Competition shapes the landscape of X-linked genetic diversity [scRNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1006019 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25657340_1.fastq.gz | Fastqsanger.gz | |||
| SRR25657340_2.fastq.gz | Fastqsanger.gz | |||
| SRR25657341_1.fastq.gz | Fastqsanger.gz | |||
| SRR25657341_2.fastq.gz | Fastqsanger.gz | |||
| SRR25657342_1.fastq.gz | Fastqsanger.gz |
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Project description:Competition shapes the landscape of X-linked genetic diversity
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Project description:Human populations harbour sequence variants even within essential genes. As a result of random X chromosome inactivation (XCI) and epigenetically stable XCI propagation, X-linked variation gives rise to genetically diverse clones that co-exist within XX individuals. Whether interactions between such clones shape the deployment of X-linked diversity remains to be explored. To address this question, we focus on benign coding variation in the X-linked STAG2 gene. Mouse models reveal that clones expressing Stag2 variants contribute to tissues such as skin and brain at the expected frequencies, but show reduced contributions to the haematopoietic stem and progenitor cell pool, and severely defective lymphoid specification. Unexpectedly, the absence of Xvariant clones from the lymphoid compartment is due not to cell-intrinsic defects, but requires competitive interactions with Xwt clones: in the absence of Xwt, Xvariant cells generate normal numbers of functional lymphocytes. X-linked competition has hallmarks of non-cell-autonomous 'cell competition', known to operate in a range of biological processes including embryonic development, aging, and cancer. These findings show that interactions between genetically diverse clones that may operate in any XX individual can shape the contribution of X-linked diversity to specific cell types and tissues.
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Project description:Competition shapes the landscape of X-linked genetic diversity [ChIP-seq]
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Project description:Human populations harbour sequence variants even within essential genes. As a result of random X chromosome inactivation (XCI) and epigenetically stable XCI propagation, X-linked variation gives rise to genetically diverse clones that co-exist within XX individuals. Whether interactions between such clones shape the deployment of X-linked diversity remains to be explored. To address this question, we focus on benign coding variation in the X-linked STAG2 gene. Mouse models reveal that clones expressing Stag2 variants contribute to tissues such as skin and brain at the expected frequencies, but show reduced contributions to the haematopoietic stem and progenitor cell pool, and severely defective lymphoid specification. Unexpectedly, the absence of Xvariant clones from the lymphoid compartment is due not to cell-intrinsic defects, but requires competitive interactions with Xwt clones: in the absence of Xwt, Xvariant cells generate normal numbers of functional lymphocytes. X-linked competition has hallmarks of non-cell-autonomous 'cell competition', known to operate in a range of biological processes including embryonic development, aging, and cancer. These findings show that interactions between genetically diverse clones that may operate in any XX individual can shape the contribution of X-linked diversity to specific cell types and tissues.
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Project description:Although increasing studies have proved cell competition widely involved in the growth and homeostasis of multicellular organisms is closely linked to tumorigenesis and development, the mechanistic contributions between drug resistance and tumor cell competition remain ill-defined. In this paper, we applied MS of cell competition group to determine the dominant characteristics of lenvatinib resistance and its metabolic differences in cell competition. Our results showed a vital role of HSP90-IDH1 mediated lipid accumulation in maintaining the competitive outcome of HCC drug-resistant cells via regulating lipid metabolism. HSP90-IDH1 axis could be a promising target to overcome HCC drug resistance.
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Project description:Competition between antigen-specific T cells for peptide:MHC (p:MHC) complexes shapes the ensuing T cell response. T cells also compete for access to antigen presenting cells (APCs), which results in competition between T cells of different antigen specificities and is referred to as cross-competition. When both mechanisms are in place, a memory T cell population specific for just a single epitope can effectively limit de novo antigen-specific T cell responses. Whether human cytomegalovirus (CMV)-specific T cell responses prevent other de novo T cell responses is unknown, but of interest in a transplant context as well as the development of CMV-based vaccines. We assessed the extent of T cell competition and cross-competition in a cohort of non-myeloablative hematopoietic stem cell transplant (nmHSCT) patients. In our cohort, HSCT donors and recipients were CMV-seronegative and -positive, respectively, thus providing genetically distinct memory and naïve T cell populations. We used single-cell transcriptomics to track donor versus recipient-derived T cell clones. We found that recipient-derived CMV-specific memory T cells outcompeted donor-derived responses of identical specificity; however, expansion of other donor-derived T cell clones still occurred averaging 24 rounds of cell division. The transcriptional programs between expanding donor and recipient-derived cells were largely congruent and consistent with an effector T cell response. Our data further indicated that the composition of the T cell compartment changed due to expanding and contracting clones in the first 90 days post-nmHSCT. Overall, our data suggest that CMV-specific memory T cells compete for p:MHC but not APC access during CMV reactivation.
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