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ABSTRACT Diverse marine animals undergo a metamorphic larval-to-juvenile transition in response to surface-bound bacteria. Although this host-microbe interaction is critical to establishing and maintaining marine animal populations, the functional activity of bacterial products and how they activate the host’s metamorphosis program has not yet been defined for any animal. The marine bacteriumPseudoalteromonas luteoviolaceastimulates the metamorphosis of a tubeworm calledHydroides elegansby producing a molecular syringe called metamorphosis-associated contractile structures (MACs). MACs stimulate metamorphosis by injecting a protein effector termed metamorphosis-inducing factor 1 (Mif1) into tubeworm larvae. Here, we show that MACs bind to tubeworm cilia and form visible pores on the cilia membrane surface, which are smaller and less numerous in the absence of Mif1.In vitro, Mif1 associates with eukaryotic lipid membranes and possesses phospholipase activity. MACs can also deliver Mif1 to human cell lines and cause parallel phenotypes, including cell surface binding, membrane disruption, calcium flux, and mitogen-activated protein kinase activation. Finally, MACs can also stimulate metamorphosis by delivering two unrelated membrane-disrupting proteins, MLKL and RegIIIɑ. Our findings demonstrate that membrane disruption by MACs and Mif1 is necessary forHydroidesmetamorphosis, connecting the activity of a bacterial protein effector to the developmental transition of a marine animal. IMPORTANCEThis research describes a mechanism wherein a bacterium prompts the metamorphic development of an animal from larva to juvenile form by injecting a protein that disrupts membranes in the larval cilia. Specifically, results show that a bacterial contractile injection system and the protein effector it injects form pores in larval cilia, influencing critical signaling pathways like mitogen-activated protein kinase and calcium flux, ultimately driving animal metamorphosis. This discovery sheds light on how a bacterial protein effector exerts its activity through membrane disruption, a phenomenon observed in various bacterial toxins affecting cellular functions, and elicits a developmental response. This work reveals a potential strategy used by marine organisms to respond to microbial cues, which could inform efforts in coral reef restoration and biofouling prevention. The study’s insights into metamorphosis-associated contractile structures’ delivery of protein effectors to specific anatomical locations highlight prospects for future biomedical and environmental applications. 

Sea urchins are basal deuterostomes that share key molecular components of innate immunity with vertebrates. They are a powerful model for the study of innate immune system evolution and function, especially during early development. Here we characterize the morphology and associated molecular markers of larval immune cell types in a newly developed model sea urchin, Lytechinus pictus. We then challenge larvae through infection with an established pathogenic Vibrio and characterize phenotypic and molecular responses. We contrast these to the previously described immune responses of the purple sea urchin Strongylocentrotus purpuratus . The results revealed shared cellular morphologies and homologs of known pigment cell immunocyte markers ( PKS, srcr142 ) but a striking absence of subsets of perforin‐like macpf genes in blastocoelar cell immunocytes. We also identified novel patterning of cells expressing a scavenger receptor cysteine rich (SRCR) gene in the coelomic pouches of the larva (the embryonic stem cell niche). The SRCR signal becomes further enriched in both pouches in response to bacterial infection. Collectively, these results provide a foundation for the study of immune responses in L. pictus. The characterization of the larval immune system of this rapidly developing and genetically enabled sea urchin species will facilitate more sophisticated studies of innate immunity and the crosstalk between the immune system and development. 

Abstract Throughout the past decade, many studies have reported adverse effects in biota following microplastic exposure. Yet, the field is still emerging as the current understanding of microplastic toxicity is limited. At the same time, recent legislative mandates have required environmental regulators to devise strategies to mitigate microplastic pollution and develop health-based thresholds for the protection of human and ecosystem health. The current publication rate also presents a unique challenge as scientists, environmental managers, and other communities may find it difficult to keep up with microplastic research as it rapidly evolves. At present, there is no tool that compiles and synthesizes the data from these studies to allow for visualization, interpretation, or analysis. Here, we present the Toxicity of Microplastics Explorer (ToMEx), an open access database and open source accompanying R Shiny web application that enables users to upload, search, visualize, and analyze microplastic toxicity data. Though ToMEx was originally created to facilitate the development of health-based thresholds to support California legislations, maintaining the database by the greater scientific community will be invaluable to furthering research and informing policies globally. The database and web applications may be accessed at https://microplastics.sccwrp.org/ . Graphical Abstract