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[P162]: The role of GATA‐2 in neurite outgrowth and neuronal migration
Author(s) -
Willett R.,
Greene L.
Publication year - 2006
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2006.09.222
Subject(s) - columbia university , citation , neurite , library science , sociology , neuroscience , media studies , biology , computer science , genetics , in vitro
The GATA family of zinc finger transcription factors have been shown to function in central roles to regulate cell lineage selection, tissue specification, proliferation and migration during development of a wide variety of organisms. One member, GATA-2, is expressed in the intermediate zone of the embryonic mesencephalon and in dorsal diencephalon, ventral hindbrain, and sympathetic ganglia. Here, we provide evidence that GATA2 may function as a negative regulator of neurite outgrowth during development, and that its expression in early neuronal precursors after cell cycle exit may function to delay morphologic differentiation until the cells migrate to their appropriate positions in the developing brain. NGF treatment of PC12 cells causes down-regulation of GATA-2 expression concomitant with neurite outgrowth. Constitutive expression of GATA-2 in PC12 cells suppresses neurite outgrowth induced by NGF, and those neurites that do escape the inhibition are significantly reduced in length compared to controls. Preliminary evidence indicates that knockdown of GATA-2 in e16 embryonic organotypic cultures of rat mesencephalon by retrovirally delivered rhRNA interferes with the migration of neural progenitors away from the ventricular zone and may hasten their maturation. In conclusion, we provide evidence that GATA-2 is required for midbrain development and that it may function to suppress neurite outgrowth so as to permit normal migration to occur.