PU.1 exhibits partial functional redundancy with Spi-B, but not with Ets-1 or Elf-1. Blood 2001 May 01;97(9):2908-12
Date
04/21/2001Pubmed ID
11313289DOI
10.1182/blood.v97.9.2908Scopus ID
2-s2.0-0035353165 (requires institutional sign-in at Scopus site) 45 CitationsAbstract
Previously it was shown that the Ets proteins, PU.1 and Spi-B, exhibit functional redundancy in B lymphocytes. To investigate the possibility that PU.1 or Spi-B or both share overlapping roles with Ets-1 or Elf-1, PU.1(+/-)Ets-1(-/-), PU.1(+/-)Elf-1(-/-), and Spi-B(-/-)Ets-1(-/-) animals were generated. No blood cell defects were observed in these animals except those previously reported for Ets-1(-/-) mice. Therefore, no genetic overlap was detected between PU.1 or Spi-B with Ets-1 or Elf-1. In contrast, the results confirmed functional redundancy for PU.1 and Spi-B in that PU.1(+/-)Spi-B(-/-) bone marrow progenitors yielded smaller colonies in methylcellulose cultures than did wild-type, PU.1(+/-) or Spi-B(-/-) progenitors. In addition, PU.1(+/-)Spi-B(+/+), PU.1(+/-)Spi-B(+/-), and PU.1(+/-) Spi-B(-/-) mice displayed extramedullary splenic hematopoiesis. In summary, PU.1 and Spi-B regulate common target genes required for proliferation of hematopoietic progenitors or their committed descendants, whereas Ets-1 or Elf-1 do not appear to regulate shared target genes with PU.1 or Spi-B.
Author List
Garrett-Sinha LA, Dahl R, Rao S, Barton KP, Simon MCAuthor
Sridhar Rao MD, PhD Associate Professor in the Pediatrics department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsDNA-Binding Proteins
Gene Expression Regulation
Hematopoietic Stem Cells
Mice
Nuclear Proteins
Proto-Oncogene Protein c-ets-1
Proto-Oncogene Proteins
Proto-Oncogene Proteins c-ets
Trans-Activators
Transcription Factors