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Sloppy paired 1/2 regulate glial cell fates by inhibiting Gcm Function
Author(s) -
Mondal Soma,
Ivanchuk Stacey M.,
Rutka James T.,
Boulianne Gabrielle L.
Publication year - 2007
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.20456
Subject(s) - biology , gcm transcription factors , cell fate determination , embryonic stem cell , downregulation and upregulation , function (biology) , microbiology and biotechnology , cell , mutant , neuroglia , gene , neuroscience , central nervous system , genetics , transcription factor , general circulation model , ecology , climate change
Abstract Organization of the central nervous system during embryonic development is an intricate process involving a host of molecular players. The Drosophila segmentation genes, sloppy paired (slp) 1/2 have been shown to be necessary for development of a neuronal precursor cell subtype, the NB4‐2 cells. Here, we show that slp1/2 also have roles in regulating glial cell fates. Using slp1/2 loss‐of‐function mutants, we show an increase in glial cell markers, glial cells missing ( gcm ) and reversed polarity. In contrast, misexpression of either slp1 or slp2 causes downregulation of glial cell‐specific genes and alters the fate of glial and neuronal cells. Furthermore, we demonstrate that Slp1 and its mammalian ortholog, Foxg1, inhibit Gcm transcriptional activity as well as bind Gcm. Taken together, these data show that Slp1/Foxg1 regulate glial cell fates by inhibiting Gcm function. © 2006 Wiley‐Liss, Inc.