Laurent Mène-Saffrané

In Arabidopsis mature seeds, the onset of the embryo-to-seedling transition is nonautonomously controlled, being blocked by endospermic abscisic acid (ABA) release under unfavorable conditions. Whether the mature endosperm governs additional nonautonomous developmental processes during this transition is unknown. Mature embryos have a more permeable cuticle than seedlings consistent with their endospermic ABA uptake capability. Seedlings acquire their well-sealing cuticles adapted to aerial lifestyle during germination. Endosperm removal prevents seedling cuticle formation and seed reconstitution by endosperm grafting onto embryos shows that the endosperm promotes seedling cuticle development. Grafting different endosperm and embryo mutant combinations, together with biochemical, microscopy and mass spectrometry approaches, reveals that release of tyrosylprotein sulfotransferase (TPST)-sulfated CIF2 and PSY1 peptides from the endosperm promotes seedling cuticle development. Endosperm-deprived embryos produced nonviable seedlings bearing numerous developmental defects, not related to embryo malnutrition, all restored by exogenously provided endosperm. Hence, seedling establishment is nonautonomous, requiring the mature endosperm.

Plants face many biotic and abiotic challenges in nature; one of them is attack by disease-causing microbes. Phytophthora infestans, the causal agent of late blight is one of the most prominent pathogens of the potato responsible for multi-billion-dollar losses every year. We have previously reported that potato-associated Pseudomonas strains inhibited P. infestans at various developmental stages. A comparative genomics approach identified several factors putatively involved in this anti-oomycete activity, among which was the production of hydrogen cyanide (HCN). Here, we report the relative contribution of HCN emission to the overall anti-Phytophthora activity of two cyanogenic Pseudomonas strains, P. putida R32 and P. chlororaphis R47. To quantify this contribution, we generated HCN-negative mutants (Δhcn) and compared their activities to those of their respective wild types in different experiments assessing P. infestans mycelial growth, zoospore germination, and infection of potato leaf disks. Using in vitro experiments allowing only volatile-mediated interactions, we observed that HCN accounted for most of the mycelial growth inhibition (57% in R47 and 80% in R32). However, when allowing both volatile and diffusible compound-mediated interactions, HCN only accounted for 1% (R47) and 18% (R32) of mycelial growth inhibition. Likewise, both mutants inhibited zoospore germination in a similar way as their respective wild types. More importantly, leaf disk experiments showed that both wild-type and Δhcn strains of R47 and R32 were able to limit P. infestans infection to a similar extent. Our results suggest that while HCN is a major contributor to the in vitro volatile-mediated restriction of P. infestans mycelial growth, it does not play a major role in the inhibition of other disease-related features such as zoospore germination or infection of plant tissues.

BACKGROUND: Solar radiation is assumed to be a major factor limiting the efficacy of entomopathogenic fungi used as biocontrol agents in open field applications. We evaluated 12 natural UV‐protective co‐formulants for their effect on the survival of UV‐exposed Beauveria bassiana spores on agar plates, colza leaf discs and in the field.RESULTS: Colony‐forming unit (CFU) counts of unformulated conidia on agar plates and leaf discs dropped to ≤ 50% after exposure to UV radiation. The highest UV protection was achieved with humic acid, which provided > 90% protection of UV‐B‐exposed conidia in laboratory experiments. In the field, 10% humic acid increased spore persistence up to 87% at 7 days after application. Sesame and colza oil also provided high UV protection in both assays (> 73% and > 70%, respectively).CONCLUSIONS: This study shows that it is possible to increase the persistence of B. bassiana spores under exposure to UV radiation by formulation with natural UV‐protective additives. UV protectants might, therefore, increase the efficacy of entomopathogenic fungi as biocontrol agents in open field applications. © 2018 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Vitamin E is one of the 13 vitamins that are essential to animals that do not produce them. To date, six natural organic compounds belonging to the chemical family of tocochromanols—four tocopherols and two tocotrienols—have been demonstrated as exhibiting vitamin E activity in animals. Edible plant-derived products, notably seed oils, are the main sources of vitamin E in the human diet. Although this vitamin is readily available, independent nutritional surveys have shown that human populations do not consume enough vitamin E, and suffer from mild to severe deficiency. Tocochromanols are mostly produced by plants, algae, and some cyanobacteria. Tocochromanol metabolism has been mainly studied in higher plants that produce tocopherols, tocotrienols, plastochromanol-8, and tocomonoenols. In contrast to the tocochromanol biosynthetic pathways that are well characterized, our understanding of the physiological and molecular mechanisms regulating tocochromanol biosynthesis is in its infancy. Although it is known that tocochromanol biosynthesis is strongly conditioned by the availability in homogentisate and polyprenyl pyrophosphate, its polar and lipophilic biosynthetic precursors, respectively, the mechanisms regulating their biosyntheses are barely known. This review summarizes our current knowledge of tocochromanol biosynthesis in plants, and highlights future challenges regarding the understanding of its regulation.

