State Key Laboratory of Plant Physiology and Biochemistry, College of Agriculture and Biotechnology, China Agricultural University, Beijing 100193, China.
College of Life Sciences, Capital Normal University, Beijing 100048, China.
Plant Physiol. 2022 Aug 1;189(4):2193-2209. doi: 10.1093/plphys/kiac241.
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.
茎尖分生组织（SAM）在胚胎发生过程中形成，在植物生命周期中产生叶片、茎和花器官。SAM 的发育受 SHOOT MERISTEMLESS（STM）的控制，STM 是一种保守的 I 类 KNOX 转录因子，它与另一个亚类同源域蛋白 BELL 相互作用形成异二聚体，在拟南芥中调节转录水平的基因表达。与此同时，SKI-INTERACTING PROTEIN（SKIP）是一种在真核生物中保守的蛋白，在植物中既作为剪接因子，又作为转录调节因子，通过与不同的伴侣相互作用，在转录和转录后水平上控制基因表达。在这里，我们表明，与 STM 功能丧失的植物类似，SKIP 功能丧失或 SKIP 在 SAM 区域的特异性敲除导致 SAM 发育失败，突变体无法完成其生命周期。相比之下，在 SAM 区域特异性表达 SKIP 的拟南芥突变体形成了正常的 SAM，并能够生成包括叶片和花器官在内的茎系统。进一步的分析证实，SKIP 在体内与 STM 相互作用，并且 SKIP 和 STM 通过结合其启动子调节相似的基因表达。此外，STM 还与早期开花 7（ELF7）相互作用，ELF7 是聚合酶相关因子 1 复合物的一个组成部分，ELF7 的突变表现出与 STM 和 SKIP 相似的 SAM 缺陷。这项工作确定了 STM 转录复合物的一个组成部分，并揭示了 SKIP 介导的拟南芥 SAM 形成的机制。
