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Related Experiment Video

Updated: Feb 5, 2026

Overexpressing Long Noncoding RNAs Using Gene-activating CRISPR
13:04

Overexpressing Long Noncoding RNAs Using Gene-activating CRISPR

Published on: March 1, 2019

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Overexpression of the

Fabienne E Bayer1, Mirjam Zimmermann1, Anette Preiss1

  • 1Universität Hohenheim, Institut für Genetik, Garbenstr. 30, 70599 Stuttgart, Germany.

Hereditas
|September 12, 2018
PubMed
Summary

Overexpressing the Drosophila ATR homologue, mei-41, triggers a DNA damage response and activates p53, even without DNA damage. This study introduces a gain-of-function allele for mei-41 research.

Area of Science:

  • Cellular signaling pathways
  • DNA damage response mechanisms
  • Drosophila melanogaster genetics

Background:

  • DNA damage activates ATM/ATR kinases and Chk1/Chk2 checkpoint kinases.
  • The Drosophila ATR homologue, mei-41, is crucial for DNA repair and cell cycle checkpoints.
  • No gain-of-function mei-41 alleles were previously available.

Purpose of the Study:

  • To generate and analyze a gain-of-function allele of mei-41 in Drosophila.
  • To investigate the effects of mei-41 overexpression on cell proliferation and checkpoints.
  • To explore the role of mei-41 in activating downstream signaling pathways.

Main Methods:

  • Generated transgenic Drosophila for temporal and tissue-specific induction of mei-41.
  • Analyzed proliferation and G2/M checkpoint in wing and eye anlagen.
Keywords:
ATRDNA damage checkpointMei-41Overexpressionp53 activation

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  • Utilized a p53R-GFP biosensor to assess p53 activation in vivo.

    • Main Results:

    • Overexpression of mei-41 disrupted proliferation and G2/M checkpoints without genomic stress.
    • Ectopic mei-41 prolonged irradiation-induced cell cycle arrest.
    • mei-41 triggered Grapes (Grp) phosphorylation and robust p53 activation in vivo.

    Conclusions:

    • Overexpression of Drosophila ATR homologue mei-41 induces a DNA damage response independently of irradiation.
    • The gain-of-function mei-41 allele provides a novel tool for studying DNA damage response pathways.
    • mei-41 activation is sufficient to elicit a p53-mediated response in vivo.