Tocochromanols are organic compounds mostly produced by photosynthetic organisms that exhibit vitamin E activity in animals. They result from the condensation of homogentisate with four different polyprenyl side chains derived all from geranylgeranyl pyrophosphate. The core tocochromanol biosynthesis has been investigated in several photosynthetic organisms and is now well-characterized. In contrast, our current knowledge of the biosynthesis and transport of tocochromanol biosynthetic precursors is much more limited. While tocochromanol synthesis occurs in plastids, converging genetic data in Arabidopsis and soybean demonstrate that the synthesis of the polar precursor homogentisate is located in the cytoplasm. These data implies that tocochromanol synthesis involves several plastidic membrane transporter(s) that remain to be identified. In addition, the metabolic origin of the lipophilic isoprenoid precursor is not fully elucidated. While some genetic data exclusively attribute the synthesis of the prenyl component of tocochromanols to the plastidic methyl erythritol phosphate pathway, multiple lines of evidence provided by feeding experiments and metabolic engineering studies indicate that it might partially originate from the cytoplasmic mevalonate pathway. Although this question is still open, these data demonstrate the existence of membrane transporter(s) capable of importing cytosolic polyprenyl pyrophosphate such as farnesyl pyrophosphate into plastids. Since the availability of both homogentisate and polyprenyl pyrophosphates are currently accepted as major mechanisms controlling the type and amount of tocochromanols produced in plant tissues, we summarized our current knowledge and research gaps concerning the biosynthesis, metabolic origins and transport of tocochromanol biosynthetic precursors in plant cells.

Summary: Photosynthetic organisms such as plants, algae and some cyanobacteria synthesize tocochromanols, a group of compounds that encompasses tocopherols and tocotrienols and that exhibits vitamin E activity in animals. While most vitamin E biosynthetic genes have been identified in plant genomes, regulatory genes controlling tocopherol accumulation are currently unknown. We isolated by forward genetics Arabidopsis enhanced vitamin E (eve) mutants that overaccumulate the classic tocopherols and plastochromanol‐8, and a tocochromanol unknown in this species. We mapped eve1 and eve4, and identified the unknown Arabidopsis tocochromanol by using a combination of analytical tools. In addition, we determined its biosynthetic pathway with a series of tocochromanol biosynthetic mutants and transgenic lines. eve1 and eve4 are two seed lipid mutants affecting the WRINKLED1 (WRI1) and ACYL‐COA:DIACYLGLYCEROL ACYLTRANSFERASE1 (DGAT1) genes, respectively. The unknown tocochromanol is 11′‐12′ γ‐tocomonoenol, whose biosynthesis is VITAMIN E 1 (VTE1) ‐ and VTE2‐dependent and is initiated by the condensation of homogentisate (HGA) and tetrahydrogeranylgeranyl pyrophosphate. This study identifies the first two regulatory genes, WRI1 and DGAT1, that control the synthesis of all tocochromanol forms in seeds, and shows the existence of a metabolic trade‐off between lipid and tocochromanol metabolisms. Moreover, it shows that Arabidopsis possesses a tocomonoenol biosynthetic pathway that competes with tocopherol synthesis.