ArticlePLoS genetics2021
dRTEL1 is essential for the maintenance of Drosophila male germline stem cells.
Article in PLoS genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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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
4 citing papers in PubMed, 19 citations in OpenAlex.
- A comparison of spermatogenesis between flies and men-conserved processes of male gamete production.Human reproduction update · 2025Review
- Telomere-to-telomere genome assembly uncovers Wolbachia-driven recurrent male bottleneck effect and selection in a sawfly.Communications biology · 2025Article
- Sex-Specific Ultraviolet Radiation Tolerance AcrossEcology and evolution · 2025Article
- Different mechanisms of X-ray irradiation-induced male and female sterility in Aedes aegypti.BMC biology · 2023Article
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Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Stem cells have the potential to maintain undifferentiated state and differentiate into specialized cell types. Despite numerous progress has been achieved in understanding stem cell self-renewal and differentiation, many fundamental questions remain unanswered. In this study, we identify dRTEL1, the Drosophila homolog of Regulator of Telomere Elongation Helicase 1, as a novel regulator of male germline stem cells (GSCs). Our genome-wide transcriptome analysis and ChIP-Seq results suggest that dRTEL1 affects a set of candidate genes required for GSC maintenance, likely independent of its role in DNA repair. Furthermore, dRTEL1 prevents DNA damage-induced checkpoint activation in GSCs. Finally, dRTEL1 functions to sustain Stat92E protein levels, the key player in GSC maintenance. Together, our findings reveal an intrinsic role of the DNA helicase dRTEL1 in maintaining male GSC and provide insight into the function of dRTEL1.
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