Project description:Asymmetric partitioning of fate-determinants is a mechanism that contributes to T cell differentiation. However, it remained unclear whether the ability of T cells to divide asymmetrically is influenced by their differentiation state, as well as if enforcing asymmetric cell division rates would have an impact on T cell differentiation and memory formation. Using the murine LCMV infection model, we established a correlation between cell stemness and the ability of CD8+ T cells to undergo asymmetric cell division (ACD). Transient mTOR inhibition proved to increase ACD rates in naïve and memory cells, and to install this ability in exhausted CD8+ T cells. Functionally, enforced ACD correlated with increased memory potential, leading to more efficient recall response and viral control upon acute or chronic LCMV infection. Moreover, transient mTOR inhibition also increased ACD rates in human CD8+ T cells. Transcriptional profiling of first daughter cells, obtained by sorting CD8lo and CD8hi cells after in vitro stimulation, revealed that progenies emerging from enforced ACD exhibited more pronounced early memory signatures, which functionally endowed these cells with strengthened memory features.

2019-02-14 | E-MTAB-7651 | biostudies-arrayexpress

Islr regulates satellite cells asymmetric division through Sparc/p-ERK1/2 signaling pathway

Project description:Satellite cells are adult muscle stem cells responsible for muscle regeneration after acute or chronic injuries. The balance between stem cell self-renewal and differentiation impacts the kinetics and efficiency of skeletal muscle regeneration. This study elucidated the function of Islr in satellite cell asymmetric division. Satellite cell specific deletion of Islr compromises muscle regeneration in adult mice by impairing the satellite cell pool. Islr is pivotal for satellite cell proliferation and its deletion promotes asymmetric cell fate segregation of satellite cells. A mechanistic search revealed that Islr interacts and stabilizes the Sparc protein, which activates p-ERK1/2 signaling required for asymmetric division. In combination, the findings have identified Islr as a key regulator of satellite cell asymmetric division through the Sparc/p-ERK1/2 signaling pathway, which provides a new insight into satellite cell biology and open avenues for the treatment of myopathy.

2023-08-16 | GSE210951 | GEO

Asymmetric Histone Inheritance Regulates Differential Transcription Re-initiation and Cell Fate Decisions in Mouse Olfactory Horizontal Basal Cells

Project description:Histones, major carriers of epigenetic information, play critical roles in regulating gene expression patterns and cell fate decisions. While asymmetric histone inheritance has been shown to regulate distinct cell fates in Drosophila adult stem cells, its relevance in mammals remains unclear. In this study, we investigated cell division modes and histone inheritance patterns in horizontal basal cells (HBCs) of the mouse olfactory epithelium following injury. We found that approximately 40% of telophase HBCs show asymmetric division, with a corresponding asymmetric segregation of histone H4. In primary cultured HBCs, we observed asymmetric cell division accompanied by asymmetric distribution of histones, including H4, H3, and H3.3, but not H2A-H2B. Asymmetric histone segregation leads to asymmetric association of a key ‘stemness’ transcription factor p63 and asynchronous transcription re-initiation during mitotic exit. Single-cell RNA sequencing of paired daughter cells further revealed asymmetric cell fate priming in cultured HBCs. Disruption of asymmetric cell division abolished asymmetric transcription re-initiation, asymmetric histone inheritance in culture HBCs and further caused regeneration defects in OE. These findings reveal the conservation of asymmetric histone inheritance in mammalian adult stem cells and highlight its biological significance in tissue regeneration.

2025-03-26 | GSE286046 | GEO

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