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Blood, 1 May 2001, Vol. 97, No. 9, pp. 2908-2912
BRIEF REPORT
PU.1 exhibits partial functional redundancy with Spi-B, but
not with Ets-1 or Elf-1
Lee Ann Garrett-Sinha,
Richard Dahl,
Sridhar Rao,
Kevin P. Barton, and
M. Celeste Simon
From the Department of Medicine and Pathology,
University of Chicago, Chicago, IL; Cardinal Bernardin Cancer Center,
Loyola University Chicago, Maywood, IL; Abramson Family Cancer Research
Institute and Howard Hughes Medical Institute, University of
Pennsylvania, Philadelphia, PA.
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.
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