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Proliferative stem cells maintain quiescence of their niche by secreting the Activin inhibitor Follistatin

Aging causes stem cell dysfunction as a result of extrinsic and intrinsic changes. Decreased function of the stem cell niche is an important contributor to this dysfunction. We use the Drosophila testis to investigate what factors maintain niche cells. The testis niche comprises quiescent “hub” cell...

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Autores principales: Herrera, Salvador C., Sainz de la Maza, Diego, Grmai, Lydia, Margolis, Shally, Plessel, Rebecca, Burel, Michael, O’Connor, Michael, Amoyel, Marc, Bach, Erika A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Cell Press 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8387025/
https://www.ncbi.nlm.nih.gov/pubmed/34363758
http://dx.doi.org/10.1016/j.devcel.2021.07.010
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author Herrera, Salvador C.
Sainz de la Maza, Diego
Grmai, Lydia
Margolis, Shally
Plessel, Rebecca
Burel, Michael
O’Connor, Michael
Amoyel, Marc
Bach, Erika A.
author_facet Herrera, Salvador C.
Sainz de la Maza, Diego
Grmai, Lydia
Margolis, Shally
Plessel, Rebecca
Burel, Michael
O’Connor, Michael
Amoyel, Marc
Bach, Erika A.
author_sort Herrera, Salvador C.
collection PubMed
description Aging causes stem cell dysfunction as a result of extrinsic and intrinsic changes. Decreased function of the stem cell niche is an important contributor to this dysfunction. We use the Drosophila testis to investigate what factors maintain niche cells. The testis niche comprises quiescent “hub” cells and supports two mitotic stem cell pools: germline stem cells and somatic cyst stem cells (CySCs). We identify the cell-cycle-responsive Dp/E2f1 transcription factor as a crucial non-autonomous regulator required in CySCs to maintain hub cell quiescence. Dp/E2f1 inhibits local Activin ligands through production of the Activin antagonist Follistatin (Fs). Inactivation of Dp/E2f1 or Fs in CySCs or promoting Activin receptor signaling in hub cells causes transdifferentiation of hub cells into fully functional CySCs. This Activin-dependent communication between CySCs and hub regulates the physiological decay of the niche with age and demonstrates that hub cell quiescence results from signals from surrounding stem cells.
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spelling pubmed-83870252021-08-31 Proliferative stem cells maintain quiescence of their niche by secreting the Activin inhibitor Follistatin Herrera, Salvador C. Sainz de la Maza, Diego Grmai, Lydia Margolis, Shally Plessel, Rebecca Burel, Michael O’Connor, Michael Amoyel, Marc Bach, Erika A. Dev Cell Article Aging causes stem cell dysfunction as a result of extrinsic and intrinsic changes. Decreased function of the stem cell niche is an important contributor to this dysfunction. We use the Drosophila testis to investigate what factors maintain niche cells. The testis niche comprises quiescent “hub” cells and supports two mitotic stem cell pools: germline stem cells and somatic cyst stem cells (CySCs). We identify the cell-cycle-responsive Dp/E2f1 transcription factor as a crucial non-autonomous regulator required in CySCs to maintain hub cell quiescence. Dp/E2f1 inhibits local Activin ligands through production of the Activin antagonist Follistatin (Fs). Inactivation of Dp/E2f1 or Fs in CySCs or promoting Activin receptor signaling in hub cells causes transdifferentiation of hub cells into fully functional CySCs. This Activin-dependent communication between CySCs and hub regulates the physiological decay of the niche with age and demonstrates that hub cell quiescence results from signals from surrounding stem cells. Cell Press 2021-08-23 /pmc/articles/PMC8387025/ /pubmed/34363758 http://dx.doi.org/10.1016/j.devcel.2021.07.010 Text en © 2021 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Herrera, Salvador C.
Sainz de la Maza, Diego
Grmai, Lydia
Margolis, Shally
Plessel, Rebecca
Burel, Michael
O’Connor, Michael
Amoyel, Marc
Bach, Erika A.
Proliferative stem cells maintain quiescence of their niche by secreting the Activin inhibitor Follistatin
title Proliferative stem cells maintain quiescence of their niche by secreting the Activin inhibitor Follistatin
title_full Proliferative stem cells maintain quiescence of their niche by secreting the Activin inhibitor Follistatin
title_fullStr Proliferative stem cells maintain quiescence of their niche by secreting the Activin inhibitor Follistatin
title_full_unstemmed Proliferative stem cells maintain quiescence of their niche by secreting the Activin inhibitor Follistatin
title_short Proliferative stem cells maintain quiescence of their niche by secreting the Activin inhibitor Follistatin
title_sort proliferative stem cells maintain quiescence of their niche by secreting the activin inhibitor follistatin
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8387025/
https://www.ncbi.nlm.nih.gov/pubmed/34363758
http://dx.doi.org/10.1016/j.devcel.2021.07.010
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