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The Linker Domain of Stat1 Is Required for Gamma Interferon-Driven Transcription

机译：γ1干扰素驱动转录需要Stat1的连接子域

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Upon binding of gamma interferon (IFN-γ) to its receptor, the latent transcription factor Stat1 becomes phosphorylated, dimerizes, and enters the nucleus to activate transcription. In response to IFN-α, Stat1 binds to Stat2 in a heterodimer that recruits p48, an IRF family member, to activate transcription. A number of functional domains of the STATs, including a C-terminal transactivation domain, a dimerization domain, and an SH2 domain, are known. However, the highly conserved residues between the DNA binding and SH2 domains (463 to 566), recently christened the linker domain on the basis of crystallographic studies, have remained without a known function. In the present study, we report that KE544-545AA point mutants in Stat1 abolish transcriptional responses to IFN-γ but not to IFN-α. We further show that this mutant Stat1 undergoes normal phosphorylation, nuclear translocation, and DNA binding. Taken together with recent structural evidence, these results suggest that the linker domain acts as a critical contact point during the construction of a Stat1-driven transcriptional complex.
机译：γ干扰素（IFN-γ）与其受体结合后，潜在的转录因子Stat1磷酸化，二聚化并进入细胞核以激活转录。响应于IFN-α，Stat1在募集IRF家族成员p48的异二聚体中与Stat2结合以激活转录。已知STAT的许多功能结构域，包括C端反式激活结构域，二聚结构域和SH2结构域。然而，DNA结合和SH2结构域之间的高度保守的残基（463至566），最近根据晶体学研究命名为接头结构域，仍然没有已知功能。在本研究中，我们报告Stat1中的KE544-545AA点突变消除了对IFN-γ的转录反应，但没有消除对IFN-α的转录反应。我们进一步表明，该突变体Stat1经历正常的磷酸化，核易位和DNA结合。结合最新的结构证据，这些结果表明，在构建Stat1驱动的转录复合体期间，接头结构域充当关键的接触点。

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