Apical extracellular matrices (aECMs) form a physical barrier to the environment. In Caenorhabditis elegans, the epidermal aECM, the cuticle, is composed mainly of different types of collagen, associated in circumferential ridges separated by furrows. Here, we show that in mutants lacking furrows, the normal intimate connection between the epidermis and the cuticle is lost, specifically at the lateral epidermis, where, in contrast to the dorsal and ventral epidermis, there are no hemidesmosomes. At the ultrastructural level, there is a profound alteration of structures that we term ‘meisosomes,’ in reference to eisosomes in yeast. We show that meisosomes are composed of stacked parallel folds of the epidermal plasma membrane, alternately filled with cuticle. We propose that just as hemidesmosomes connect the dorsal and ventral epidermis, above the muscles, to the cuticle, meisosomes connect the lateral epidermis to it. Moreover, furrow mutants present marked modifications of the biomechanical properties of their skin and exhibit a constitutive damage response in the epidermis. As meisosomes co-localise to macrodomains enriched in phosphatidylinositol (4,5) bisphosphate, they could conceivably act, like eisosomes, as signalling platforms, to relay tensile information from the aECM to the underlying epidermis, as part of an integrated stress response to damage.

Diazachlorin and diazabacteriochlorin have been prepared through reduction of diazaporphyrin and their in vitro and in vivo activity in photodynamic therapy has been investigated.

Animals and plants need to defend themselves from pathogen attack. Their defences drive innovation in virulence mechanisms, leading to never-ending cycles of co-evolution in both hosts and pathogens. A full understanding of host immunity therefore requires examination of pathogen virulence strategies. Here, we take advantage of the well-studied innate immune system ofCaenorhabditis elegansto dissect the action of two virulence factors from its natural fungal pathogenDrechmeria coniospora. We show that these two enterotoxins have strikingly different effects when expressed individually in the nematode epidermis. One is able to interfere with diverse aspects of host cell biology, altering vesicle trafficking and preventing the key STAT-like transcription factor STA-2 from activating defensive antimicrobial peptide gene expression. The second increases STA-2 levels in the nucleus, modifies the nucleolus, and, potentially as a consequence of a host surveillance mechanism, causes increased defence gene expression. Our results highlight the remarkably complex and potentially antagonistic mechanisms that come into play in the interaction between co-evolved hosts and pathogens.

Botryosphaeria dieback (BD) is a worldwide grapevine trunk disease constituting a serious threat to sustainable grapevine production, especially in the context of climate change. Effective treatments to control BD are still lacking, prompting the exploration of new non-chemical alternatives. Among these, biocontrol agents (BCAs), such as Trichoderma spp. and Bacillus spp., are described as promising. This study aimed to thoroughly investigate the physiological changes in grapevines induced by two BCAs, Bacillus subtilis ( Bs PTA-271) and Trichoderma atroviride ( Ta SC1), which are used to protect two cultivars from Neofusicoccum parvum Bt67 (Np-Bt67) infection. Using nontarget transcriptomic analysis (RNA-seq) and validation by qRT-PCR, this research offers novel insights into the molecular responses associated with Np-Bt67 infection in Chardonnay and Tempranillo cultivars in relation to the protective mechanisms conferred by each BCA. RNA-seq revealed that the cultivars showed no common transcriptional changes upon pathogen challenge. In Chardonnay, changes were mainly related to terpene/carotenoid pathways, whereas in Tempranillo, they mostly related to amino acid transport and photosynthesis. Following the inoculation of protective BCA, changes were also distinct between the infected cultivars: Bs PTA-271’s protective effect against infection in Chardonnay was mainly related to the phenylpropanoid pathway and secondary metabolic processes, whereas that of Ta SC1 for Tempranillo correlated with more metabolic changes. Consecutive validation by qRT-PCR provided markers indicating grapevine susceptibility versus protection against Np-Bt67, some of which are shared by both cultivars. These markers could offer valuable tools for monitoring the health status of grapevine toward N. parvum.

Efficient early pathogen detection, before symptom apparition, is crucial for optimizing disease management. In barley, the fungal pathogen Pyrenophora teres is the causative agent of net blotch disease, which exists in two forms: P. teres f. sp. teres (Ptt), causing net-form of net blotch (NTNB), and P. teres f. sp. maculata (Ptm), responsible for spot-form of net blotch (STNB). In this study, we developed primers and a TaqMan probe to detect both Ptt and Ptm. A comprehensive k-mer based analysis was performed across a collection of P. teres genomes to identify the conserved regions that had potential as universal genetic markers. These regions were then analyzed for their prevalence and copy number across diverse Moroccan P. teres strains, using both a k-mer analysis for sequence identification and a phylogenetic assessment to establish genetic relatedness. The designed primer-probe set was successfully validated through qPCR, and early disease detection, prior to symptom development, was achieved using ddPCR. The k-mer analysis performed across the available P. teres genomes suggests the potential for these sequences to serve as universal markers for P. teres, transcending environmental variations.

Apical extracellular matrices (aECMs) form a physical barrier to the environment. In C. elegans , the epidermal aECM, the cuticle, is composed mainly of different types of collagen, associated in circumferential ridges separated by furrows. Here, we show that in mutants lacking furrows, the normal intimate connection between the epidermis and the cuticle is lost, specifically at the lateral epidermis, where, in contrast to the dorsal and ventral epidermis, there are no hemidesmosomes. At the ultrastructural level, there is a profound alteration of structures that we term “meisosomes”, in reference to eisosomes in yeast. We show that meisosomes are composed of stacked parallel folds of the epidermal plasma membrane, alternately filled with cuticle. We propose that just as hemidesmosomes connect the dorsal and ventral epidermis, above the muscles, to the cuticle, meisosomes connect the lateral epidermis to it. Moreover, furrow mutants present marked modifications of the biomechanical properties of their skin and exhibit a constitutive damage response in the epidermis. As meisosomes co-localise to macrodomains enriched in phosphatidylinositol (4,5) bisphosphate, they might act, like eisosomes, as signalling platforms, to relay tensile information from the aECM to the underlying epidermis, as part of an integrated stress response to damage.