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Pectin is a major cell wall component that plays important roles in plant development and response to environmental stresses. Arabidopsis thaliana plants expressing a fungal polygalacturonase (PG plants) that degrades homogalacturonan (HG), a major pectin component, as well as loss-of-function mutants for QUASIMODO2 (QUA2), encoding a putative pectin methyltransferase important for HG biosynthesis, show accumulation of reactive oxygen species (ROS), reduced growth and almost complete resistance to the fungal pathogen Botrytis cinerea. Both PG and qua2 plants show increased expression of the class III peroxidase AtPRX71 that contributes to their elevated ROS levels and reduced growth. In this work, we show that leaves of PG and qua2 plants display greatly increased cuticle permeability. Both increased cuticle permeability and resistance to B. cinerea in qua2 are suppressed by loss of AtPRX71. Increased cuticle permeability in qua2, rather than on defects in cuticle ultrastructure or cutin composition, appears to be dependent on reduced epidermal cell adhesion, which is exacerbated by AtPRX71, and is suppressed by the esmeralda1 mutation, which also reverts the adhesion defect and the resistant phenotype. Increased cuticle permeability, accumulation of ROS, and resistance to B. cinerea are also observed in mutants lacking a functional FERONIA, a receptor-like kinase thought to monitor pectin integrity. In contrast, mutants with defects in other structural components of primary cell wall do not have a defective cuticle and are normally susceptible to the fungus. Our results suggest that disrupted cuticle integrity, mediated by peroxidase-dependent ROS accumulation, plays a major role in the robust resistance to B. cinerea of plants with altered HG integrity.

39 pages, 6 figures, 2 tables, This paper presents major gaps and challenges for implementing the UN Decade of Ocean Science for Sustainable Development (2021-2030) in the Mediterranean region. The authors make recommendations on the scientific knowledge needs and co-design actions identified during two consultations, part of the Decade preparatory-phase, framing them in the Mediterranean Sea’s unique environmental and socio-economic perspectives. According to the ‘Mediterranean State of the Environment and Development Report 2020’ by the United Nations Environment Programme Mediterranean Action Plan and despite notable progress, the Mediterranean region is not on track to achieve and fully implement the Sustainable Development Goals of Agenda 2030. Key factors are the cumulative effect of multiple human-induced pressures that threaten the ecosystem resources and services in the global change scenario. The basin, identified as a climate change vulnerability hotspot, is exposed to pollution and rising impacts of climate change. This affects mainly the coastal zones, at increasing risk of extreme events and their negative effects of unsustainable management of key economic assets. Transitioning to a sustainable blue economy is the key for the marine environment’s health and the nourishment of future generations. This challenging context, offering the opportunity of enhancing the knowledge to define science-based measures as well as narrowing the gaps between the Northen and Southern shores, calls for a joint (re)action. The paper reviews the state of the art of Mediterranean Sea science knowledge, sets of trends, capacity development needs, specific challenges, and recommendations for each Decade’s societal outcome. In the conclusions, the proposal for a Mediterranean regional programme in the framework of the Ocean Decade is addressed. The core objective relies on integrating and improving the existing ocean-knowledge, Ocean Literacy, and ocean observing capacities building on international cooperation to reach the “Mediterranean Sea that we want”, With the institutional support of the ‘Severo OchoaCentre of Excellence’ accreditation (CEX2019-000928-S)

Background Plant biomass is a potentially important renewable source of energy and industrial products. The natural recalcitrance of the cell walls to enzymatic degradation (saccharification), which plants have evolved to defend themselves from biotic stresses, represents a major bottleneck for the industrial bioconversion of lignocellulosic biomasses. The identification of factors that influence the cell wall recalcitrance to saccharification may help to overcome the existing limitations that hamper the utilization of biomass. Results Here we have investigated in Arabidopsis thaliana the impact of homogalacturonan (HG) content and structure on tissue saccharification. We characterized mutants affected in genes encoding proteins involved in HG biosynthesis (quasimodo2-1; qua2-1) and methylesterification (pectin methylesterase 3; pme3). We also analyzed the natural variation of Arabidopsis through the characterization of a nested core collection of 24 accessions generated to maximize genetic variability. We found a negative correlation between the level of de-methyl-esterified HG (HGA) and cellulose degradability. Conclusions We propose to use the level of HGA domains as a biochemical marker of the cell wall recalcitrance to saccharification. This may be utilized for selecting, on a large scale, natural variants or mutants with improved bioconversion features.

Plant cell walls represent an abundant, renewable source of biofuels and other useful products. The major bottleneck for the industrial scale-up of their conversion to simple sugars (saccharification) is their recalcitrance to enzymatic hydrolysis. We demonstrated that the structure of pectin affects the exposure of cellulose to enzymes and consequently the process of saccharification. Le pareti cellulari vegetali rappresentano una abbondante e rinnovabile sorgente di biocarburanti ed altri prodotti utili. Una delle maggiori difficoltà nell’utilizzo delle pareti cellulari a livello industriale è la loro conversione in zuccheri semplici (saccarificazione) in quanto sono estremamente resistenti all’idrolisi enzimatica. In questo lavoro dimostriamo che la struttura della pectina influenza l’esposizione della cellulosa all’azione enzimatica e conseguentemente il processo di saccarificazione. This work was supported by the European Research Council [ERC Advanced Grant 233083 (F. C.)], the Institute Pasteur-Fondazione Cenci Bolognetti, the Italian Ministry of University and Research [PRIN 2007 Grant (G. D. L., F.C. and R.D) and AgroGen Grant (R.D.)] and the European Union COST Action 928 (D.B.).

Arabidopsis (Arabidopsis thaliana) genes MILDEW RESISTANCE LOCUS O2 (MLO2), MLO6, and MLO12 exhibit unequal genetic redundancy with respect to the modulation of defense responses against powdery mildew fungi and the control of developmental phenotypes such as premature leaf decay. We show that early chlorosis and necrosis of rosette leaves in mlo2 mlo6 mlo12 mutants reflects an authentic but untimely leaf senescence program. Comparative transcriptional profiling revealed that transcripts of several genes encoding tryptophan biosynthetic and metabolic enzymes hyperaccumulate during vegetative development in the mlo2 mlo6 mlo12 mutant. Elevated expression levels of these genes correlate with altered steady-state levels of several indolic metabolites, including the phytoalexin camalexin and indolic glucosinolates, during development in the mlo2 single mutant and the mlo2 mlo6 mlo12 triple mutant. Results of genetic epistasis analysis suggest a decisive role for indolic metabolites in mlo2-conditioned antifungal defense against both biotrophic powdery mildews and a camalexin-sensitive strain of the necrotrophic fungus Botrytis cinerea. The wound- and pathogen-responsive callose synthase POWDERY MILDEW RESISTANCE4/GLUCAN SYNTHASE-LIKE5 was found to be responsible for the spontaneous callose deposits in mlo2 mutant plants but dispensable for mlo2-conditioned penetration resistance. Our data strengthen the notion that powdery mildew resistance of mlo2 genotypes is based on the same defense execution machinery as innate antifungal immune responses that restrict the invasion of nonadapted fungal pathogens.