ArticlePLoS genetics2020
Dis3L2 regulates cell proliferation and tissue growth through a conserved mechanism.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Male sterility in Drosophila hybrids revealed by a multi-generational transcriptomic analysis of genes and transposable elements in testes.BMC biology · 2026Article
- Ribonucleases in Mendelian disease: Characterization and insight from model organisms.Genes & diseases · 2025Review
- Dis3l2 is essential for neural crest survival by modulating Akt signaling.Cell communication and signaling : CCS · 2025Article
- Characterisation of the in-vivo miRNA landscape in Drosophila ribonuclease mutants reveals Pacman-mediated regulation of the highly conserved let-7 cluster during apoptotic processes.Frontiers in genetics · 2024Article
- Conditional ablation of DIS3L2 ribonuclease in pre-meiotic germ cells causes defective spermatogenesis and infertility in male mice.Theranostics · 2024Article
- tRNARNA (New York, N.Y.) · 2023Article
- How hydrolytic exoribonucleases impact human disease: Two sides of the same story.FEBS open bio · 2023Review
- DIS3L2 ribonuclease degrades terminal-uridylated RNA to ensure oocyte maturation and female fertility.Nucleic acids research · 2023Article
- A shape-shifting nuclease unravels structured RNA.Nature structural & molecular biology · 2023Article
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- ZFC3H1 prevents RNA trafficking into nuclear speckles through condensation.Nucleic acids research · 2021Article
- Genome-wide analyses of XRN1-sensitive targets in osteosarcoma cells identify disease-relevant transcripts containing G-rich motifs.RNA (New York, N.Y.) · 2021Article
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Dis3L2 is a highly conserved 3'-5' exoribonuclease which is mutated in the human overgrowth disorders Perlman syndrome and Wilms' tumour of the kidney. Using Drosophila melanogaster as a model system, we have generated a new dis3L2 null mutant together with wild-type and nuclease-dead genetic lines in Drosophila to demonstrate that the catalytic activity of Dis3L2 is required to control cell proliferation. To understand the cellular pathways regulated by Dis3L2 to control proliferation, we used RNA-seq on dis3L2 mutant wing discs to show that the imaginal disc growth factor Idgf2 is responsible for driving the wing overgrowth. IDGFs are conserved proteins homologous to human chitinase-like proteins such as CHI3L1/YKL-40 which are implicated in tissue regeneration as well as cancers including colon cancer and non-small cell lung cancer. We also demonstrate that loss of DIS3L2 in human kidney HEK-293T cells results in cell proliferation, illustrating the conservation of this important cell proliferation pathway. Using these human cells, we show that loss of DIS3L2 results in an increase in the PI3-Kinase/AKT signalling pathway, which we subsequently show to contribute towards the proliferation phenotype in Drosophila. Our work therefore provides the first mechanistic explanation for DIS3L2-induced overgrowth in humans and flies and identifies an ancient proliferation pathway controlled by Dis3L2 to regulate cell proliferation and tissue growth.
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Registered trials
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