No abstract

Recent genomic analyses have highlighted parallel divergence in response to ecological gradients, but the extent to which altitude can underpin such repeated speciation remains unclear. Wing reduction and flight loss have apparently evolved repeatedly in montane insect assemblages, and have been suggested as important drivers of hexapod diversification. We test this hypothesis using genomic analyses of a widespread wing-polymorphic stonefly species complex in New Zealand. We identified over 50,000 polymorphic genetic markers generated across almost 200 Zelandoperla fenestrata stonefly specimens using a newly generated plecopteran reference genome, to reveal widespread parallel speciation between sympatric full-winged and wing-reduced ecotypes. Rather than the existence of a single, widespread, flightless taxon (Zelandoperla pennulata), evolutionary genomic data reveal that wing-reduced upland lineages have speciated repeatedly and independently from full-winged Z. fenestrata. This repeated evolution of reproductive isolation between local ecotype pairs that lack mitochondrial DNA differentiation suggests that ecological speciation has evolved recently. A cluster of outlier SNPs detected in independently wing-reduced lineages, tightly linked in an approximately 85 kb genomic region that includes the developmental ‘supergene’ doublesex, suggests that this ‘island of divergence’ may play a key role in rapid ecological speciation.

There is growing interest in the role of structural variants (SVs) as drivers of local adaptation and speciation. From a biodiversity genomics perspective, the characterization of genome‐wide SVs provides an exciting opportunity to complement single nucleotide polymorphisms (SNPs). However, little is known about the impacts of SV discovery and genotyping strategies on the characterization of genome‐wide SV diversity within and among populations. Here, we explore a near whole‐species resequence data set, and long‐read sequence data for a subset of highly represented individuals in the critically endangered kākāpō (Strigops habroptilus). We demonstrate that even when using a highly contiguous reference genome, different discovery and genotyping strategies can significantly impact the type, size and location of SVs characterized genome‐wide. Further, we found that the mean number of SVs in each of two kākāpō lineages differed both within and across generations. These combined results suggest that genome‐wide characterization of SVs remains challenging at the population‐scale. We are optimistic that increased accessibility to long‐read sequencing and advancements in bioinformatic approaches including multireference approaches like genome graphs will alleviate at least some of the challenges associated with resolving SV characteristics below the species level. In the meantime, we address caveats, highlight considerations, and provide recommendations for the characterization of genome‐wide SVs in biodiversity genomic research.

8 9 3 1human MAIT cells to TCR and cytokine stimulation. We report that MAIT cells rapidly respond 3 2 to TCR stimulation through the production of multiple effector cytokines and chemokines, 3 3 alteration of their cytotoxic granule content and transcription factor expression, and upregulation 3 4 of co-stimulatory proteins CD40L and 4-1BB. In contrast, cytokine-mediated activation is slower 3 5and results in more limited production of cytokines, chemokines, and co-stimulatory proteins; 3 6 differences in granule content and transcription factor expression are also evident. Therefore, we 3 7 propose that in infections by riboflavin-synthesizing bacteria, MAIT cells play a key early role in 3 8 effecting and coordinating the immune response, while in the absence of TCR stimulation (e.g. 3 9 viral infection) their role is likely to differ. 4 0 4 1

The Developmental Origins of Health and Disease hypothesis predicts that early-life environmental exposures can be detrimental to later-life health and that mismatch between the pre- and post-natal environment may contribute to the growing non-communicable disease epidemic. Within this is an increasingly recognized role for epigenetic mechanisms; for example, epigenetic modifications can be influenced by nutrition and can alter gene expression in mothers and offspring. Currently, there are few whole-genome transcriptional studies of response to nutritional alteration. Thus, we sought to explore how nutrition affects the expression of genes involved in epigenetic processes in Drosophila melanogaster. We manipulated Drosophila food macronutrient composition at the F0 generation, mismatched F1 offspring back to a standard diet and analysed the transcriptome of the F0–F3 generations by RNA sequencing. At F0, the altered (high-protein, low-carbohydrate) diet increased expression of genes classified as having roles in epigenetic processes, with co-ordinated down-regulation of genes involved in immunity, neurotransmission and neurodevelopment, oxidative stress and metabolism. Upon reversion to standard nutrition, mismatched F1 and F2 generations displayed multigenerational inheritance of altered gene expression. By the F3 generation, gene expression had reverted to F0 (matched) levels. These nutritionally induced gene expression changes demonstrate that dietary alterations can up-regulate epigenetic genes, which may influence the expression of genes with broad biological functions. Furthermore, the multigenerational inheritance of the gene expression changes in F1 and F2 mismatched generations suggests a predictive adaptive response to maternal nutrition, aiding the understanding of the interaction between maternal diet and offspring health, with direct implications for the current non-communicable disease epidemic.