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NFIX-mediated transcriptional regulation in skeletal muscle cells

ABSTRACT: Skeletal muscle plays a central role in voluntary movement and possesses remarkable regenerative capacity following injury. NFIX, a member of the Nuclear Factor I (NFI) family of transcription factors, is essential for skeletal muscle development and regeneration. Despite its increasing importance, the molecular mechanisms by which NFIX mediates transcriptional regulation in skeletal muscle remain unclear. In this study, we performed siRNA-mediated knockdown of NFIX in human immortalized skeletal muscle cells and conducted RNA-seq analysis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE305570 | GEO | 2026/03/03

REPOSITORIES: GEO

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Nfix is a novel regulator of murine hematopoietic stem and progenitor cell survival

Project description:Hematopoietic stem cells are both necessary and sufficient to sustain the complete blood system of vertebrates. Here we show that Nfix, a member of the nuclear factor I (Nfi) family of transcription factors, is highly expressed by hematopoietic stem and progenitor cells (HSPC) of murine adult bone marrow. Although shRNA mediated knockdown of Nfix expression in Lineage-Sca-1+c-Kit+ HSPC had no effect on in vitro cell growth or viability, Nfix-depleted HSPC displayed a significant loss of colony forming potential, as well as short- and long-term in vivo hematopoietic repopulating activity. Analysis of recipient mice 4-20 days post-transplant revealed that Nfix-depleted HSPC establish in the bone marrow but fail to persist due to increased apoptotic cell death. Gene expression profiling of Nfix-depleted HSPC reveals that loss of Nfix expression in HSPC is concomitant with a decrease in the expression of multiple genes known to be important for HSPC survival, such as Erg, Mecom, Mpl and Prdm16. These data reveal that Nfix is a novel regulator of HSPC survival post-transplantation and establish, for the first time, a role for Nfi genes in the regulation of this cellular compartment. 3 NFIX depleted samples are compared to 3 wt samples

2013-09-05 | E-GEOD-45492 | biostudies-arrayexpress

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2015-06-30 | E-GEOD-65337 | biostudies-arrayexpress

NFI Transcription Factors Govern Stem Cell Chromatin Accessibility and Guard Against Irreversible Hair Loss [scRNA-seq]

Project description:Tissue homeostasis and regeneration rely upon resident stem cells (SCs), whose behavior is regulated through niche-dependent crosstalk. The mechanisms underlying SC maintenance are still unfolding. Here, using hair follicles (HFs) as model and spatiotemporal gene ablation in mice, we uncover transcription factors (TFs) NFIB and NFIX as guardians of the process. Complete NFI ablation causes SC depletion and hair loss which resembles irreversible alopecia in humans, who intriguingly also display reduced NFI. Through single cell transcriptomics, ATAC- and ChIP-seq profiling, we uncover a key role for NFIB/NFIX in governing chromatin accessibility of HFSC master TFs . When NFIB/NFIX are genetically removed, the stemness epigenetic landscape is lost, as enhancers driving HFSC identity are decommissioned and those of epidermal differentiation and wound-repair are de-repressed. Together, our findings expose NFIB/NFIX as crucial rheostats of tissue homeostasis, functioning to safeguard the SC epigenome from a breach in lineage confinement that otherwise triggers irreversible tissue degeneration.

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