Drosophila MOF regulates DIAP1 and induces apoptosis in a JNK dependent pathway

Sreerangam N C V L Pushpavalli1, Arpita Sarkar2, M Janaki Ramaiah2,3

  • 1Agricultural Research Station, Prof. Jayashankar Telangana State Agricultural University, Tandur, 501141, Telangana, India.

Insights

The study reveals that Mof protein regulates apoptosis in Drosophila by controlling histone acetylation and activating caspases and JNK pathways. Mof

Area of Science:

  • Molecular Biology
  • Developmental Biology
  • Genetics

Background:

  • Histone modifications regulate gene expression and cellular processes.
  • Mof (Male-specific lethal withoutНomolog) protein in Drosophila is crucial for H4K16 acetylation.
  • Mof's role in apoptosis and its regulatory pathways are not fully understood.

Purpose of the Study:

  • To investigate the role of Mof in apoptosis during Drosophila development.
  • To elucidate the molecular mechanisms underlying Mof-mediated apoptosis, including caspase and JNK pathway involvement.
  • To determine if Mof directly regulates the expression of apoptosis-related genes like Diap1.

Main Methods:

  • Utilized Drosophila melanogaster models, including mof mutants and RNAi.
  • Induced apoptosis using mof knockdown and pro-apoptotic genes (Hid, Reaper, Grim).
  • Assessed apoptosis via caspase activation, caspase inhibitors (P35, Diap1), JNK pathway mutants (bsk, tak1), and Mof localization studies.

Main Results:

  • Mof deficiency leads to reduced larval imaginal disc size and increased apoptosis.
  • Knockdown of mof induces apoptosis dependent on caspases and the JNK pathway.
  • Overexpression of Mof rescues apoptosis and restores eye development, suggesting a direct role in regulating Diap1 transcription via H4K16 acetylation.

Conclusions:

  • Mof plays a critical role in regulating programmed cell death in Drosophila.
  • Mof-induced apoptosis involves caspase activation and is mediated by the JNK signaling pathway.
  • Mof directly upregulates Diap1 expression through histone H4K16 acetylation at the Diap1 promoter.

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