Related Experiment Video
Updated: Mar 28, 2026

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila
Published on: November 27, 2016
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.
Abstract:
Histone modulations have been implicated in various cellular and developmental processes where in Drosophila Mof is involved in acetylation of H4K16. Reduction in the size of larval imaginal discs is observed in the null mutants of mof with increased apoptosis. Deficiency involving Hid, Reaper and Grim [H99] alleviated mof (RNAi) induced apoptosis in the eye discs. mof (RNAi) induced apoptosis leads to activation of caspases which is suppressed by over expression of caspase inhibitors like P35 and Diap1 clearly depicting the role of caspases in programmed cell death. Also apoptosis induced by knockdown of mof is rescued by JNK mutants of bsk and tak1 indicating the role of JNK in mof (RNAi) induced apoptosis. The adult eye ablation phenotype produced by ectopic expression of Hid, Rpr and Grim, was restored by over expression of Mof. Accumulation of Mof at the Diap1 promoter 800 bp upstream of the transcription start site in wild type larvae is significantly higher (up to twofolds) compared to mof (1) mutants. This enrichment coincides with modification of histone H4K16Ac indicating an induction of direct transcriptional up regulation of Diap1 by Mof. Based on these results we propose that apoptosis triggered by mof (RNAi) proceeds through a caspase-dependent and JNK mediated pathway.
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.
Related Concept Videos
The Extrinsic Apoptotic Pathway
The Intrinsic Apoptotic Pathway
Apoptosis
MAPK Signaling Cascades

