Transposon silencing in the Drosophila female germline is essential for genome stability in progeny embryos
| Autor: | Anne Ephrussi, Ramesh S. Pillai, Zeljko Durdevic |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Transposable element 030102 biochemistry & molecular biology Ecology DNA damage urogenital system Health Toxicology and Mutagenesis fungi RNA Plant Science Biology Biochemistry Genetics and Molecular Biology (miscellaneous) RNA Helicase A Nurse cell Germline Cell biology 03 medical and health sciences chemistry.chemical_compound 030104 developmental biology chemistry Gene silencing DNA Research Articles Research Article |
| Zdroj: | Life Science Alliance |
| ISSN: | 2575-1077 |
| Popis: | Suppression of transposons by the Piwi-interacting RNA biogenesis factor Vasa in the supporting nurse cells is essential to prevent their accumulation in the developing oocyte, ensuring proper Drosophila embryonic development. The Piwi-interacting RNA pathway functions in transposon control in the germline of metazoans. The conserved RNA helicase Vasa is an essential Piwi-interacting RNA pathway component, but has additional important developmental functions. Here, we address the importance of Vasa-dependent transposon control in the Drosophila female germline and early embryos. We find that transient loss of vasa expression during early oogenesis leads to transposon up-regulation in supporting nurse cells of the fly egg-chamber. We show that elevated transposon levels have dramatic consequences, as de-repressed transposons accumulate in the oocyte where they cause DNA damage. We find that suppression of Chk2-mediated DNA damage signaling in vasa mutant females restores oogenesis and egg production. Damaged DNA and up-regulated transposons are transmitted from the mother to the embryos, which sustain severe nuclear defects and arrest development. Our findings reveal that the Vasa-dependent protection against selfish genetic elements in the nuage of nurse cell is essential to prevent DNA damage–induced arrest of embryonic development. |
| Databáze: | OpenAIRE |
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