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Abstract Reports of diverse vermiform and peloidal structures in Neoproterozoic to Mesozoic open marine to peritidal carbonates include cases interpreted to be keratose sponges. However, living keratose sponges have elaborate, highly elastic skeletons of spongin (a mesoscopic end‐member of a hierarchical assemblage of collagenous structures) lacking spicules, thus have poor preservation potential in contrast to the more easily fossilized spicule‐bearing sponges. Such interpreted fossil keratose sponges comprise diverse layered, network, amalgamated, granular and variegated microfabrics of narrow curved, branching, vesicular–cellular to irregular areas of calcite cement, thought to represent former spongin, embedded in microcrystalline to peloidal carbonate. Interpreted keratose sponges are presented in publications almost entirely in two‐dimensional (thin section) studies, usually displayed normal to bedding, lacking mesoscopic three‐dimensional views in support of a sponge body fossil. For these structures to be keratose sponges critically requires conversion of the spongin skeleton into the calcite cement component, under shallow‐burial conditions and this must have occurred prior to compaction. However, there is no robust petrographic–geochemical evidence that the fine‐grained carbonate component originated from sponge mummification (automicritic body fossilsviacalcification of structural tissue components) because in the majority of cases the fine‐grained component is homogenous and thus likely to be deposited sediment. Thus, despite numerous studies, verification of fossil keratose sponges is lacking. Although some may be sponges, all can be otherwise explained. Alternatives include: (i) meiofaunal activity; (ii) layered microbial (spongiostromate) accretion; (iii) sedimentary peloidal to clotted micrites; (iv) fluid escape and capture resulting in bird's eye to vuggy porosities; and (v) moulds of siliceous sponge spicules. Uncertainty of keratose sponge identification is fundamental and far‐reaching for understanding: (i) microfacies and diagenesis where they occur; (ii) fossil assemblages; and (iii) wider aspects of origins of animal clades, sponge ecology, evolution and the systemic recovery from mass extinctions. Thus, alternative explanations must be considered. 

Abstract BackgroundAnimals with polyploid, hybrid nuclei offer a challenge for models of gene expression and regulation during embryogenesis. To understand how such organisms proceed through development, we examined the timing and prevalence of mortality among embryos of unisexual salamanders in the genusAmbystoma. ResultsOur regional field surveys suggested that heightened rates of embryo mortality among unisexual salamanders begin in the earliest stages of embryogenesis. Although we expected elevated mortality after zygotic genome activation in the blastula stage, this is not what we found among embryos which we reared in the laboratory. Once embryos entered the first cleavage stage, we found no difference in mortality rates between unisexual salamanders and their bisexual hosts. Our results are consistent with previous studies showing high rates of unisexual mortality, but counter to reports that heightened embryo mortality continues throughout embryo development. ConclusionsPossible causes of embryonic mortality in early embryogenesis suggested by our results include abnormal maternal loading of RNA during meiosis and barriers to insemination. The surprising survival rates of embryos post-cleavage invites further study of how genes are regulated during development in such polyploid hybrid organisms. 

The blood–brain barrier (BBB) is a multicellular construct that regulates the diffusion and transport of metabolites, ions, toxins, and inflammatory mediators into and out of the central nervous system (CNS). Its integrity is essential for proper brain physiology, and its breakdown has been shown to contribute to neurological dysfunction. The BBB in vertebrates exists primarily through the coordination between endothelial cells, pericytes, and astrocytes, while invertebrates, which lack a vascularized circulatory system, typically have a barrier composed of glial cells that separate the CNS from humoral fluids. Notably, the invertebrate barrier is molecularly and functionally analogous to the vertebrate BBB, and the fruit fly, Drosophila melanogaster, is increasingly recognized as a useful model system in which to investigate barrier function. The most widely used technique to assess barrier function in the fly is the dye-exclusion assay, which involves monitoring the infiltration of a fluorescent-coupled dextran into the brain. In this study, we explore analytical and technical considerations of this procedure that yield a more reliable assessment of barrier function, and we validate our findings using a traumatic injury model. Together, we have identified parameters that optimize the dye-exclusion assay and provide an alternative framework for future studies examining barrier function in Drosophila.