Cell Wall Signalling in Arabidopsis thaliana

复杂的多细胞生物是如何通过协调的细胞增殖、分化和生长来完成发育的是一个基本的生物学问题。在动物中，干细胞的维持和细胞身份规范部分由细胞外基质（ECM）控制。植物细胞壁这一刚性但动态的外基质，通过选择性限制细胞扩增来指导形态发生。为了控制生长，也为了响应外部扰动，细胞壁状态被认为受到与细胞内信号传导相关的细胞表面受体的持续监视。然而，关于细胞壁特性是如何被感知的，信号是如何被转导的，以及细胞壁介导的反馈信号是如何与植物发育的调节机制交叉的，我们知之甚少。基于我们最近的发现，我们假设细胞壁信号通路通过控制细胞命运的维持在发育中发挥重要作用，这让人想起动物中ECM的调节作用。我们发现了一种新的细胞壁信号通路，它依赖于质膜定位受体样蛋白RLP44。RLP44与细胞壁果胶成分相互作用，并通过与各自的受体复合物相互作用并促进其活性，连接两种众所周知的信号通路，油菜素内酯（BR）和植物硫代激素（PSK）信号通路。有趣的是，rlp44促进的PSK信号是维持根原形成层细胞身份所必需的，这是该途径的一种新功能。PSK相关突变体与RLP44的缺失类似，在原形成层的位置显示异位木质部，而RLP44突变体可以被外源PSK拯救。在这里，我们主要想回答两个问题。首先，BRI1-RLP44-PSK信号模块是如何促进前层身份的？基于广泛的初步结果，我们想要测试PSK信号在一定程度上通过控制蛋白质翻译起作用的假设。此外，我们想要剖析PSK信号如何与已知的原形成层身份调节因子相交，即相互抑制的生长素和细胞分裂素形态发生场。第二，rlp44介导的细胞壁感应是否对调节生长发育的细胞内网络有直接影响？为此，我们将利用我们的发现，RLP44直接与果胶相互作用，并评估细胞壁结合对信号读数以及受体复合物中蛋白质-蛋白质相互作用的影响。

How the development of complex multicellular organisms is accomplished through coordinated cell proliferation, differentiation, and growth is a fundamental biological question. In animals, stem cell maintenance and cell identity specification are in part controlled by the extracellular matrix (ECM). The rigid, yet dynamic ECM of plants, the cell wall, is known to guide morphogenesis through selective restriction of cell expansion. To control growth, but also to respond to extrinsic perturbations, cell wall state is believed to be under constant surveillance by cell surface receptors connected to intracellular signalling. However, very little is known about how cell wall properties are sensed, how signals are transduced, and how cell wall-mediated feedback signalling intersects with the regulatory mechanisms of plant development. Based on our recent discoveries, we hypothesize that cell wall signalling pathways play major roles in development by controlling the maintenance of cell fate, reminiscent of the regulatory role of the ECM in animals. We discovered a novel cell wall signalling pathways that depends on the plasma membrane localized receptor-like protein RLP44. RLP44 interacts with the pectate component of the cell wall and connects two well-known signalling pathways, brassinosteroid (BR) and phytosulfokine (PSK) signalling, by interacting with the respective receptor complexes and promoting their activity. Interestingly, RLP44-promoted PSK signalling is required for the maintenance of procambial cell identity in the root, a novel function for this pathway. Mimicking the loss of RLP44, PSK-related mutants show ectopic xylem in the position of procambium, whereas RLP44 mutants can be rescued by exogenous PSK. Here, we want to address mainly two questions. First, how does the BRI1-RLP44-PSK signalling module promote procambial identity? Building on extensive preliminary results, we want to test the hypothesis that PSK signalling acts in part through the control of protein translation. In addition, we want to dissect how PSK signalling intersects with the known regulators of procambial identity, namely the mutually inhibitory auxin and cytokinin morphogenetic fields. Second, does RLP44-mediated cell wall sensing have a direct effect on intracellular networks regulating growth and development? To this end, we will leverage our finding that RLP44 directly interacts with pectate and assess the influence of cell wall binding on signalling readouts as well as on protein-protein interactions in the receptor complexes.