SKI-INTERACTING PROTEIN interacts with SHOOT MERISTEMLESS to regulate shoot apical meristem formation

编号 040036101

推送时间 20220919

研究领域 森林培育 

年份 2022 

类型 期刊 

语种 英语

标题 SKI-INTERACTING PROTEIN interacts with SHOOT MERISTEMLESS to regulate shoot apical meristem formation

来源期刊 Plant Physiology

期 第361期

发表时间 20220528

关键词 Arabidopsis thaliana;  SKI-INTERACTING PROTEIN (SKIP);  SHOOT MERISTEMLESS (STM);  shoot apical meristem (SAM);  splicing factor;  transcriptional regulator;  genes; 

摘要 The shoot apical meristem (SAM), which is formed during embryogenesis, generates leaves, stems, and floral organs during the plant life cycle. SAM development is controlled by SHOOT MERISTEMLESS (STM), a conserved Class I KNOX transcription factor that interacts with another subclass homeodomain protein, BELL, to form a heterodimer, which regulates gene expression at the transcriptional level in Arabidopsis (Arabidopsis thaliana). Meanwhile, SKI-INTERACTING PROTEIN (SKIP), a conserved protein in eukaryotes, works as both a splicing factor and as a transcriptional regulator in plants to control gene expression at the transcriptional and posttranscriptional levels by interacting with distinct partners. Here, we show that, similar to plants with a loss of function of STM, a loss of function of SKIP or the specific knockout of SKIP in the SAM region resulted in failed SAM development and the inability of the mutants to complete their life cycle. In comparison, Arabidopsis mutants that expressed SKIP specifically in the SAM region formed a normal SAM and were able to generate a shoot system, including leaves and floral organs. Further analysis confirmed that SKIP interacts with STM in planta and that SKIP and STM regulate the expression of a similar set of genes by binding to their promoters. In addition, STM also interacts with EARLY FLOWERING 7 (ELF7), a component of Polymerase-Associated Factor 1 complex, and mutation in ELF7 exhibits similar SAM defects to that of STM and SKIP. This work identifies a component of the STM transcriptional complex and reveals the mechanism underlying SKIP-mediated SAM formation in Arabidopsis.

服务人员 孙小满

服务院士 尹伟伦

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