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. 2021 Apr 6;7:68. doi: 10.1038/s41420-021-00452-w

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 8 — a, b Graphical representation of the apical tips of normal testes and testes with GSC differentiation defects. c, d Mechanisms of CG6015 and EGFR signaling. In normal testes, the stem cell niche is composed of GSCs, CySCs, and hub cells, which occupy the apical tips of the testis. For the integrity of germ cell differentiation, somatic cells should envelop germ cells, and fusomes gradually transition from dot to bifurcate. Somatic inactivation of CG6015 and key targets in the EGFR signaling pathway lead to the accumulation of undifferentiated germ cells, and eventually the formation of tumor-like germ cell cysts with pointed fusomes in the Drosophila testis. Our results show the maintenance of stem cell niche homeostasis by CG6015 and EGFR signaling via germline dpERK signals.