Current opinion in plant biology最新文献

Plant cell walls are essential elements for disease resistance that pathogens need to overcome to colonise the host. Certain pathogens secrete a large battery of enzymes to hydrolyse plant cell wall polysaccharides, which leads to the release of carbohydrate-based molecules (glycans) that are perceived by plant pattern recognition receptors and activate pattern-triggered immunity and disease resistance. These released glycans are used by colonizing microorganisms as carbon source, chemoattractants to locate entry points at plant surface, and as signals triggering gene expression reprogramming. The release of wall glycans and their perception by plants and microorganisms determines plant-microbial interaction outcome. Here, we summarise and discuss the most recent advances in these less explored aspects of plant-microbe interaction.

Plant genomes possess hundreds of candidate surface localized receptors capable of recognizing microbial components or modified-self molecules. Surface-localized pattern recognition receptors (PRRs) can recognize proteins, peptides, or structural microbial components as nonself, triggering complex signaling pathways leading to defense. PRRs possess diverse extracellular domains capable of recognizing epitopes, lipids, glycans and polysaccharides. Recent work highlights advances in our understanding of the diversity and evolution of PRRs recognizing pathogen components. We also discuss PRR functional diversification, pathogen strategies to evade detection, and the role of tissue and age-related resistance for effective plant defense.

Plant pathogens represent a critical threat to global agriculture and food security, particularly under the pressures of climate change and reduced agrochemical use. Most plant pathogens initially colonize the extracellular space or apoplast and understanding the host–pathogen interactions that occur here is vital for engineering sustainable disease resistance in crops. Structural biology has played important roles in elucidating molecular mechanisms underpinning plant-pathogen interactions but only few studies have reported structures of extracellular complexes. This article highlights these resolved extracellular complexes by describing the insights gained from the solved structures of complexes consisting of CERK1-chitin, FLS2-flg22-BAK1, RXEG1-XEG1-BAK1 and PGIP2-FpPG. Finally, we discuss the potential of AI-based structure prediction platforms like AlphaFold as an alternative hypothesis generator to rapidly advance our molecular understanding of plant pathology and develop novel strategies to increase crop resilience against disease.

The recent relaxation of psychedelic drug regulations has prompted extensive clinical investigation into their potential use to treat diverse mental health conditions including anxiety, depression, post-traumatic stress, and substance-abuse disorders. Most clinical trials have relied on a small number of known molecules found in nature, such as psilocybin, or long-known synthetic analogs of natural metabolites, including lysergic acid diethylamide (LSD). Elucidation of biosynthetic pathways leading to several psychedelic compounds has established an opportunity to use synthetic biology as a complement to synthetic chemistry for the preparation of novel derivatives with potentially superior pharmacological properties compared with known drugs. Herein we review the metabolic biochemistry of pathways from plants, fungi and animals that yield the medicinally important hallucinogenic specialized metabolites ibogaine, mescaline, psilocybin, lysergic acid, and N,N-dimethyltryptamine (DMT). We also summarize the reconstitution of these pathways in microorganisms and comment on the integration of native and non-native enzymes to prepare novel derivatives.

Filamentous pathogens need to overcome plant barriers for successful infection. To this end, special structures, most commonly appressoria, are used for penetration. In differentiated appressoria, the generation of high turgor pressure is mandatory to breach plant cell wall and cuticle. However, quantitative description of turgor pressure and resulting invasive forces are only described for a handful of plant pathogens. Recent advances in methodology allowed determination of surprisingly high pressures and corresponding forces in oomycetes and a necrotrophic fungus. Here, we describe turgor generation in appressoria as essential function for host penetration. We summarize the known experimentally determined turgor pressure as well as invasive forces and discuss their universal role in plant pathogen infection.

Gibberellin (GA) is a classical plant hormone that regulates many physiological processes, such as plant growth, development, and environmental responses. GA inhibits arbuscular mycorrhizal (AM) symbiosis, the most ancient and widespread type of mycorrhizal symbiosis. Knowledge about mycorrhizal symbioses at the molecular level has been obtained mainly in model plants such as legumes and rice. In contrast, molecular mechanisms in non-model plants are still unclear. Recent studies have revealed the novel roles of GA in mycorrhizal symbioses: its positive effect in Paris-type AM symbiosis in Eustoma grandiflorum and its negative effect on both seed germination and mycorrhizal symbiosis in orchids. This review focuses on the recent data on GA function in AM and orchid mycorrhizal symbioses.

Plants associate with a wealth of microbes, collectively referred to as the plant microbiota, whose composition is determined by host plant genetics, immune responses, environmental factors and intermicrobial relations. Unsurprisingly, microbiota compositions change during disease development. Recent evidence revealed that some of these changes can be attributed to effector proteins with antimicrobial activities that are secreted by plant pathogens to manipulate host microbiota to their advantage. Intriguingly, many of these effectors have ancient origins, predating land plant emergence, and evolved over long evolutionary trajectories to acquire selective antimicrobial activities to target microbial antagonists in host plant microbiota. Thus, we argue that host-pathogen co-evolution likely involved arms races within the host-associated microbiota.