Biodiversity is of crucial importance for ecosystem functioning, sustainability and resilience, but the magnitude and organization of marine diversity at a range of spatial and taxonomic scales are undefined. In this paper, we use second-generation sequencing to unmask putatively diverse marine metazoan biodiversity in a Scottish temperate benthic ecosystem. We show that remarkable differences in diversity occurred at microgeographical scales and refute currently accepted ecological and taxonomic paradigms of meiofaunal identity, rank abundance and concomitant understanding of trophic dynamics. Richness estimates from the current benchmarked Operational Clustering of Taxonomic Units from Parallel UltraSequencing analyses are broadly aligned with those derived from morphological assessments. However, the slope of taxon rarefaction curves for many phyla remains incomplete, suggesting that the true alpha diversity is likely to exceed current perceptions. The approaches provide a rapid, objective and cost-effective taxonomic framework for exploring links between ecosystem structure and function of all hitherto intractable, but ecologically important, communities.
SummaryWhile components of the pathway that establishes left-right asymmetry have been identified in diverse animals, from vertebrates to flies, it is striking that the genes involved in the first symmetry-breaking step remain wholly unknown in the most obviously chiral animals, the gastropod snails. Previously, research on snails was used to show that left-right signaling of Nodal, downstream of symmetry breaking, may be an ancestral feature of the Bilateria [1, 2]. Here, we report that a disabling mutation in one copy of a tandemly duplicated, diaphanous-related formin is perfectly associated with symmetry breaking in the pond snail. This is supported by the observation that an anti-formin drug treatment converts dextral snail embryos to a sinistral phenocopy, and in frogs, drug inhibition or overexpression by microinjection of formin has a chirality-randomizing effect in early (pre-cilia) embryos. Contrary to expectations based on existing models [3, 4, 5], we discovered asymmetric gene expression in 2- and 4-cell snail embryos, preceding morphological asymmetry. As the formin-actin filament has been shown to be part of an asymmetry-breaking switch in vitro [6, 7], together these results are consistent with the view that animals with diverse body plans may derive their asymmetries from the same intracellular chiral elements [8].
Aim Meiofaunal communities that inhabit the marine benthos offer unique opportunities to simultaneously study the macroecology of numerous phyla that exhibit different life-history strategies. Here, we ask: (1) if the macroecology of meiobenthic communities is explained mainly by dispersal constraints or by environmental conditions; and (2) if levels of meiofaunal diversity surpass existing estimates based on morphological taxonomy.Location UK and mainland European coast.Methods Next-generation sequencing techniques (NGS; Roche 454 FLX platform) using 18S nuclear small subunit ribosomal DNA (rDNA) gene. Pyrosequences were analysed using AmpliconNoise followed by chimera removal using Perseus.Results Rarefaction curves revealed that sampling saturation was only reached at 15% of sites, highlighting that the bulk of meiofaunal diversity is yet to be discovered. Overall, 1353 OTUs were recovered and assigned to 23 different phyla. The majority of sampled sites had c. 60-70 unique operational taxonomic units (OTUs) per site, indicating high levels of beta diversity. The environmental parameters that best explained community structure were seawater temperature, geographical distance and sediment size, but most of the variability (R 2 = 70%-80%) remains unexplained.Main conclusions High percentages of endemic OTUs suggest that meiobenthic community composition is partly niche-driven, as observed in larger organisms, but also shares macroecological features of microorganisms by showing high levels of cosmopolitanism (albeit on a much smaller scale). Meiobenthic communities exhibited patterns of isolation by distance as well as associations between niche, latitude and temperature, indicating that meiobenthic communities result from a combination of niche assembly and dispersal processes. Conversely, isolation-bydistance patterns were not identified in the featured protists, suggesting that animals and protists adhere to radically different macroecological processes, linked to life-history strategies.
In previous work (Davison et al., 2016), we used both genetic mapping and a chemical knockdown to show that a frameshift mutation in one copy of a duplicated formin gene is most likely the mutation that causes changes in left-right (LR) asymmetry, or chirality, in the pond snail Lymnaea stagnalis. We also showed that the asymmetric morphology is preceded by asymmetric formin expression in snails, and that overexpressing the same gene in frogs reverses LR asymmetry. We are therefore pleased that research by Abe and Kuroda (2019) not only corroborates our own findings, but gains definitive proof for causation. The new work puts beyond any doubt that LR asymmetry in snails originates in the cellular architecture. However, we are troubled by several errors or omissions, and also that the authors dismiss previous experimental work, by ourselves and others. These points need making because they detract from what is otherwise an important step forward, causing confusion amongst colleagues in an important area of developmental biology. (1) The new work confuses the gene names, to the extent that several colleagues mistakenly believed that we misidentified the locus in 2016. In being the first to identify the causative gene (Davison et al., 2016; submitted in August 2015, published in February 2016), we named it Ldia2 because it is evidently the derived version, compared with Ldia1. Ldia2 is located on a long branch (evidence of rapid evolution), and Ldia2 transcripts are enriched in the embryo relative to Ldia1 (indicating specialized function). Despite submitting their work after ours was published (Kuroda et al., 2016; received in July 2016, published in October 2016), the Kuroda group reversed the naming of the same genes, Lsdia1 for the mutated version and Lsdia2 for the other copy. This fact is not mentioned at all in their new work (Abe and Kuroda, 2019). It is therefore important that these differences are made clear, and that, as in other fields, precedence should be used for describing the genes in future publications. (2) The authors' title is that the work 'establishes the formin Lsdia1 as the long-sought gene for snail dextral/sinistral coiling'. Notwithstanding the fact that we established the formin as the causative gene (Davison et al., 2016), and they gained definitive proof (Abe and Kuroda, 2019), all experiments prior to ∼2003 were carried out in another species, L. peregra, for which the causative gene remains CORRESPONDENCE Development (2020) 147
Although the pond snail Lymnaea stagnalis is an emerging model organism for molecular studies in a wide variety of fields, there are a limited number of verified endogenous control genes for use in quantitative real-time PCR. As part of a larger study on snail chirality, or left–right asymmetry, we assayed gene expression in pond snail embryos. We evaluated six candidate control genes, by comparing their expression in three tissues (ovotestis, foot and embryo) and used three software programmes (geNorm, Normfinder and Bestkeeper) to do so. The specific utility of these control genes was then tested by investigating the relative expression of six experimental transcripts, including formin Ldia2, a gene that has been associated with chiral variation in L. stagnalis. All six control genes were found to be suitable for use in the three tissues tested. Of the six experimental genes, it was found that all were relatively depleted in the early embryo compared with other tissues, except the formin Ldia2 gene. Instead, transcripts of the wild-type Ldia2dex were enriched in the embryo, whereas a nonfunctional frameshifted version, Ldia2sin, was severely depleted. These differences in Ldia2sin expression were less evident in the ovotestis and were not evident in the foot tissue, possibly because nonsense-mediated decay is obscured in actively transcribing tissues. Our work provides a set of control genes that may be useful to the wider community and illustrates how these genes may be used to assay differences in expression in a variety of tissues.
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