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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

04/21/2001

Pubmed ID

11313289

DOI

10.1182/blood.v97.9.2908

Scopus ID

2-s2.0-0035353165 (requires institutional sign-in at Scopus site)   45 Citations

Abstract

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 MC

Author

Sridhar Rao MD, PhD Associate Professor in the Pediatrics department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
DNA-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