RT Journal Article
SR Electronic
T1 Hipk is required for JAK/STAT activity and promotes hemocyte-derived tumorigenesis
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 058156
DO 10.1101/058156
A1 Blaquiere, Jessica A.
A1 Wray, Nathan B.
A1 Verheyen, Esther M.
YR 2016
UL http://biorxiv.org/content/early/2016/06/10/058156.abstract
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.