Opposing functions of the Ets factors NERF and ELF-1 during chicken blood vessel development.
OBJECTIVE
The purpose of this study was to evaluate the role of the Ets factor NERF in the regulation of the Tie1 and Tie2 genes during chicken blood vessel development.


RESULTS
We have isolated the full-length cDNA for the chicken homologue of the human Ets factor NERF2 (cNERF2). Northern blot analysis and in situ hybridization demonstrate that cNERF2 is enriched in the developing blood vessels of the chicken chorioallantoic membrane. Interestingly, cNERF2 functions as a competitive inhibitor of a highly related Ets factor cELF-1, which we have previously shown to be enriched in chicken blood vessel development. Although in vitro-translated cELF-1 and cNERF2 can bind equally well to conserved Ets binding sites in the promoters of the Tie1 and Tie2 genes, cELF-1 preferentially binds to the Ets sites in these promoters during early stages of chicken blood vessel development, suggesting that cNERF may bind during later stages of blood vessel development and vascular remodeling.


CONCLUSIONS
cNERF2 is enriched during embryonic and extraembryonic blood vessel development in the chicken and facilitates tight control of Tie1 and Tie2 gene regulation.
Cardiology Division, New England Baptist Bone and Joint Institute, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Mass, USA.
John
J
Gaspar
Shelley
S
Thai
Carole
C
Voland
Antoinise
A
Dube
Towia A
TA
Libermann
M Luisa
ML
Iruela-Arispe
Peter
P
Oettgen
D000818:Animals; D002460:Cell Line; D002642:Chick Embryo; D002645:Chickens; D004268:DNA-Binding Proteins / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D020869:Gene Expression Profiling; D018507:Gene Expression Regulation, Developmental / Q000235:genetics / Q000502:physiology; D015971:Gene Expression Regulation, Enzymologic / Q000235:genetics / Q000502:physiology; D006801:Humans; D017403:In Situ Hybridization; D007668:Kidney / Q000166:cytology; D051379:Mice; D018919:Neovascularization, Physiologic / Q000235:genetics; D009687:Nuclear Proteins; D011401:Promoter Regions, Genetic / Q000235:genetics; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000502:physiology*; D050783:Proto-Oncogene Proteins c-ets; D020794:Receptor Protein-Tyrosine Kinases / Q000235:genetics / Q000378:metabolism; D042810:Receptor, TIE-1; D042787:Receptor, TIE-2; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D042764:Receptors, TIE; D014157:Transcription Factors / Q000037:antagonists & inhibitors / Q000235:genetics / Q000302:isolation & purification / Q000378:metabolism / Q000502:physiology*
D004268:DNA-Binding Proteins; C512897:ELF1 protein, human; C512896:Elf1 protein, mouse; D009687:Nuclear Proteins; D011518:Proto-Oncogene Proteins; D050783:Proto-Oncogene Proteins c-ets; D011956:Receptors, Cell Surface; D014157:Transcription Factors; C101003:ELF2 protein, human; D020794:Receptor Protein-Tyrosine Kinases; D042810:Receptor, TIE-1; D042787:Receptor, TIE-2; D042764:Receptors, TIE