Expression of the Runt Domain-Encoding <i>PEBP2</i> α Genes in T cells during Thymic Development

Masanobu Satake(Kyoto University), Shintaro Nomura(The University of Osaka), Yuko Yamaguchi‐Iwai(Kyoto University), Yousuke Takahama(Nippon Institute of Technology), Yasuhiro Hashimoto(Nippon Institute of Technology), Masaru Niki(Institute of Aging), Yukihiko Kitamura(The University of Osaka), Yoshiaki Ito(Kyoto University)
Molecular and Cellular Biology
March 1, 1995
Cited by 160Open Access
Full Text

Abstract

The PEBP2 alpha A and PEBP2 alpha B genes encode the DNA-binding subunit of a murine transcription factor, PEBP2, which is implicated as a T-cell-specific transcriptional regulator. These two related genes share the evolutionarily conserved region encoding the Runt domain. PEBP2 alpha B is the murine counterpart of human AML1, which is located at the breakpoints of the 8;21 and 3;21 chromosome translocations associated with acute myeloid leukemia. Northern (RNA) blots of various adult mouse tissues revealed that the levels of expression of both genes were most prominent in the thymus. Furthermore, transcripts of PEBP2 alpha A and mouse AML1/PEBP2 alpha B were detected in T lymphocytes in the thymuses from day 16 embryos and newborns, as well as 4-week-old adult mice, by in situ hybridization. The expression of the genes persisted in peripheral lymph nodes of adult mice. The transcripts were detected in all the CD4- CD8-, CD4+ CD8+, CD4+ CD8-, and CD4- CD8+ cell populations. The results indicated that both genes are expressed in T cells throughout their development, supporting the notion that PEBP2 is a T-cell-specific transcription factor. Transcripts of mouse AML1/PEBP2 alpha B were also detected in day 12 fetal hematopoietic liver and in the bone marrow cells of newborn mice. The implication of mouse AML1/PEBP2 alpha B expression in hematopoietic cells other than those of T-cell lineage is discussed in relation to myeloid leukemogenesis.


Related Papers

No related papers found

Powered by citation graph analysis