chinmo Is a Functional Effector of the JAK/STAT Pathway that Regulates Eye Development, Tumor Formation, and Stem Cell Self-Renewal in Drosophila

SummaryThe Drosophila STAT transcription factor Stat92E regulates diverse functions, including organ development and stem cell self-renewal. However, the Stat92E functional effectors that mediate these processes are largely unknown. Here we show that chinmo is a cell-autonomous, downstream mediator of Stat92E that shares numerous functions with this protein. Loss of either gene results in malformed eyes and head capsules due to defects in eye progenitor cells. Hyperactivation of Stat92E or misexpression of Chinmo results in blood cell tumors. Both proteins are expressed in germline (GSCs) and cyst stem cells (CySCs) in the testis. While Stat92E is required for the self-renewal of both populations, chinmo is only required in CySCs, indicating that Stat92E regulates self-renewal in different stem cells through independent effectors. Like hyperactivated Stat92E, Chinmo misexpression in CySCs is sufficient to maintain GSCs nonautonomously. Chinmo is therefore a key effector of JAK/STAT signaling in a variety of developmental and pathological contexts.

Graphical AbstractFigure optionsDownload high-quality image (287 K)Download as PowerPoint slideHighlights
► chinmo is a critical functional effector of the JAK/STAT signaling pathway
► Manipulating chinmo recapitulates STAT-related developmental and tumor phenotypes
► chinmo is required for self-renewal of somatic stem cells (CySCs) in the gonad
► Excess chinmo in CySCs expands the germline stem cell (GSC) population