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Aberrant activation of p53/p66Shc-mInsc axis increases asymmetric divisions and attenuates proliferation of aged mammary stem cells.

ABSTRACT: Aberrant activation of p53/p66Shc-mInsc axis increases asymmetric divisions and attenuates proliferation of aged mammary stem cells.

PROVIDER: PRJNA830505 | ENA |

REPOSITORIES: ENA

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Aberrant activation of p53/p66Shc-mInsc axis increases asymmetric divisions and attenuates proliferation of aged mammary stem cells.

Project description:Mammary gland aging is due to aberrant activation of p66Shc, which induces p53/p44 signaling, leading to failure of symmetric divisions, decreased proliferation and reduced regenerative potential of MaSCs. Age-related changes in mammary epithelial cells derived from C57BL/6J WT and p66Shc knockedout mice cultured as stem cell-enriched mammospheres.

2022-12-21 | GSE201253 | GEO

Asymmetric Segregation of the Nucleosome Remodeling and Deacetylase Complex during Asymmetric Cell Divisions

Project description:Asymmetric Segregation of the Nucleosome Remodeling and Deacetylase Complex during Asymmetric Cell Divisions

| PRJNA704418 | ENA

Asymmetric Segregation of the Nucleosome Remodeling and Deacetylase Complex during Asymmetric Cell Divisions

Project description:Asymmetric cell divisions (ACDs) generate two daughter cells with identical genetic information but distinct cell fates. Epigenetic mechanisms are crucial for cell fate specification, and it remains unclear how epigenetic information is inherited. Here, we report asymmetric segregation of the nucleosome remodeling and deacetylase complex (NuRD) during ACDs in Caenorhabditis elegans. NuRD is enriched to chromosomes of the future surviving but not apoptotic daughter cell, whereas NuRD evenly distributes to two viable siblings. Disruption of ACDs causes symmetric NuRD inheritance, and an ectopic gain of NuRD in apoptotic daughters allows cell survival and differentiation. Lack of NuRD upregulates the expression of the vital cell death-inducing gene egl-1 by increasing H3K27 acetylation on the egl-1 locus, which activates the EGL-1-CED-9-CED-4-CED-3 pathway to promote apoptosis. We propose that biased NuRD segregation during ACDs provides a previously unrecognized yet common mechanism for asymmetrically partitioning epigenetic information that contributes to binary cell fate decisions.

2022-12-30 | GSE167379 | GEO

Regulators of cellular heterogeneity in basal-like breast cancer influence symmetric versus asymmetric division rates (shRNA targeting)

Project description:Differentiation events contribute to cellular heterogeneity within tumors and influence disease progression and response to therapy. Here we dissect the mechanisms controlling intratumoral heterogeneity within basal-like breast cancers. We show that cancer cells can transition between a differentiation state related to that of normal luminal progenitors and a state closer to that of mature luminal cells, and that this occurs through asymmetric cell divisions. The Polycomb factor EZH2 and the Notch pathway act to increase the rates of symmetric divisions that produce progenitor-like cells, while the FOXA1 transcription factor promotes asymmetric divisions that reduce the numbers of such cells. Through functional screening, we identified a group of regulators that control cancer cell differentiation state and the relative proportions of tumor cell subpopulations. Our findings highlight the regulation of asymmetric cell divisions as a mechanism controlling intratumoral heterogeneity, and identify molecular pathways that control breast cancer cellular composition.

2018-08-26 | GSE84143 | GEO

Regulators of cellular heterogeneity in basal-like breast cancer influence symmetric versus asymmetric division rates (Expression profiles)

2018-08-26 | GSE84080 | GEO

Regulation of cellular heterogeneity and rates of symmetric and asymmetric divisions in triple-negative breast cancer

Project description:Regulation of cellular heterogeneity and rates of symmetric and asymmetric divisions in triple-negative breast cancer

| PRJNA328149 | ENA

Distinct types of stem cell divisions determine organ regeneration and aging in hair follicles

