PT - JOURNAL ARTICLE AU - Jessica A. Blaquiere AU - Nathan B. Wray AU - Esther M. Verheyen TI - Hipk is required for JAK/STAT activity and promotes hemocyte-derived tumorigenesis AID - 10.1101/058156 DP - 2016 Jan 01 TA - bioRxiv PG - 058156 4099 - http://biorxiv.org/content/early/2016/06/10/058156.short 4100 - http://biorxiv.org/content/early/2016/06/10/058156.full AB - 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.