Osmotic Regulation of a Peptide Ligand-Mediated Signaling

摘要 多细胞有机体中的细胞不断地通过配体受体介导的信号传递 协调它们的生长、发展和对环境的适应。多肽配体触发 信号在人类的这个网络中是最丰富的，它的失调导致了许多流行的 人类疾病。然而，关于多肽配体触发的信号是如何由 环境仍然不完整。我们研究了一个经典的多肽配体-受体介导的信号通路 调节拟南芥的表皮气孔发育，一种自然简化的和实验的 可访问的系统。气孔是植物地上表面的微孔，它促进植物与植物之间的气体交换。 环境。气孔发育在不同的环境条件下灵活调整，以优化植物 适应，使其成为研究多肽配体触发的环境调节的一个有吸引力的系统 信号通路。在气孔信号通路的上游有一组分泌配体，名为 表皮图案化因子(EPF)，其中许多对环境线索高度敏感。我们发现 这种渗透胁迫导致气孔密度急剧下降。有趣的是，一位推定的 EPF配体在渗透胁迫下优先诱导。与野生型植物相比，EPF突变体产生了 渗透胁迫下气孔前体细胞增多。根据这些新发现，我们假设渗透胁迫 通过增强候选EPF配体触发的信号来抑制气孔发育。我们的研究和其他人 以前已经指出，不同的EPF触发的信号通路针对气孔的不同步骤 发展过程。这种特异性至少部分是由于一种基因的精确时空表达 特异性EPF配体和包括ERECTA-like 1在内的受体激酶的不同亚细胞行为， 来转导EPF信号。这份Mira提案旨在全面评估渗透胁迫-- 通过解决以下三个问题来诱导EPF配体触发的信号通路：1)阐明 对候选EPF基因转录的渗透调节；2)剖析了EPF基因转录的渗透调节 气孔受体复合体；3)确定渗透胁迫诱导EPF信号通路的靶点。 这项工作的完成可能会为我们理解渗透调节提供有价值的见解。 通过多肽配体触发的信号通路实现生物体发育。

Abstract Cells in a multicellular organism constantly communicate by ligand-receptor-mediated signaling to coordinate their growth, development, and adaptation to the environment. The peptide ligands-triggered signaling is the most abundant in this network in humans, dysregulation of which contributes to many prevalent human diseases. However, knowledge of how the peptide ligand-triggered signaling is regulated by the environment remains incomplete. We study a classical peptide ligand-receptor-mediated signaling pathway that regulates the epidermal stomatal development in Arabidopsis thaliana, a naturally simplified and experimentally accessible system. Stomata are micropores on the aerial surface of plants that facilitate gas exchange with the environment. Stomatal development is flexibly adjusted under variable environmental conditions to optimize plant adaptation, making it an attractive system for studies on environmental regulation of peptide ligand-triggered signaling pathways. Upstream of the stomatal signaling pathway are a group of secretory ligands named Epidermal Patterning Factors (EPFs), many of which are highly responsive to environmental cues. We found that osmotic stress caused a dramatic reduction in stomatal density. Interestingly, the transcript of a putative EPF ligand is preferentially induced under osmotic stress. Compared to wild-type plants, the epf mutants produce more stomatal precursor cells under osmotic stress. With these new findings, we hypothesize that osmotic stress inhibits stomatal development via enhancing the candidate EPF ligand-triggered signaling. Our study and others have previously indicated that distinct EPF-triggered signaling pathways target different steps of the stomatal developmental process. The specificity is, at least partially, due to the precise spatiotemporal expression of a particular EPF ligand and the differential subcellular behavior of the receptor kinases including ERECTA-LIKE 1, that transduce the EPF signaling. This MIRA proposal aims to comprehensively evaluate the osmotic stress- induced EPF ligand-triggered signaling pathway by addressing the following three questions: 1) Elucidate the osmotic regulation of the transcription of the candidate EPF gene; 2) Dissect the osmotic regulation of the stomatal receptor complex; 3) Identify the targets of the osmotic stress-induced EPF signaling pathway. Completion of this work is likely to provide valuable insight into our understanding of osmotic regulation of organism development via peptide ligand-triggered signaling pathways.