Project description:Aging organs functionally and structurally decline with the loss of their regenerative capabilities, yet the existence of distinct cell division programs that determine organ fates is unknown. Hair follicles, mammalian mini-organs that grow hair, miniaturize by aging. Here we report that hair follicle regeneration and aging are driven by distinct cell division types of hair follicle stem cells (HFSCs). Cell fate tracing and cell division axis analysis in mice revealed that HFSCs undergo symmetric and asymmetric cell divisions to generate a new bulge, yet preferentially provoke “stress-responsive type” asymmetric cell divisions that generate aberrantly differentiating cells upon age/stress. That dynamic program with repetitive divisions efficiently eradicates those cells through defective association and stabilization of a hemidesmosomal protein COL17A1 and a cell-polarity-protein aPKCλ in HFSCs, thereby causing organ aging. The forced stabilization of COL17A1 rescued organ aging through aPKCλ stabilization. These results demonstrate that distinct cell division programs govern tissue/organ fates.

2020-12-25 | GSE124119 | GEO

Identification of long-lived proteins retained in cells undergoing repeated asymmetric divisions

Project description:To identify long-lived proteins that are retained in yeast mother cells, we combined a method developed in our lab with a pulse-chase protocol using total proteome analysis. Cells were initially grown in medium with stable heavy-isotope amino acids to label proteins. The cells were then switched into media containing light-isotope amino acids and cultured for an additional ~18 cell divisions with the MEP engaged. Finally, we determined whether any of the original heavy-labeled proteins were still present in the aged mother cells

2014-09-01 | PXD001251 | Pride

Spatially resolved proteomics of the Arabidopsis stomatal lineage identifies polarity complexes for cell divisions and stomatal pores

Project description:Cell polarity is used to guide asymmetric divisions and create morphologically diverse cells. We find that two oppositely oriented cortical polarity domains present during the asymmetric divisions in the Arabidopsis stomatal lineage are reconfigured into polar domains marking ventral (pore-forming) and outward facing domains of maturing stomatal guard cells. Proteins that define these opposing polarity domains were used as baits in miniTurboID-based proximity labeling. Among differentially enriched proteins we find SOSEKIs and their effector ANGUSTIFOLIA, protein kinase CKII and LC8-type DYNEIN LIGHT CHAIN1 as polar scaffolds. Using AI-facilitated protein structure prediction models, we identify their potential interaction interfaces. Functional and localization analysis of polarity protein OPL2 and its newly discovered partners suggest a positive interaction with mitotic microtubules and a potential role in cytokinesis. This combination of cutting-edge proteomics and structural modeling with live cell imaging provides insights into how polarity is rewired in different cell types and cell cycle stages.

2024-03-21 | PXD050287 | Pride

Egf signaling directs neoblast repopulation by regulating asymmetric cell division in planarians

Project description:The goal of this experiment is to identify target genes of Egf signaling which regulate recovery of the neoblast population following exposure to a sublethal dose of radiation. A large population of highly proliferative stem cells (neoblasts) is required for physiological tissue homeostasis and regeneration after injury in planarians. Recent studies indicate that survival of a few neoblasts after sublethal irradiation results in the clonal expansion of the surviving stem cells and the eventual restoration of tissue homeostasis and regenerative capacity. Many genes are known to be required for the normal function of neoblasts, but the precise mechanisms regulating the population dynamics of these adult pluripotent stem cells remain largely unknown. By coupling RNAi screening and sublethal irradiation, we uncovered a central role for Epidermal Growth Factor (EGF) signaling during in vivo neoblast expansion mediated by Smed-egfr-3 (egfr-3) and its putative ligand Smed-neuregulin-7 (nrg-7). Furthermore, the EGFR-3 protein localizes asymmetrically on the cytoplasmic membrane of neoblasts and the ratio of asymmetric to symmetric cell divisions decreases significantly in egfr-3(RNAi) worms. Our results not only provide the first molecular evidence of asymmetric stem cell divisions in planarian, but also demonstrate that EGF signaling likely functions as an essential regulator of neoblast clonal expansion.

2016-08-18 | GSE84025 | GEO

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