@article{d308aea040314810897bd13e7f28f35f,
title = "Reciprocal interactions of Pit1 and GATA2 mediate signaling gradient- induced determination of pituitary cell types",
abstract = "The mechanisms by which transient gradients of signaling molecules lead to emergence of specific cell types remain a central question in mammalian organogenesis. Here, we demonstrate that the appearance of four ventral pituitary cell types is mediated via the reciprocal interactions of two transcription factors, Pit1 and GATA2, which are epistatic to the remainder of the cell type-specific transcription programs and serve as the molecular memory of the transient signaling events. Unexpectedly, this program includes a DNA binding-independent function of Pit1, suppressing the ventral GATA2- dependent gonadotrope program by inhibiting GATA2 binding to gonadotrope- but not thyrotrope-specific genes, indicating that both DNA binding-dependent and -independent actions of abundant determining factors contribute to generate distinct cell phenotypes.",
author = "Dasen, {Jeremy S.} and O'Connell, {Shawn M.} and Flynn, {Sarah E.} and Mathias Treier and Gleiberman, {Anatoli S.} and Szeto, {Daniel P.} and Farideh Hooshmand and Aggarwal, {Aneel K.} and Rosenfeld, {Michael G.}",
note = "Funding Information: We thank P. Meyer for expertise in figure preparation; S. Orkin and Y. Fujiwara for providing anti-GATA2 antisera and other reagents; the transgenic core facility at Scripps Research Institute; C. Nelson for cell culture; Mary Ayers for animal care; and Kathleen Scully, Lorin Olson, and Grace Zhao for their contributions. J. S. D. was supported by a Lucille Markey Fund Fellowship, A. S. G. by a National Research Service Award from NIH, and M. T. by a Boehringer Ingelheim Fonds postdoctoral fellowship. M. G. R. is an Investigator with the Howard Hughes Medical Institute. This work was supported by a grant from NIH (NIDDK).",
year = "1999",
month = may,
day = "28",
doi = "10.1016/S0092-8674(00)80770-9",
language = "English",
volume = "97",
pages = "587--598",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "5",
}