Mutation of Arabidopsis SPLICEOSOMAL TIMEKEEPER LOCUS1 Causes Circadian Clock Defects
Mutation of Arabidopsis SPLICEOSOMAL TIMEKEEPER LOCUS1 Causes Circadian Clock Defects
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DOI：
10.1105/tpc.112.104828
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发表时间：
2012-10-01
期刊：
影响因子：
11.6
通讯作者：
Harmer, Stacey L.
中科院分区：
文献类型：
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作者：
Jones, Matthew A.;Williams, Brian A.;Harmer, Stacey L.
生物钟在协调植物代谢和生理功能与可预测的环境变量（例如黄昏和黎明）方面发挥着至关重要的作用，同时还调节对生物和非生物挑战的反应。昼夜节律系统的大部分初始特征都集中在转录起始上，但现在很明显，在这一关键的调节步骤之后，会施加相当大的调节。据报道，转录处理、蛋白质稳定性和辅因子可用性都会影响多种物种的昼夜节律。我们使用基因筛选来鉴定假定的 RNA 结合蛋白（SPLICEOSOMAL TIMEKEEPER LOCUS1 [STIPL1]）内的突变，该突变在恒定条件下诱导长昼夜节律表型。 STIPL1 是参与剪接体分解的剪接体蛋白 TFP11（智人）和 Ntr1p（酿酒酵母）的同源物。使用高分辨率 RT-PCR 系统对一般剪接和选择性剪接的分析表明，该蛋白质的突变导致大多数但不是全部分析的内含子的剪接效率较低。特别是，昼夜节律相关转录物积累的改变可能有助于观察到的突变表型。有趣的是，STIPL1 的密切同源物 STIP-LIKE2 的突变不会引起昼夜节律表型，这表明这些家族成员之间的功能存在差异。我们的工作强调了时钟机制中转录后控制的重要性。
The circadian clock plays a crucial role in coordinating plant metabolic and physiological functions with predictable environmental variables, such as dusk and dawn, while also modulating responses to biotic and abiotic challenges. Much of the initial characterization of the circadian system has focused on transcriptional initiation, but it is now apparent that considerable regulation is exerted after this key regulatory step. Transcript processing, protein stability, and cofactor availability have all been reported to influence circadian rhythms in a variety of species. We used a genetic screen to identify a mutation within a putative RNA binding protein (SPLICEOSOMAL TIMEKEEPER LOCUS1 [STIPL1]) that induces a long circadian period phenotype under constant conditions. STIPL1 is a homolog of the spliceosomal proteins TFP11 (Homo sapiens) and Ntr1p (Saccharomyces cerevisiae) involved in spliceosome disassembly. Analysis of general and alternative splicing using a high-resolution RT-PCR system revealed that mutation of this protein causes less efficient splicing of most but not all of the introns analyzed. In particular, the altered accumulation of circadian-associated transcripts may contribute to the observed mutant phenotype. Interestingly, mutation of a close homolog of STIPL1, STIP-LIKE2, does not cause a circadian phenotype, which suggests divergence in function between these family members. Our work highlights the importance of posttranscriptional control within the clock mechanism.