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Defensin-like proteins are conserved in multicellular organisms and contribute to innate immune responses against fungal pathogens. In rice, defensins play a novel role in regulating cadmium (Cd) efflux from the cytosol. However, whether the antifungal activity of defensins correlates with Cd-efflux function remains unknown. In this study, we isolated an endophytic Fusarium , designed Fo 10, by a comparative microbiome analysis of rice plants grown in a paddy contaminated with Cd. Fo 10 is tolerant to high levels of Cd, but is sensitive to the defensin-like protein OsCAL1, which mediates Cd efflux to the apoplast. We found that Fo 10 symbiosis in rice is regulated by OsCAL1 dynamics, and Fo 10 coordinates multiple plant processes, including Cd uptake, vacuolar sequestration, efflux to the environment, and formation of Fe plaques in the rhizosphere. These processes are dependent on the salicylic acid signaling pathway to keep Cd levels low in the cytosol of rice cells and to decrease Cd levels in rice grains without any yield penalty. Fo 10 also plays a role in Cd tolerance in the poaceous crop maize and wheat, but has no observed effects in the eudicot plants Arabidopsis and tomato. Taken together, these findings provide insights into the mechanistic basis underlying how a fungal endophyte and host plant interact to control Cd accumulation in host plants by adapting defense responses to promote the establishment of a symbiosis that permits adaptation to high-Cd environments. This study identifies an endophytic Fusarium Fo 10 that interacts reciprocally with the defensin-like protein OsCAL1 to reduce cytosolic Cd levels in rice. Fo10 modulates iron plaque formation, vacuolar Cd sequestration, and rhizosphere Cd efflux likely by activating SA signaling pathway. [ABSTRACT FROM AUTHOR]

Root hairs are tubular-shaped outgrowths of epidermal cells essential for plants acquiring water and nutrients from the soil. Despite their importance, the growth of root hairs is finite. How this determinate growth is precisely regulated remains largely unknown. Here we identify LONG ROOT HAIR (LRH), a GYF domain-containing protein, as a unique repressor of root hair growth. We show that LRH inhibits the association of eukaryotic translation initiation factor 4Es (eIF4Es) with the mRNA of ROOT HAIR DEFECTIVE6-LIKE4 (RSL4) that encodes the master regulator of root hair growth, repressing RSL4 translation and thus root hair elongation. RSL4 in turn directly transactivates LRH expression to maintain a proper LRH gradient in the trichoblasts. Our findings reveal a previously uncharacterized LRH-RSL4 feedback regulatory loop that limits root hair growth, shedding new light on the mechanism underlying the determinate growth of root hairs. [Display omitted] • Long Root Hair (LRH) is required for the determinate growth of root hairs • LRH inhibits root hair elongation via repression of RSL4 protein accumulation • LRH interacts with eIF4Es to repress RSL4 translation in root hair cells • RSL4 directly transactivates LRH expression to form a feedback regulatory loop How the determinate growth of root hairs is precisely controlled remains largely unknown. Cui et al. identify a novel factor, LRH, that represses RSL4-dependent root hair elongation at the translational level. RSL4 in turn directly transactivates LRH expression to form a feedback regulatory loop, fine-tuning the determinate growth of root hairs. [ABSTRACT FROM AUTHOR]

Toxic signaling by extrasynaptic NMDA receptors (eNMDARs) is considered an important promoter of amyotrophic lateral sclerosis (ALS) disease progression. To exploit this therapeutically, we take advantage of TwinF interface (TI) inhibition, a pharmacological principle that, contrary to classical NMDAR pharmacology, allows selective elimination of eNMDAR-mediated toxicity via disruption of the NMDAR/TRPM4 death signaling complex while sparing the vital physiological functions of synaptic NMDARs. Post-disease onset treatment of the SOD1 G93A ALS mouse model with FP802, a modified TI inhibitor with a safe pharmacology profile, stops the progressive loss of motor neurons in the spinal cord, resulting in a reduction in the serum biomarker neurofilament light chain, improved motor performance, and an extension of life expectancy. FP802 also effectively blocks NMDA-induced death of neurons in ALS patient-derived forebrain organoids. These results establish eNMDAR toxicity as a key player in ALS pathogenesis. TI inhibitors may provide an effective treatment option for ALS patients., Competing Interests: Declaration of interests H.B. and J.Y. are named inventors of the patent application for a novel class of neuroprotectants (PCT/EP2018/078577); H.B. is co-founder of FundaMental Pharma GmbH, Heidelberg, Germany, which licenses FP802; H.B. and J.Y. are shareholders of FundaMental Pharma GmbH., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)