-stimulation or MHCII-expression on B cells are central for the induction of IgA following colonization by T.mu, implicating a previously underappreciated mode of IgA induction following protozoan commensal colonization. Finally, the commensal T.mu further improves the induction of IgA-secreting plasma cells and their peripheral dissemination, even against non-protozoan, orally ingested antigens, identifying T.mu as natural adjuvant for IgA. Collectively, these findings propose a previously unknown, protozoa-driven mode of IgA induction that supports intestinal immune homeostasis even against non-microbial antigens.

immunology↗

Microbial Energy Metabolism Fuels a CSF2-dependent Intestinal Macrophage Niche within Tertiary Lymphoid Organs

Maintaining intestinal macrophage (MP) heterogeneity is critical to ensure tissue homeostasis and host defense. The gut microbiota and host factors are thought to synergistically shape colonic MP development, although there remains a fundamental gap in our understanding of the details of such collaboration. Here, we report tertiary lymphoid organs (TLOs), enriched in group 3 innate lymphoid cells (ILC3s), as a microbiota-operated intestinal niche for the development of monocyte-derived MPs. ILC3-derived colony stimulating factor 2 (CSF2) serves as a developmental and functional determinant for MPs and required microbe-derived extracellular adenosine 5-triphosphate (ATP) as a trigger. Microbial communities rich in extracellular ATP promoted MP turnover via ILC3 activity in an NLRP3-dependent fashion. Single cell RNA-sequencing of MPs revealed unique TLO-associated, CSF2-dependent MP populations critical for anti-microbial defense against enteric infection. Collectively, these findings describe a fundamental framework that constitutes an intestinal MP niche fueled by microbial energy metabolism.

immunology↗

NLRP1B and NLRP3 control the host response following colonization by the commensal protist Tritrichomonas musculis.

Commensal intestinal protozoa, unlike their pathogenic relatives, are neglected members of the mammalian microbiome. These microbes have a significant impact on the hosts intestinal immune homeostasis, typically by elevating anti-microbial host defense. Tritrichomonas musculis (T. mu), a protozoan gut commensal, strengthens the intestinal host defense against enteric Salmonella infections through Asc- and Il1r1-dependent Th1 and Th17 cell activation. However, the underlying inflammasomes mediating this effect remain unknown. Here, we report that colonization with T. mu results in an increase in luminal extracellular ATP, elevated levels of IL-1{beta}, and increased numbers of IL-18 receptor-expressing Th1 and Th17 cells in the colon. Mice deficient in either Nlrp1b or Nlrp3 failed to display these protozoan-driven immune changes and lost resistance to enteric Salmonella infections even in the presence of T. mu. These findings demonstrate that T. mu-mediated host protection requires sensors of extra and intracellular ATP to confer resistance to enteric Salmonella infections. KEY POINTSO_LIIntestinal colonization with the commensal Tritrichomonas musculis elevates luminal ATP levels C_LIO_LINLRP1B and NLRP3 activation is required for Tritrichomonas musculis-driven Th cell response. C_LI

immunology↗

ShinyCell: Simple and sharable visualisation of single-cell gene expression data

MotivationAs the generation of complex single-cell RNA sequencing datasets becomes more commonplace it is the responsibility of researchers to provide access to these data in a way that can be easily explored and shared. Whilst it is often the case that data is deposited for future bioinformatic analysis many studies do not release their data in a way that is easy to explore by non-computational researchers. ResultsIn order to help address this we have developed ShinyCell, an R package that converts single-cell RNA sequencing datasets into explorable and shareable interactive interfaces. These interfaces can be easily customised in order to maximise their usability and can be easily uploaded to online platforms to facilitate wider access to published data. AvailabilityShinyCell is available at https://github.com/SGDDNB/ShinyCell. Contactowen.rackham@duke-nus.edu.sg

bioinformatics↗

Single-cell analysis of EphA clustering phenotypes to probe cancer cell heterogeneity

Eph receptors, a family of receptor tyrosine kinases, play a crutial role in the assembly and maintenance of healthy tissues. Dysfunction in Eph signaling are causally and correlatively associated with cancer progression. In breast cancer cells, dysregulated Eph signaling has been largely linked to alterations in receptor clustering abilities. In the present study, we implemented a single-cell assay and a scoring scheme to systematically probe the spatial organization of activated EphA receptor in carcinoma cells of different origin. Using this assay, we found that cancer cells retained EphA clustering phenotype upon cell division for several generations and degree of clustering reported for population as well as single-cell migration potential. Finally, using patient-derived cancer cell lines, we probed the evolution of EphA signalling in cancer cell populations that underwent metastatic transformation and acquisition of drug resistance. Taken together, our simple and scalable approach provides a reliable quantitation of EphA associated gene expression and phenotypes in multiple carcinomas and can assay the heterogeneity of cancer cell populations in a cost- and time-effective manner.

cancer biology↗