38 research outputs found

    Acid secretion by the boring organ of the burrowing giant clam, Tridacna crocea

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    The giant clam Tridacna crocea, native to Indo-Pacific coral reefs, is noted for its unique ability to bore fully into coral rock and is a major agent of reef bioerosion. However, T. crocea\u27s mechanism of boring has remained a mystery despite decades of research. By exploiting a new, two-dimensional pH-sensing technology and manipulating clams to press their presumptive boring tissue (the pedal mantle) against pH-sensing foils, we show that this tissue lowers the pH of surfaces it contacts by greater than or equal to 2 pH units below seawater pH day and night. Acid secretion is likely mediated by vacuolar-type H+-ATPase, which we demonstrate (by immunofluorescence) is abundant in the pedal mantle outer epithelium. Our discovery of acid secretion solves this decades-old mystery and reveals that, during bioerosion, T. crocea can liberate reef constituents directly to the soluble phase, rather than producing sediment alone as earlier assumed

    Seek, and ye shall find: Accessing the global epidemiological literature in different languages.

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    The thematic series Beyond English: Accessing the global epidemiological literature in Emerging Themes in Epidemiology highlights the wealth of epidemiological and public health literature in the major languages of the world, and the bibliographic databases through which they can be searched and accessed. This editorial suggests that all systematic reviews in epidemiology and public health should include literature published in the major languages of the world and that the use of regional and non-English bibliographic databases should become routine.Published versio

    A brain-infecting parasite impacts host metabolism both during exposure and after infection is established

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    Metabolic costs associated with parasites should not be limited to established infections. Even during initial exposure to questing and attacking parasites, hosts can enact behavioural and physiological responses that could also incur metabolic costs. However, few studies have measured these costs directly. Hence, little is known about metabolic costs arising from parasite exposure. Furthermore, no one has yet measured whether and how previous infection history modulates metabolic responses to parasite exposure. Here, using the California killifish Fundulus parvipinnis and its brain‐infecting parasite Euhaplorchis californiensis, we quantified how killifish metabolism, behaviour and osmoregulatory phenotype changed upon acute exposure to parasite infectious stages (i.e. cercariae), and with long‐term infection. Exposure to cercariae caused both naïve and long‐term infected killifish to acutely increase their metabolic rate and activity, indicating detection and response to parasite infectious stages. Additionally, these metabolic and behavioural effects were moderately stronger in long‐term infected hosts than naïve killifish, suggesting that hosts may develop learned behavioural responses, nociceptor sensitization and/or acute immune mechanisms to limit new infections. Although established infection altered the metabolic response to parasite exposure, established infection did not alter standard metabolic rate, routine metabolic rate, maximum metabolic rate, aerobic scope or citrate synthase enzyme activity. Unexpectedly, established infection reduced lactate dehydrogenase enzyme activity in killifish brains and relative Na+/K+‐ATPase abundance in gills, suggesting novel mechanisms by which E. californiensis may alter its hosts\u27 behaviour and osmoregulation. Thus, we provide empirical evidence that parasites can disrupt the metabolism of their host both during parasite exposure and after infection is established. This response may be modulated by previous infection history, with probable knock‐on effects for host performance, brain energy metabolism, osmoregulation and ecology. A free Plain Language Summary can be found within the Supporting Information of this article

    Seawater carbonate chemistry and blood and endolymph acid-base parameters in control and OA-exposed rockfish

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    Over a decade ago, ocean acidification (OA) exposure was reported to induce otolith overgrowth in teleost fish. This phenomenon was subsequently confirmed in multiple species; however, the underlying physiological causes remain unknown. Here, we report that splitnose rockfish (Sebastes diploproa) exposed to 1600 μatm pCO2 (pH 7.5) were able to fully regulated the pH of both blood and endolymph (the fluid that surrounds the otolith within the inner ear). However, while blood was regulated around pH 7.80, the endolymph was regulated around pH 8.30. These different pH setpoints result in increased pCO2 diffusion into the endolymph, which in turn leads to proportional increases in endolymph [HCO3−] and [CO32−]. Endolymph pH regulation despite the increased pCO2 suggests enhanced H+ removal. However, a lack of differences in inner ear bulk and cell-specific Na+/K+-ATPase and vacuolar type H+-ATPase protein abundance localization pointed out to activation of preexisting ATPases, non-bicarbonate pH buffering, or both, as the mechanism for endolymph pH-regulation. These results provide the first direct evidence showcasing the acid-base chemistry of the endolymph of OA-exposed fish favors otolith overgrowth, and suggests that this phenomenon will be more pronounced in species that count with more robust blood and endolymph pH regulatory mechanisms
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