Affiliations: 1) University of Dayton; 2) Premedical Program, University of Dayton, Dayton, OH; 3) Center for Tissue Regeneration & Engineering (TREND), University of Dayton, Dayton, OH; 4) Integrative Science and Engineering (ISE), University of Dayton, Dayton, OH; 5) Center for Genomic Advocacy (TCGA), Indiana State University, Terre Haute, IN
Keywords: f. autophagy; f. autophagy
In all multicellular organisms, transcriptional regulation is crucial to regulate differential gene expression, which is important during development and growth. Transcriptional pausing is one such mechanism used to control gene expression. Recently, we have shown that M1BP, a transcriptional pausing factor, promotes eye development by suppressing wingless (wg) expression. We showed that loss of M1BP induces ectopic caspase-mediated cell death that is triggered by wg induction. Blocking caspase-dependent cell death using p35 showed significant but incomplete rescue. M1BP is the functional homolog of ZKSCAN3, an autophagy repressor in humans. Jun-amino-terminal-(NH2)-Kinase (JNK) signaling is known to activate both caspase-dependent and -independent cell death. We hypothesized that M1BP could have a role in mediating multiple forms of cell death via JNK signaling during eye development. In our study, we have used the Drosophila melanogaster (Fruit fly) model to study the role of JNK pathway modulation during M1BP mediated eye suppression. Using the GAL4-UAS system, we modulated JNK signaling components along with downregulating M1BP. Here we present data that shows that the absence of M1BP results in activation of autophagic marker and JNK signaling. We also show that activation of JNK signaling enhances M1BPRNAi phenotype and downregulation of JNK signaling rescues the M1BPRNAi no eye phenotype.