TY - JOUR
T1 - Genesis, a Winged Helix transcriptional repressor, has embryonic expression limited to the neural crest, and stimulates proliferation in vitro in a neural development model
AU - Hromas, Robert
AU - Ye, Honggang
AU - Spinella, Michael
AU - Dmitrovsky, Ethan
AU - Xu, Dawei
AU - Costa, Robert H.
N1 - Funding Information:
The murine monoclonal antibody SSEA-3 (IgM) was obtained from the Developmental Studies Hybridoma Bank maintained by the Department of Pharmacology and Molecular Sciences, Johns Hopkins University School of Medicine, Baltimore, MD, and the Department of Biological Sciences, University of Iowa, Iowa City, Iowa, under contract N01-HD-6–2915 from the National Institute for Child Health and Human Development (NICHD). The murine hybridoma A2B5 (IgM) was obtained from the American Type Culture Collection (ATCC).
Funding Information:
This work was supported by Public Health Service grants RO1 HL48914 to R.H. and RO1 GM43241 to R.H.C. R.H.C. is an Established Investigator of the American Heart Association/Bristol-Myers Squibb. R.H. is a Scholar of the Leukemia Society of America
Copyright:
Copyright 2021 Elsevier B.V., All rights reserved.
PY - 1999
Y1 - 1999
N2 - A novel repressor of the Winged Helix (formerly HNF-3/Forkhead) transcriptional regulatory family, termed Genesis (also called HFH2), was previously found to be exclusively expressed in primitive embryonic cell lines. In this study in situ cRNA hybridization experiments revealed that Genesis was expressed during embryogenesis only in developing neural crest cells. Its expression diminished upon their terminal differentiation into sympathetic and parasympathetic neurons. Based on that finding, Genesis was retrovirally transduced into pluripotent N-Tera-2 clone D1 (NT2/D1) teratocarcinoma cells, which are a well-described in vitro model of neural development. Retinoic acid (RA) treatment will drive these cells to differentiation toward the neuronal lineage and cause an increase in expression of the cyclin-dependent kinase inhibitor p21 protein, which leads to an inhibition in cellular proliferation. Although RA-induced expression of neuronal differentiation markers was not influenced by forced overexpression of Genesis in NT2-D1 cells, proliferation of Genesis-transduced cells continued following RA treatment. RA was unable to induce the expression of the cyclin-dependent kinase inhibitor p21 in the Genesis-transduced cells, but Go/G1 tumor suppressor p53 expression was induced normally. Therefore, Genesis may play a role in the regulation of primitive neural crest development by preventing terminal quiescence through inhibition of p21 protein expression. These data also lend evidence for the hypothesis that proliferation and differentiation pathways are not irrevocably linked, but can function independently.
AB - A novel repressor of the Winged Helix (formerly HNF-3/Forkhead) transcriptional regulatory family, termed Genesis (also called HFH2), was previously found to be exclusively expressed in primitive embryonic cell lines. In this study in situ cRNA hybridization experiments revealed that Genesis was expressed during embryogenesis only in developing neural crest cells. Its expression diminished upon their terminal differentiation into sympathetic and parasympathetic neurons. Based on that finding, Genesis was retrovirally transduced into pluripotent N-Tera-2 clone D1 (NT2/D1) teratocarcinoma cells, which are a well-described in vitro model of neural development. Retinoic acid (RA) treatment will drive these cells to differentiation toward the neuronal lineage and cause an increase in expression of the cyclin-dependent kinase inhibitor p21 protein, which leads to an inhibition in cellular proliferation. Although RA-induced expression of neuronal differentiation markers was not influenced by forced overexpression of Genesis in NT2-D1 cells, proliferation of Genesis-transduced cells continued following RA treatment. RA was unable to induce the expression of the cyclin-dependent kinase inhibitor p21 in the Genesis-transduced cells, but Go/G1 tumor suppressor p53 expression was induced normally. Therefore, Genesis may play a role in the regulation of primitive neural crest development by preventing terminal quiescence through inhibition of p21 protein expression. These data also lend evidence for the hypothesis that proliferation and differentiation pathways are not irrevocably linked, but can function independently.
KW - Differentiation
KW - Embryonal carcinoma
KW - Forkhead/Winged helix
KW - Mouse
KW - Retinoic acid
KW - Transcription factors
KW - Transcriptional repression
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U2 - 10.1007/s004410051365
DO - 10.1007/s004410051365
M3 - Article
C2 - 10460485
AN - SCOPUS:0032843174
SN - 0302-766X
VL - 297
SP - 371
EP - 382
JO - Cell and Tissue Research
JF - Cell and Tissue Research
IS - 3
ER -