Mondal Soma, Ivanchuk Stacey M, Rutka James T, Boulianne Gabrielle L
The Arthur and Sonia Labatt Brain Tumour Research Center, Hospital for Sick Children, Toronto, Ontario, Canada.
Glia. 2007 Feb;55(3):282-93. doi: 10.1002/glia.20456.
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.
胚胎发育过程中中枢神经系统的组织是一个复杂的过程，涉及许多分子参与者。果蝇的分节基因，稀松配对（slp）1/2已被证明对于一种神经元前体细胞亚型NB4-2细胞的发育是必需的。在这里，我们表明slp1/2在调节神经胶质细胞命运方面也发挥作用。使用slp1/2功能丧失突变体，我们发现神经胶质细胞标记物、神经胶质细胞缺失（gcm）增加且极性反转。相反，slp1或slp2的错误表达会导致神经胶质细胞特异性基因的下调，并改变神经胶质细胞和神经元细胞的命运。此外，我们证明Slp1及其哺乳动物直系同源物Foxg1抑制Gcm转录活性并与Gcm结合。综上所述，这些数据表明Slp1/Foxg1通过抑制Gcm功能来调节神经胶质细胞命运。
