Analysis of alternative splicing mechanisms coordinately regulated by high-light responsive SR proteins

我们已经证明拟南芥SR蛋白atSR45a和atSR30通过其他剪接因子参与剪接体组装，并在强光胁迫下显著诱导其表达。这些事实表明，atSR45a和atSR30参与了高光胁迫响应-选择性剪接事件的调控。在这里，我们通过全基因组拼接阵列技术确定了atSR45a和atSR30调节选择性剪接效率的基因，并通过一系列结构域缺失突变体证明了atSR30和atSR45a中的结构域参与亚细胞和亚核分布。

We have demonstrated that Arabidopsis SR proteins, atSR45a and atSR30 participates in a spliceosomal assembly through other splicing factors and its expression is markedly induced by high-light stress. These facts suggest that atSR45a and atSR30 are involved in the regulation of high-light stress responsive-alternative splicing events. Here, we identified genes of which alternative splicing efficiencies are regulated by atSR45a and atSR30, by a whole genome tiling array technology, and demonstrated the involvement of the domains in atSR30 and atSR45a in subcellular and subnuclear distribution using a series of structural domain-deleted mutants.