Presenter(s)

    Anuradha Chimata Venkatakrishnan, Hannah Paige Darnell

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    Description

    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 known to activate caspase-mediated cell death. We hypothesize that M1BP could have a role in mediating cell death via JNK signaling during eye development. In our studies, we explore the modulation of JNK signaling and its effect on M1BP mediated cell death by using the GAL4-UAS system. We present preliminary data that shows that the absence of M1BP function results in activation of autophagic cell death markers and JNK signaling.

    Publication Date

    4-22-2021

    Project Designation

    Independent Research

    Primary Advisor

    Amit Singh

    Primary Advisor's Department

    Biology

    Keywords

    Stander Symposium project, College of Arts and Sciences

    United Nations Sustainable Development Goals

    Good Health and Well-Being

    Role of Motif 1 Binding Protein (M1BP), a transcriptional pausing transcription factor in JNK-mediated cell death during eye development

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