Beyond their function as structural barriers, plant cell walls are essential elements for the adaptation of plants to environmental conditions. Cell walls are dynamic structures whose composition and integrity can be altered in response to environmental challenges and developmental cues. These wall changes are perceived by plant sensors/receptors triggering adaptative responses during development and upon stress perception. Plant cell wall damage caused by pathogen infection, wounding or other stresses leads to the release of wall molecules, like carbohydrates (glycans), that function as Damage-Associated Molecular Patterns (DAMPs). DAMPs are perceived by the Extracellular Ectodomains (ECDs) of Pattern Recognition Receptors (PRRs) activating Pattern-Triggered Immunity (PTI) and disease resistance. Similarly, glycans released from walls and extracellular layers of microorganisms interacting with plants are recognised as Microbe-Associated Molecular Patterns (MAMPs) by specific ECD-PRRs triggering PTI responses. The number of oligosaccharides DAMPs/MAMPs identified that are perceived by plants has increased in recent years. However, the structural mechanisms underlying glycans recognition by plant PRRs remain limited. Currently, this knowledge is mainly focused on receptors of the LysM-PRRs family, which are involved in the perception of various molecules, such as chitooligosaccharides from fungi and lipo-chitooligosaccharides (i.e. Nod/MYC factors from bacteria and mycorrhiza, respectively) that trigger differential physiological responses. Nevertheless, additional families of plant PRRs have recently been implicated in oligosaccharide/polysaccharide recognition. These include Receptor Kinases (RKs) with Leucine-Rich Repeat and Malectin domains in their ECDs (LRR-MAL RKs), Catharanthus roseus RECEPTOR-LIKE KINASE 1 LIKE group (CrRLK1L) with Malectin-like (MLL) domains in their ECDs, as well as Wall-Associated Kinases (WAKs), lectin-RKs and LRR-extensins. The characterization of the structural basis of glycans recognition by these new plant receptors will shed light on their similarities with those of mammalians involved in glycan perception. This gained knowledge holds the potential to facilitate the development of sustainable, glycan-based crop protection solutions.

Synthetic ether-linked analogues of phosphatidylcholine and lysophosphatidylcholine, collectively named as antitumour lipids (ATLs), were initially synthesized in the late 60s, but have attracted a renewed interest since the finding that the ether lipid 1-O-octadecyl-2-O-methyl-rac-glycero-3- phosphocholine (ET-18-OCH3, edelfosine), a synthetic analogue of 2-lysophosphatidylcholine considered the ATL prototype, induces a selective apoptotic response in tumour cells, sparing normal cells. Unlike most chemotherapeutic agents currently used, ET-18-OCH3 does not interact with DNA, but act at the cell membrane, and thereby its effects seem to be independent of the proliferative state of target cells. Each part of the molecular structure of ET-18-OCH3 is important for its optimal proapoptotic activity. Recent progress has unveiled the molecular mechanism underlying the apoptotic action of ET-18-OCH3, involving membrane rafts and Fas / CD95 death receptor, and has led to the proposal of a two-step model for the ET-18-OCH3 selective action on cancer cells, namely: a) ET-18-OCH3 uptake into the tumour cell, but not in normal cells; b) intracellular activation of Fas / CD95 through its translocation and capping into membrane rafts. ET-18-OCH3 constitutes the first antitumour drug acting through the intracellular activation of the Fas / CD95 death receptor. Computational docking studies have allowed us to propose a molecular model for the putative interaction of ET-18-OCH3 with the intracellular Fas/CD95 death domain. This novel mechanism of action represents a new way to target tumour cells in cancer chemotherapy and can be of interest as a new framework in designing novel and more selective proapoptotic antitumour drugs.