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First published online September 18, 2007

Journal of Cell Science 120, 1804e (2007)
© The Company of Biologists Limited
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In this issue

Loopy chromatin fights infection


Figure 1

Activation of genes within the major histocompatibility complex (MHC) on chromosome 6 by interferon {gamma} (IFN{gamma}) is a critical trigger of the immune response. IFN{gamma} 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{gamma}-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{gamma}-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.


Related articles in JCS:

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




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