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Hipk is required for JAK/STAT activity and promotes hemocyte-derived tumorigenesis

Jessica A. Blaquiere, Nathan B. Wray, Esther M. Verheyen
doi: https://doi.org/10.1101/058156
Jessica A. Blaquiere
Department of Molecular Biology and Biochemistry Centre for Cell Biology, Development and Disease Simon Fraser University, Burnaby, B.C Canada
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Nathan B. Wray
Department of Molecular Biology and Biochemistry Centre for Cell Biology, Development and Disease Simon Fraser University, Burnaby, B.C Canada
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Esther M. Verheyen
Department of Molecular Biology and Biochemistry Centre for Cell Biology, Development and Disease Simon Fraser University, Burnaby, B.C Canada
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Abstract

Dysregulation of key signaling molecules and pathways are causative of many Human diseases and cancers. A point mutation in the Drosophila Janus kinase (called hop) causes constitutive activation of the JAK/STAT pathway and results in blood cell tumours. We provide robust genetic evidence that Hipk is required for endogenous JAK/STAT activity. Overexpression of Hipk can phenocopy the effects of overactive JAK/STAT mutations and lead to melanized tumors and loss of Hipk can suppress the effects of hyperactive JAK/STAT. Furthermore, Hipk expression in blood cell progenitors causes tumors. PLA experiments show that Hipk can interact with the pathway effector Stat92E. Together our results show that Hipk is a novel factor required for effective JAK/STAT signaling.

Summary Statement Loss of hipk impairs JAK/STAT activity in multiple tissue types and elevated Hipk leads to the formation of blood cell tumors in Drosophila.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. All rights reserved. No reuse allowed without permission.
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Posted June 10, 2016.
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Hipk is required for JAK/STAT activity and promotes hemocyte-derived tumorigenesis
Jessica A. Blaquiere, Nathan B. Wray, Esther M. Verheyen
bioRxiv 058156; doi: https://doi.org/10.1101/058156
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Hipk is required for JAK/STAT activity and promotes hemocyte-derived tumorigenesis
Jessica A. Blaquiere, Nathan B. Wray, Esther M. Verheyen
bioRxiv 058156; doi: https://doi.org/10.1101/058156

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