PDF(Pubmed)
Abstract：
Programed cell death (PCD) plays fundamental roles in plant development and responses to environmental stresses. Here, we report a protein, SICKLE (SIC), which represses PCD. In Arabidopsis (Arabidopsis thaliana), the loss-of-function mutant of SIC, sic-4, hyperaccumulated lariat intronic RNAs (lariRNAs) and exhibited PCD. The gene encoding an RNA debranching enzyme 1 (DBR1), a rate-limiting enzyme for lariRNAs decay, was overexpressed to reduce the level of lariRNAs in the sic-4 mutant, which led to suppression of PCD. Meanwhile, another lariRNAs hyper-accumulating mutant, dbr1-2, also exhibited PCD, further indicating that sic-4 PCD is caused by hyper-accumulation of lariRNAs. Transcriptional profiling analyses revealed that the sic-4 mutation disturbed alternative splicing and decay of mRNAs associated with salicylic acid (SA) homeostasis, a well-known molecule functioning in PCD regulation. Moreover, SA is dramatically increased in sic-4 and the disruption of SA biosynthesis and signaling suppressed PCD in the mutant, demonstrating that SA functions downstream of sic-4. Taken together, our results demonstrate that SIC is involved in regulating SA-triggered PCD.
摘要：
细胞程序性死亡（PCD）在植物发育和对环境胁迫的响应中起着重要作用。这里,我们报告了一种蛋白质，SICKLE(SIC),抑制PCD。在拟南芥（拟南芥）中，SIC的功能丧失突变体,sic-4，过度积累的套索内含子RNA（lariRNAs）并表现出PCD。编码RNA脱支酶1（DBR1）的基因，lariRNAs衰变的限速酶，过表达以降低sic-4突变体中lariRNAs的水平，这导致PCD的抑制。同时,另一个lariRNAs超积累突变体，dbr1-2，也表现出PCD，进一步表明sic-4PCD是由lariRNAs的过度积累引起的。转录谱分析显示，sic-4突变干扰了与水杨酸（SA）稳态相关的mRNA的可变剪接和衰减，在PCD调节中起作用的众所周知的分子。此外，SA在sic-4中急剧增加，并且SA生物合成的破坏和信号传导抑制了突变体中的PCD，证明SA在sic-4的下游起作用。一起来看,我们的结果表明SIC参与调节SA触发的PCD.
