Mouse major histocompatibility class I gene expression begins at midsomite stage and is inducible in earlier-stage embryos by interferon

To determine the timing of major histocompatibility complex class I gene expression during embryonic development, binding of anti-class I antibodies and appearance of class I gene transcripts were examined in mouse embryos from the egg-cylinder stage through day 16 of gestation. By using two series...

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Veröffentlicht in:Proc. Natl. Acad. Sci. U.S.A.; (United States) 1985-04, Vol.82 (8), p.2427-2431
Hauptverfasser: Ozato, K, Wan, Y.J, Orrison, B.M
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Sprache:eng
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Zusammenfassung:To determine the timing of major histocompatibility complex class I gene expression during embryonic development, binding of anti-class I antibodies and appearance of class I gene transcripts were examined in mouse embryos from the egg-cylinder stage through day 16 of gestation. By using two series of monoclonal antibodies reactive with monomorphic and polymorphic determinants of class I antigens, it was found that cell-surface expression of the antigens becomes detectable at a low level only after midsomite stage on gestation day 10, at a time when embryos are developed beyond primordial organogenesis and have partial blood circulation. In agreement with the above finding, a low level of class I mRNA became detectable in day 9 and older embryos in blot hybridization. The level of class I transcripts in embryos at least to day 13 remained less than 1/50th that in adult spleen cells. Cells from head-fold stage embryos (gestation day 8), which otherwise do not have an appreciable amount of class I mRNA or surface antigens, begin to express a high level of antigens upon treatment with mouse α /β or γ interferon. This induction of class I antigen expression appears to be stage specific in that embryos in an earlier egg-cylinder stage (day 6) failed to express the antigens after interferon treatment. A possible role of interferons in activating class I genes during in vivo embryonic development is suggested.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.82.8.2427