ArticleDevelopment (Cambridge, England)2025
Maintenance of niche architecture requires actomyosin and enables proper stem cell signaling and oriented division in the Drosophila testis.
Article in Development (Cambridge, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- The Tbx1 ortholog org-1 is required to establish testis stem cell niche identity in Drosophila.Development (Cambridge, England) · 2026Article
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3 authors.
Funding
Abstract
Stem cells are essential to repair and regenerate tissues, and often reside in a niche that controls their behavior. Here, we use the Drosophila testis niche, a paradigm for niche-stem cell interactions, to address the cell biological features that maintain niche structure and function during its steady-state operation. We report enrichment of Myosin II (MyoII) and a key regulator of actomyosin contractility (AMC), Rho Kinase (ROK), within the niche cell cortex at the interface with germline stem cells (GSCs). Compromising MyoII and ROK disrupts niche architecture, suggesting that AMC in niche cells is important to maintain its reproducible structure. Furthermore, defects in niche architecture disrupt GSC function. Our data suggest that the niche signals less robustly to adjacent germ cells yet permits increased numbers of cells to respond to the signal. Finally, compromising MyoII in niche cells leads to increased misorientation of centrosomes in GSCs as well as defects in the centrosome orientation checkpoint. Ultimately, this work identifies a crucial role for AMC-dependent maintenance of niche structure to ensure a proper complement of stem cells that correctly execute divisions.
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