Kumaran R Ileng, Muralikrishna Bhattiprolu, Parnaik Veena K
Centre for Cellular and Molecular Biology, Hyderabad-500 007, India.
J Cell Biol. 2002 Dec 9;159(5):783-93. doi: 10.1083/jcb.200204149.
The A-type lamins have been observed to colocalize with RNA splicing factors in speckles within the nucleus, in addition to their typical distribution at the nuclear periphery. To understand the functions of lamin speckles, the effects of transcriptional inhibitors known to modify RNA splicing factor compartments (SFCs) were examined. Treatment of HeLa cells with alpha-amanitin or 5,6-dichlorobenzimidazole riboside (DRB) inhibited RNA polymerase II (pol II) transcription and led to the enlargement of lamin speckles as well as SFCs. Removal of the reversible inhibitor DRB resulted in the reactivation of transcription and a rapid, synchronous redistribution of lamins and splicing factors to normal-sized speckles, indicating a close association between lamin speckles and SFCs. Conversely, the expression of NH2-terminally modified lamin A or C in HeLa cells brought about a loss of lamin speckles, depletion of SFCs, and down-regulation of pol II transcription without affecting the peripheral lamina. Our results suggest a unique role for lamin speckles in the spatial organization of RNA splicing factors and pol II transcription in the nucleus.
除了在核周的典型分布外，还观察到 A 型核纤层蛋白与核内斑点中的 RNA 剪接因子共定位。为了了解核纤层蛋白斑点的功能，研究了已知可改变 RNA 剪接因子区室（SFCs）的转录抑制剂的作用。用α-鹅膏蕈碱或 5,6-二氯苯并咪唑核糖核苷（DRB）处理 HeLa 细胞会抑制 RNA 聚合酶 II（pol II）转录，并导致核纤层蛋白斑点以及 SFCs 增大。去除可逆抑制剂 DRB 会导致转录重新激活，核纤层蛋白和剪接因子迅速同步重新分布到正常大小的斑点中，这表明核纤层蛋白斑点与 SFCs 之间存在密切关联。相反，在 HeLa 细胞中 NH2 末端修饰的核纤层蛋白 A 或 C 的表达导致核纤层蛋白斑点消失、SFCs 减少以及 pol II 转录下调，而不影响核周层。我们的结果表明核纤层蛋白斑点在细胞核中 RNA 剪接因子的空间组织和 pol II 转录中具有独特作用。
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