Role of M1BP, a transcriptional pausing transcription factor in JNK-mediated cell death during eye development
Anuradha Chimata Venkatakrishnan, Hannah paige Darnell
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 transcription factor, promotes eye development by suppressing wingless (wg) expression. We also showed that M1BP regulates caspase-mediated cell death that is triggered by wg induction. M1BP is a functional homolog of ZKSCAN3, an autophagy repressor in humans. Jun-amino-terminal-(NH2)-Kinase (JNK) signaling is a pro-death pathway that is also known to activate caspase-mediated cell death. We hypothesized that M1BP could have a role in mediating cell death via JNK signaling during eye development. We used the Drosophila melanogaster model to study the role of JNK signaling during M1BP mediated eye suppression. Using the GAL4-UAS system, we modulated JNK signaling components along with downregulating M1BPRNAi. We present data that shows that the absence of M1BPRNAi results in activation of autophagic marker and JNK signaling. We show that activation of JNK signaling enhances M1BPRNAi phenotype and downregulation of JNK signaling rescues the M1BPRNAi phenotype of no eye. We also show that loss of M1BPRNAi in addition to blocking cell death and autophagy resulted in a rescue of the M1BPRNAi no eye phenotype.
Madhuri Kango-Singh, Amit Singh
Primary Advisor's Department
Stander Symposium project, College of Arts and Sciences
United Nations Sustainable Development Goals
Good Health and Well-Being
"Role of M1BP, a transcriptional pausing transcription factor in JNK-mediated cell death during eye development" (2022). Stander Symposium Projects. 2421.