Fungal interactions with plants can involve specific morphogenetic developments to access host cells, the suppression of plant defenses, and the establishment of a feeding lifestyle that nourishes the colonizer oftenbut not always-at the expense of the host. Reactive oxygen species (ROS) metabolism is central to the infection process, and the stage-specific production and/or neutralization of ROS is critical to the success of the colonization process. ROS metabolism during infection is dynamicsometimes seemingly contradictory-and involves endogenous and exogenous sources. Yet, intriguingly, molecular decision-making involved in the spatio-temporal control of ROS metabolism is largely unknown. When also considering that ROS demands are similar between pathogenic and beneficial fungal-plant interactions despite the different outcomes, the intention of our review is to synthesize what is known about ROS metabolism and highlight knowledge gaps that could be hindering the discovery of novel means to mediate beneficial plant-microbe interactions at the expense of harmful plant-microbe interactions.

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Summary Fungal phytopathogens can suppress plant immune mechanisms in order to colonize living host cells. Identifying all the molecular components involved is critical for elaborating a detailed systems‐level model of plant infection probing pathogen weaknesses; yet, the hierarchy of molecular events controlling fungal responses to the plant cell is not clear. Here we show how, in the blast fungus Magnaporthe oryzae, terminating rice innate immunity requires a dynamic network of redox‐responsive E3 ubiquitin ligases targeting fungal sirtuin 2 (Sir2), an antioxidation regulator required for suppressing the host oxidative burst. Immunoblotting, immunopurification, mass spectrometry and gene functional analyses showed that Sir2 levels responded to oxidative stress via a mechanism involving ubiquitination and three antagonistic E3 ubiquitin ligases: Grr1 and Ptr1 maintained basal Sir2 levels in the absence of oxidative stress; Upl3 facilitated Sir2 accumulation in response to oxidative stress. Grr1 and Upl3 interacted directly with Sir2 in a manner that decreased and scaled with oxidative stress, respectively. Deleting UPL3 depleted Sir2 during growth in rice cells, triggering host immunity and preventing infection. Overexpressing SIR2 in the Δupl3 mutant remediated pathogenicity. Our work reveals how redox‐responsive E3 ubiquitin ligases in M. oryzae mediate Sir2 accumulation‐dependent antioxidation to modulate plant innate immunity and host susceptibility.

Concentrations of carbon dioxide (CO(2)) are increasing in the atmosphere, affecting soybean (Glycine max L.) phytohormone signaling and herbivore resistance. Whether the impact of elevated CO(2) on phytohormones and induced defenses is a generalized response within this species is an open question. We examined jasmonic acid (JA) and salicylic acid (SA) under ambient and elevated CO(2) concentrations with and without Japanese beetle (Popillia japonica Newman) damage and artificial damage across six soybean cultivars (HS93-4118, Pana, IA 3010, Loda, LN97-15076, and Dwight). Elevated CO(2) reduced constitutive levels of JA and related transcripts in some but not all soybean cultivars. In contrast to the variation in JA, constitutive levels of salicylic were increased universally among soybean cultivars grown under elevated CO(2). Variation in hormonal signaling may underpin observed variation in the response of insect herbivores and pathogens to plants grown under elevated CO(2).

Omalizumab (Xolair ) is an anti-IgE monoclonal antibody, which may benefit adults with systemic mastocytosis. We report effective treatment with omalizumab in two toddlers with severe diffuse cutaneous mastocytosis. Our cases offer preliminary evidence to support the safe use of omalizumab in paediatric patients with cutaneous mastocytosis.