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. Author manuscript; available in PMC: 2011 Jun 13.
Published in final edited form as: Epigenetics. 2008 May 9;3(3):134–142. doi: 10.4161/epi.3.3.6252

Figure 4.

Figure 4

Increased PU.1 expression in Lsh−/− hematopoietic progenitors and reactivation of endogenous retroviral elements. (A) PU.1 protein levels were examined in extracts derived from MEFs or fetal livers from three different Lsh−/− or Lsh+/+ control mice by Western blot analysis. (B) Graph of the PU.1 locus showing the five exons (open boxes), the location of the two retroviral elements ERVL and MaLR (black boxes), the transcriptional start site (arrow) and the position of the primers used for RT-PCR analysis (black triangles). The primers used for detection of PU.1 transcripts were located in exon I and exon IV. The 5' and 3' primer for MaLR and the 5' primer for ERVL were located outside of the repeat region allowing specific detection of transcripts. (C) RT-PCR analysis for detection of PU.1 transcripts and ERVL and MaLR transcripts located in the PU.1 locus. RT-PCR analysis for IAP transcripts was used for comparison and actin as a control. RNA was prepared from Lin-Sca1+Kit+ purified progenitor cells derived from Lsh−/− or Lsh+/+ fetal liver. (D) Bar graph of semi-quantitative RT-PCR analysis for detection of PU.1, IAP, ERVL and MaLR. Number represents arbitrary units relative to actin. The data for PU.1 transcripts summarizes PCR analysis performed with RNA from three independent purified Lin−Sca1+Kit+ progenitor cells. The other graphs summarize results from two independent stem cell purifications.