NDLI: chinmo is a functional effector of the JAK/STAT pathway that regulates eye development, tumor formation and stem cell self-renewal in Drosophila

Content Provider	PubMed Central
Author	Flaherty, Maria Sol Salis, Pauline Evans, Cory J. Ekas, Laura A. Marouf, Amine Zavadil, Jiri Banerjee, Utpal Bach, Erika A.
Copyright Year	2009
Abstract	The 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 non-autonomously. Chinmo is therefore a key effector of JAK/STAT signaling in a variety of developmental and pathological contexts.
Related Links	http://dx.doi.org/10.1016/j.devcel.2010.02.006
Ending Page	568
Page Count	13
Starting Page	556
File Format	PDF
ISSN	15345807
e-ISSN	18781551
Journal	Developmental cell
Issue Number	4
Volume Number	18
Language	English
Publisher Date	2010-04-01
Access Restriction	Open
Subject Keyword	Developmental Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Developmental Biology Molecular Biology

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