Areospora rohanae n.gen. n.sp. (Microsporidia; Areosporiidae n. fam.) elicits multi-nucleate giant-cell formation in southern king crab (Lithodes santolla)

Stentiford, Grant D.; Bateman, Kelly S.; Feist, Stephen W.; Oyarzún, Sylvia; Uribe, Juan Carlos; Palacios, Mauricio; Stone, David M.

doi:10.1016/j.jip.2014.02.004

Cited by 23 publications

(18 citation statements)

References 29 publications

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“…support a major economy, amounting to almost 40 billion dollars per annum from wild fisheries and aquaculture [79]. Those pathogens that target the edible musculature of crustacean hosts have the potential to render marketable meats inedible [80], while those infecting connective tissues can blight the visual esthetics and marketing of high-value captured hosts such as king crabs [81]. In aquaculture settings, farmed penaeid shrimp represent one of the highest-value traded seafood commodities (see [79]).…”

Section: Microsporidia In Major Food Production Chainsmentioning

confidence: 99%

Microsporidia – Emergent Pathogens in the Global Food Chain

Stentiford

Becnel

Weiss

et al. 2016

Trends in Parasitology

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Intensification of food production has the potential to drive increased disease prevalence in food plants and animals. Microsporidia are diversely distributed, opportunistic, and density-dependent parasites infecting hosts from almost all known animal taxa. They are frequent in highly managed aquatic and terrestrial hosts, many of which are vulnerable to epizootics, and all of which are crucial for the stability of the animal–human food chain. Mass rearing and changes in global climate may exacerbate disease and more efficient transmission of parasites in stressed or immune-deficient hosts. Further, human microsporidiosis appears to be adventitious and primarily associated with an increasing community of immune-deficient individuals. Taken together, strong evidence exists for an increasing prevalence of microsporidiosis in animals and humans, and for sharing of pathogens across hosts and biomes.

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Section: Microsporidia In Major Food Production Chainsmentioning

confidence: 99%

Microsporidia – Emergent Pathogens in the Global Food Chain

Stentiford

Becnel

Weiss

et al. 2016

Trends in Parasitology

Self Cite

260

190

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“…Further studies on the molecular and structural changes involved in the Nematocida - C. elegans interactions we described here will contribute to our understanding of how two separate cells can be joined together. Previous studies on infections of both vertebrates and invertebrates reported that microsporidia cause the formation of syncytia in host tissues 24–26 . These syncytia can occur in structures called xenomas, which are described as hypertrophic host cells that increase in size and number of nuclei 27 .…”

mentioning

confidence: 99%

Cell-to-cell spread of microsporidia causes Caenorhabditis elegans organs to form syncytia

et al. 2016

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The growth of pathogens is dictated by their interactions with the host environment1. Obligate intracellular pathogens undergo several cellular decisions as they progress through their life cycles inside of host cells2. We studied this process for microsporidian species in the genus Nematocida as they grew and developed inside their co-evolved animal host Caenorhabditis elegans3–5. We found that microsporidia can restructure multicellular host tissues into a single contiguous multinucleate cell. In particular, we found that all three Nematocida species we studied were able to spread across the cells of C. elegans tissues before forming spores, with two species causing syncytial formation in the intestine, and one species causing syncytial formation in the muscle. We also found that the decision to switch from replication to differentiation in N. parisii was altered by the density of infection, suggesting that environmental cues influence the dynamics of the pathogen life cycle. These findings show how microsporidia can maximize the use of host space for growth, and that environmental cues in the host can regulate a developmental switch in the pathogen.

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“…This presence presumably facilitates redistribution of host mitochondria and other organelles around early intracellular stages characteristic for nearly all described species of microsporidia as well as probably it ensures movement of Nosema granulosis early meronts along the spindle axis of dividing host oocytes (Terry et al 1999). Acquisition of host cell adhesion proteins such as cadherins may be a standard adaptation for microsporidia: the literature reveals a number of species, particularly in host muscle, in which the spore stages displayed filaments or bristles on the spore surface, structurally similar to those discussed in this paper, particularly in the muscle of decapod crustaceans (Johnston et al 1978;LaDouceur and Murphy 2017;Small et al 2014Small et al , 2019Stentiford et al 2014;Wang et al 2017), but also in insects (Weidner et al 1999a), and even in bryozoans (Canning et al 2002). Interestingly, the tissues known to be particularly rich in IFs include muscles and neurons (Sanghvi-Shah and Weber 2017).…”

Section: Discussionmentioning

confidence: 55%

“…1A, B), were observed previously in A. michaelis and also in other five Ameson spp. infecting muscles of various decapods (for reference see (Small et al 2019;Stentiford et al 2013), as well as in Areospora rohanae (Stentiford et al 2014). At the first glance their fine morphology does not match the one of any kind of intermediate filaments conventionally organized in 7-10 nm thick bundles (Goldmann 2018;Marceau et al 2014;Melcer et al 2007).…”

Section: Filamentous Structures Revealed On the Surface Of Microsporimentioning

confidence: 99%

Microsporidia Can Acquire Lamin‐like Intermediate Filaments and Cell Adhesion Catenin‐cadherin Complexes from the Host (?)

Weidner

Sokolova

Overstreet

2020

J Eukaryotic Microbiology

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On their spore surfaces, Microsporidia often develop a canopy of filaments with characteristics of intermediate filaments (IF), as we demonstrated in previous studies on Thelohania sp., Ameson michaelis, and Spraguea lophii. Genomic studies indicate that among invertebrates, lamins that may localize in the cytoplasm or nucleus, are the only known IF type. These IFs can bind to the substrate containing cell adhesion molecules (CAMs) cadherins, associated with β and γ catenins. The objects of this study were to determine whether microsporidia have CAMs with the attached IFs on their envelopes and to find out if these proteins are provided by the host. An examination was made for localization of lamins and CAMs on the spores of the mentioned above species and Anncaliia algerae, plus in the host animals. Then, we determined whether the spores of A. michaelis and A. algerae could bind vertebrate nuclear lamin onto the spore surface. We also tested transgenic Drosophila melanogaster stocks bearing cadherin‐GFP to see whether developing A. algerae parasites in these hosts could acquire host CAMs. The tests were positive for all these experiments. We hypothesize that microsporidia are able to acquire host lamin IFs and cell adhesion catenin–cadherin complexes from the host.

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Areospora rohanae n.gen. n.sp. (Microsporidia; Areosporiidae n. fam.) elicits multi-nucleate giant-cell formation in southern king crab (Lithodes santolla)

Cited by 23 publications

References 29 publications

Microsporidia – Emergent Pathogens in the Global Food Chain

Microsporidia – Emergent Pathogens in the Global Food Chain

Cell-to-cell spread of microsporidia causes Caenorhabditis elegans organs to form syncytia

Microsporidia Can Acquire Lamin‐like Intermediate Filaments and Cell Adhesion Catenin‐cadherin Complexes from the Host (?)

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