ArticleDevelopment (Cambridge, England)2015
Maintenance of Drosophila germline stem cell sexual identity in oogenesis and tumorigenesis.
Article in Development (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 51 citations in OpenAlex.
- The nuclear and mitochondrial genomes need to tango. How is their dance synchronized during development?NAR molecular medicine · 2026Article
- Soma-germline communication drives sex maintenance in theNational science review · 2024Article
- Spatio-temporal patterns of ovarian development andOpen biology · 2023Article
- Article
- Wolbachia infection at least partially rescues the fertility and ovary defects of several new Drosophila melanogaster bag of marbles protein-coding mutants.PLoS genetics · 2023Article
- Genetic control of a sex-specific piRNA program.Current biology : CB · 2023Article
- Targeting Endogenous Loci That Function in Drosophila Germline Stem Cells.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Safeguarding Drosophila female germ cell identity depends on an H3K9me3 mini domain guided by a ZAD zinc finger protein.PLoS genetics · 2022Article
- Germline sex determination regulates sex-specific signaling between germline stem cells and their niche.Cell reports · 2022Article
- Stonewall prevents expression of ectopic genes in the ovary and accumulates at insulator elements in D. melanogaster.PLoS genetics · 2022Article
- The Regulation of Germline Sex Determination in Drosophila by Sex lethal.Sexual development : genetics, molecular biology, evolution, endocrinology, embryology, and pathology of sex determination and differentiation · 2022Review
- Tumor models in various Drosophila tissues.WIREs mechanisms of disease · 2021Review
- Molecular population genetics of Sex-lethal (Sxl) in the Drosophila melanogaster species group: a locus that genetically interacts with Wolbachia pipientis in Drosophila melanogaster.G3 (Bethesda, Md.) · 2021Article
- Germline masculinization by Phf7 in D. melanogaster requires its evolutionarily novel C-terminus and the HP1-family protein HP1D3csd.Scientific reports · 2021Article
- An autoregulatory switch in sex-specificDevelopment (Cambridge, England) · 2020Article
- Molecular profiling of stem cell-like female germ line cells inBiology open · 2019Article
- Sex Differences in Intestinal Carbohydrate Metabolism Promote Food Intake and Sperm Maturation.Cell · 2019Article
- The histone code reader PHD finger protein 7 controls sex-linked disparities in gene expression and malignancy inScience advances · 2019Article
- Tudor-domain containing protein 5-like promotes male sexual identity in the Drosophila germline and is repressed in females by Sex lethal.PLoS genetics · 2019Article
- Dimorphic sperm formation byProceedings of the National Academy of Sciences of the United States of America · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Adult stem cells maintain tissue homeostasis by balancing self-renewal and differentiation. In Drosophila females, germline stem cells (GSCs) require Sex lethal (Sxl) to exit the stem cell state and to enter the differentiation pathway. Without Sxl GSCs do not differentiate and instead form tumors. Previous studies have shown that these tumors are not caused by a failure in the self-renewal/differentiation switch. Here, we show that Sxl is also necessary for the cell-autonomous maintenance of germ cell female identity and demonstrate that tumors are caused by the acquisition of male characteristics. Germ cells without Sxl protein exhibit a global derepression of testis genes, including Phf7, a male germline sexual identity gene. Phf7 is a key effector of the tumor-forming pathway, as it is both necessary and sufficient for tumor formation. In the absence of Sxl protein, inappropriate Phf7 expression drives tumor formation through a cell-autonomous mechanism that includes sex-inappropriate activation of Jak/Stat signaling. Remarkably, tumor formation requires a novel response to external signals emanating from the GSC niche, highlighting the importance of interactions between mutant cells and the surrounding normal cells that make up the tumor microenvironment. Derepression of testis genes, and inappropriate Phf7 expression, is also observed in germ cell tumors arising from the loss of bag of marbles (bam), demonstrating that maintenance of female sexual identity requires the concerted actions of Sxl and bam. Our work reveals that GSCs must maintain their sexual identity as they are reprogrammed into a differentiated cell, or risk tumorigenesis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.