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Effector secretion by different routes mediates the molecular interplay between host plant and pathogen, but mechanistic details in eukaryotes are sparse. This may limit the discovery of new effectors that could be utilized for improving host plant disease resistance. In fungi and oomycetes, apoplastic effectors are secreted via the conventional endoplasmic reticulum (ER)-Golgi pathway, while cytoplasmic effectors are packaged into vesicles that bypass Golgi in an unconventional protein secretion (UPS) pathway. In Magnaporthe oryzae, the Golgi bypass UPS pathway incorporates components of the exocyst complex and a t-SNARE, presumably to fuse Golgi bypass vesicles to the fungal plasma membrane. Upstream, cytoplasmic effector mRNA translation in M. oryzae requires the efficient decoding of AA-ending codons. This involves the modification of wobble uridines in the anticodon loop of cognate tRNAs and fine-tunes cytoplasmic effector translation and secretion rates to maintain biotrophic interfacial complex integrity and permit host infection. Thus, plant-fungal interface integrity is intimately tied to effector codon usage, which is a surprising constraint on pathogenicity. Here, we discuss these findings within the context of fungal and oomycete effector discovery, delivery, and function in host cells. We show how cracking the codon code for unconventional cytoplasmic effector secretion in M. oryzae has revealed AA-ending codon usage bias in cytoplasmic effector mRNAs across kingdoms, including within the RxLR-dEER motif-encoding sequence of a bona fide Phytophthora infestans cytoplasmic effector, suggesting its subjection to translational speed control. By focusing on recent developments in understanding unconventional effector secretion, we draw attention to this important but understudied area of host-pathogen interactions. [Formula: see text] Copyright © 2024 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license . 

Following leaf cuticle penetration by specialized appressorial cells, the devastating blast fungusMagnaporthe oryzaegrows as invasive hyphae (IH) in living rice cells. IH are separated from host cytoplasm by plant-derived membranes forming an apoplastic compartment and a punctate biotrophic interfacial complex (BIC) that mediate the molecular host-pathogen interaction. What molecular and cellular processes determine the temperature range for this biotrophic growth stage is an unanswered question pertinent to a broader understanding of how phytopathogens may cope with environmental stresses arising under climate change. Here, we shed light on thermal adaptation inM.oryzaeby disrupting theACB1gene encoding the single acyl-CoA-binding protein, an intracellular transporter of long-chain acyl-CoA esters. Loss ofACB1affected fatty acid desaturation levels and abolished pathogenicity at optimal (26°C) and low (22°C) but not elevated (29°C) infection temperatures (the latter following post-penetration shifts from 26°C). Relative to wild type, the Δacb1mutant strain exhibited poor vegetative growth and impaired membrane trafficking at 22°C and 26°C, but not at 29°C.In planta, Δacb1biotrophic growth was inhibited at 26°C–which was accompanied by a multi-BIC phenotype—but not at 29°C, where BIC formation was normal. Underpinning the Δacb1phenotype was impaired membrane fluidity at 22°C and 26°C but not at elevated temperatures, indicating Acb1 suppresses membrane rigidity at optimal- and suboptimal- but not supraoptimal temperatures. Deducing a temperature-dependent role for Acb1 in maintaining membrane fluidity homeostasis reveals how the thermal range for rice blast disease is both mechanistically determined and wider than hitherto appreciated. 

The Earth’s atmosphere is comprised of turbulent layers that result in speckled and blurry images from ground- based visible and infrared observations. Adaptive Optics (AO) systems are employed to measure the perturbed wavefront with a wavefront sensor (WFS) and correct for these distortions with a deformable mirror. Therefore, understanding and characterising the atmosphere is crucial for the design and functionality of AO systems. One parameter for characterizing the atmosphere is the atmospheric coherence time, which is a function of the effec- tive wind velocity of the atmosphere. This parameter dictates how fast the AO system needs to correct for the atmosphere. If not fast enough, phenomena such as the wind butterfly effect can occur, hindering high-contrast coronographic imaging. This effect is a result of fast, strong, high-altitude turbulent layers. This paper presents two methods for estimating the effective wind velocity, using pseudo-open loop WFS slopes. The first method uses a spatial-temporal covariance map and the second uses the power spectral density of the defocus term. We show both simulated results and preliminary results from the Gemini Planet Imager AO telemetry. 

Abstract The blast fungusMagnaporthe oryzaeproduces invasive hyphae in living rice cells during early infection, separated from the host cytoplasm by plant-derived interfacial membranes. However, the mechanisms underpinning this intracellular biotrophic growth phase are poorly understood. Here, we show that theM. oryzaeserine/threonine protein kinase Rim15 promotes biotrophic growth by coordinating cycles of autophagy and glutaminolysis in invasive hyphae. Alongside inducing autophagy, Rim15 phosphorylates NAD-dependent glutamate dehydrogenase, resulting in increased levels of α-ketoglutarate that reactivate target-of-rapamycin (TOR) kinase signaling, which inhibits autophagy. DeletingRIM15attenuates invasive hyphal growth and triggers plant immunity; exogenous addition of α-ketoglutarate prevents these effects, while glucose addition only suppresses host defenses. Our results indicate that Rim15-dependent cycles of autophagic flux liberate α-ketoglutarate – via glutaminolysis – to reactivate TOR signaling and fuel biotrophic growth while conserving glucose for antioxidation-mediated host innate immunity suppression.