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First published online September 18, 2007

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Loopy chromatin fights infection

Activation of genes within the major histocompatibility complex (MHC) on chromosome 6 by interferon (IFN) is a critical trigger of the immune response. IFN stimulates signalling through JAK/STAT-family proteins and, in many cell types, induces the formation of a giant chromatin loop that encompasses the MHC region. Now, on p. 3262, Denise Sheer and co-workers describe how this loop forms and propose that chromatin remodelling is necessary for activation of MHC genes. They show, for example, that a point mutation in the STAT1 transcription factor that prevents its phosphorylation abolishes chromatin remodelling in IFN-treated fibrosarcoma cells. The onset of chromatin remodelling in these cells, they report, coincides with binding of activated STAT1 and the chromatin-remodelling enzyme BRG1 to the MHC region; RNA-polymerase recruitment and histone hyperacetylation (markers of transcriptional activation) occur subsequently. The authors also report that the MHC region becomes decondensed in the IFN-induced chromatin loop. They propose, therefore, that JAK/STAT signalling drives higher-order chromatin remodelling of the MHC locus, which generates the trancriptionally permissive chromatin environment needed for activation of MHC genes.

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Related articles in JCS:

P-STAT1 mediates higher-order chromatin remodelling of the human MHC in response to IFN

Rossitza Christova, Tania Jones, Pei-Jun Wu, Andreas Bolzer, Ana P. Costa-Pereira, Diane Watling, Ian M. Kerr, and Denise Sheer
JCS 2007 120: 3262-3270. [Abstract] [Full Text]  

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in JCS Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Search for Related Content Social Bookmarking                         What's this?