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scs, slug, muscle, mice, fig, cell, cells, pinka, article, google, scholar, cas, expression, supplementary, usa, data, stem, regeneration, muscles, injury, senescence, aged, skeletal, staining, aging, selfrenewal, analysis, myoblasts, slugdeficient, students, ttest, saβgal, nature, gene, day, protein, slugcko, genes, mouse, total, source, control, transcription, transplantation, activation, results, muscs, culture, vivo, factor,

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crispr/cas9-based genome editing nature portfolio cd45−/cd11b−/cd31−/sca1−/integrin-α7+/cd34+ cd45−cd11b−cd31−sca1−integrin-α7+cd34+ privacy policy nutrient-sensitive pi3k-akt-mtor pathways o-nitrophenyl b-d-galactopyranoside nature communications advertising crispr/cas9-mediated gene tagging par-complex-dependent asymmetric activation sporadic sa-β-gal+ cells zymo research representative sa-β-gal staining sa-β-gal+ cells stained sa-β-gal staining showed sa-β-gal+pax7+ cells negative sa-β-gal staining remained open sa-β-gal staining demonstrated facilitate easier access performed sa-β-gal staining reprints zinc-finger transcription factor integrin-α7 antibody labeled efluor660-conjugated cd34 antibody zinc-finger transcription factors sa-β-gal+ cells sa-β-gal positive sa-β-gal staining bacl2-pre-injured ta muscle quick-rnatm microprep kit nature 490 nature 506 nature 443 nature 529 nature 456 nature 129/svx129/sv-cp f1 liquid nitrogen-cooled isopentane sa-β-gal−/pax7+ early-passaged slug-deficient myoblasts paav-grna-gfp expression vector fibro-adipogenic progenitors pax7-szgreen mouse strain correct site-directed integration slug−/−p16+/+ donor-derived scs slug−/−p16−/− donor-derived scs 025μg cmv-lacz plasmid specific e-box motifs

Questions {❓}

• Could senescence phenotypes strike the balance to promote tumor dormancy?

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         headline:The transcription factor Slug represses p16Ink4a and regulates murine muscle stem cell aging
         description:Activation of the p16Ink4a-associated senescence pathway during aging breaks muscle homeostasis and causes degenerative muscle disease by irreversibly dampening satellite cell (SC) self-renewal capacity. Here, we report that the zinc-finger transcription factor Slug is highly expressed in quiescent SCs of mice and functions as a direct transcriptional repressor of p16Ink4a. Loss of Slug promotes derepression of p16Ink4a in SCs and accelerates the entry of SCs into a fully senescent state upon damage-induced stress. p16Ink4a depletion partially rescues defects in Slug-deficient SCs. Furthermore, reduced Slug expression is accompanied by p16Ink4a accumulation in aged SCs. Slug overexpression ameliorates aged muscle regeneration by enhancing SC self-renewal through active repression of p16Ink4a transcription. Our results identify a cell-autonomous mechanism underlying functional defects of SCs at advanced age. As p16Ink4a dysregulation is the chief cause for regenerative defects of human geriatric SCs, these findings highlight Slug as a potential therapeutic target for aging-associated degenerative muscle disease. Muscle regeneration depends on self-renewal of muscle stem cells but how this is regulated on aging is unclear. Here, the authors identify Slug as regulating p16Ink4a in quiescent muscle stem cells, and when Slug expression reduces in aged stem cells, p16Ink4a accumulates, causing regenerative defects.
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      headline:The transcription factor Slug represses p16Ink4a and regulates murine muscle stem cell aging
      description:Activation of the p16Ink4a-associated senescence pathway during aging breaks muscle homeostasis and causes degenerative muscle disease by irreversibly dampening satellite cell (SC) self-renewal capacity. Here, we report that the zinc-finger transcription factor Slug is highly expressed in quiescent SCs of mice and functions as a direct transcriptional repressor of p16Ink4a. Loss of Slug promotes derepression of p16Ink4a in SCs and accelerates the entry of SCs into a fully senescent state upon damage-induced stress. p16Ink4a depletion partially rescues defects in Slug-deficient SCs. Furthermore, reduced Slug expression is accompanied by p16Ink4a accumulation in aged SCs. Slug overexpression ameliorates aged muscle regeneration by enhancing SC self-renewal through active repression of p16Ink4a transcription. Our results identify a cell-autonomous mechanism underlying functional defects of SCs at advanced age. As p16Ink4a dysregulation is the chief cause for regenerative defects of human geriatric SCs, these findings highlight Slug as a potential therapeutic target for aging-associated degenerative muscle disease. Muscle regeneration depends on self-renewal of muscle stem cells but how this is regulated on aging is unclear. Here, the authors identify Slug as regulating p16Ink4a in quiescent muscle stem cells, and when Slug expression reduces in aged stem cells, p16Ink4a accumulates, causing regenerative defects.
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