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An intergenic regulatory region mediates Drosophila Myc-induced apoptosis and blocks tissue hyperplasia

C Zhang1, S Casas-Tintó2, G Li3

  • 11] Department of Molecular Genetics and Microbiology and UF Shands Cancer Center, University of Florida, Gainesville, FL, USA [2] Department of Cell Biology, Emory University School of Medicine, Atlanta, GA, USA.

Oncogene
|June 17, 2014
PubMed

Insights

A key tumor-suppressive mechanism involves programmed cell death (apoptosis) triggered by oncogene-induced overproliferation. This study identifies an intergenic regulatory region (IRER) essential for dMyc-induced apoptosis in fruit flies, highlighting epigenetic control of DNA accessibility.

Area of Science:

  • Molecular Biology
  • Genetics
  • Developmental Biology

Background:

  • Cell-autonomous apoptosis is a critical tumor-suppressive mechanism in vertebrates, activated by oncogene-induced overproliferation.
  • The precise molecular mechanisms underlying this process are not fully understood.
  • Oncogenic stress, such as that induced by dMyc, can trigger apoptosis to prevent uncontrolled cell growth.

Purpose of the Study:

  • To elucidate the mechanism of dMyc-induced cell-autonomous apoptosis in Drosophila melanogaster.
  • To identify key regulatory elements involved in this tumor-suppressive pathway.
  • To investigate the role of epigenetic modifications in controlling apoptotic gene expression.

Main Methods:

  • Utilized Drosophila melanogaster as a model organism.
  • Identified and characterized an intergenic regulatory sequence, the IRER (irradiation-responsive enhancer region).
  • Employed an in vivo reporter to monitor the chromatin state and DNA accessibility of the IRER.
  • Investigated the overlap between dMyc-induced apoptosis and P53-mediated DNA damage response.

Main Results:

  • dMyc-induced apoptosis depends on the IRER, which regulates the expression of proapoptotic genes.
  • Epigenetic control of DNA accessibility within the IRER determines the strength of the apoptotic response to excess dMyc.
  • The IRER is also involved in P53-dependent proapoptotic gene induction following DNA damage.
  • Chromatin conformation within the IRER is modulated by polycomb group-mediated histone modifications.

Conclusions:

  • The IRER acts as a crucial mediator for both dMyc-induced apoptosis and P53-mediated DNA damage response.
  • Epigenetic regulation of IRER accessibility sets thresholds for apoptotic gene expression, influencing cellular sensitivity to oncogenic stress.
  • This study reveals a conserved mechanism linking oncogene-induced stress, DNA damage response, and epigenetic control of apoptosis.

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