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Macdonald, S.

Publications and source records attributed to Macdonald, S..

4 recordsLinked to original sources

Spiroplasma and heat hardening can buffer insect male fertility loss at high temperatures

Insects upper thermal limits for survival, activity, and fertility have been used to assess vulnerability to climate change, yet heritable endosymbionts - present in over 70% of insect species - are often overlooked. While emerging research suggests some endosymbionts can increase thermal tolerance, their effects on upper lethal and fertility thermal limits has rarely been investigated. Additionally, short-term exposure to sub-lethal high temperatures (heat hardening) can increase insect heat tolerance, but its impact on male fertility is unclear and potential interactions with endosymbionts has not been explored. Here, we investigate whether the endosymbiont Spiroplasma poulsonii and heat hardening influence upper survival and fertility thermal limits in a native widespread host of Spiroplasma (Drosophila hydei) and a novel host (Drosophila birchii), a rainforest-restricted species with low heat tolerance. Heat hardening generally improved survival and fertility following a heat shock. The presence of Spiroplasma increased survival and fertility of D. hydei males following heat-shock, while in D. birchii, it did not enhance survival but protected male fertility after heat-shock and modulated hardening responses at sub-lethal temperatures. While protective effects varied across species, sex, and trait, both Spiroplasma and hardening significantly buffered male fitness loss during heat shock in both host species and halved heat exposure risk under current and predicted climate change in the rainforest restricted D. birchii. These findings highlight that, beyond generating novel phenotypic variation, endosymbionts can interact with plastic responses to heat stress, emphasising the importance of accounting for endosymbiont-mediated effects on thermal tolerance when assessing insect vulnerability to climate change and exploring strategies to manipulate insect thermal tolerance.

evolutionary biology↗

Genetic Variation in Chromatin State Across Multiple Tissues in Drosophila melanogaster

We use ATAC-seq to examine chromatin accessibility for four different tissues in Drosophila melanogaster: adult female brain, ovaries, and both wing and eye-antennal imaginal discs from males. Each tissue is assayed in eight different inbred strain genetic backgrounds, seven associated with a reference quality genome assembly. We develop a method for the quantile normalization of ATAC-seq fragments and test for differences in coverage among genotypes, tissues, and their interaction at 44099 peaks throughout the euchromatic genome. For the strains with reference quality genome assemblies, we correct ATAC-seq profiles for read mis-mapping due to nearby polymorphic structural variants (SVs). Comparing coverage among genotypes without accounting for SVs results in a highly elevated rate (55%) of identifying false positive differences in chromatin state between genotypes. After SV correction, we identify 1050, 30383, and 4508 regions whose peak heights are polymorphic among genotypes, among tissues, or exhibit genotype-by-tissue interactions, respectively. Finally, we identify 3988 candidate causative variants that explain at least 80% of the variance in chromatin state at nearby ATAC-seq peaks. AUTHOR SUMMARYChromatin states are well described in Drosophila melanogaster embryos, but adult and pre-adult tissues are poorly studied, as are differences among genotypes. We carried out ATAC-seq on four different tissues in eight different inbred genotypes with biological replicates within tissue and genotype. We discover that apparent differences in coverage, and by inference chromatin openness, are often due to segregating structural variants (SVs) that can only be corrected for if strains are associated with high-quality genome assemblies. After correction for false positives associated with SVs, we identify thousands of regions that appear to vary in chromatin state between genotypes or vary between genotypes in a tissue-dependent manner. It has been widely speculated that cis-regulatory variants contribute to standing variation in complex traits. If this is true, chromatin states that vary between individuals, perhaps in a tissue-dependent manner, are likely to be enriched for quantitative trait loci.

genetics↗

Predicting evolutionary change at the DNA level in a natural Mimulus population

Evolution by natural selection occurs when the frequencies of genetic variants change because individuals differ in Darwinian fitness components such as survival or reproductive success. Differential fitness has been demonstrated in field studies of many organisms, but our ability to quantitatively predict allele frequency changes from fitness measurements remains unclear. Here, we characterize natural selection on millions of Single Nucleotide Polymorphisms (SNPs) across the genome of the annual plant Mimulus guttatus. We use fitness estimates to calibrate population genetic models that effectively predict observed allele frequency changes into the next generation. Hundreds of SNPs experienced "male selection" in 2013 with one allele at each SNP elevated in frequency among successful male gametes relative to the entire population of adults. In the following generation, allele frequencies at these SNPs consistently shifted in the predicted direction. A second year of study revealed that SNPs had effects on both viability and reproductive success with pervasive trade-offs between fitness components. SNPs favored by male selection were, on average, detrimental to survival. These trade-offs (antagonistic pleiotropy and temporal fluctuations in fitness) may be essential to the long-term maintenance of alleles undergoing substantial changes from generation to generation. Despite the challenges of measuring selection in the wild, the strong correlation between predicted and observed allele frequency changes suggests that population genetic models have a much greater role to play in forward-time prediction of evolutionary change. Author summaryFor the last 100 years, population geneticists have been deriving equations for {Delta}p, the change in allele frequency owing to mutation, selection, migration, and genetic drift. Seldom are these equations used directly, to match a prediction for {Delta}p to an observation of {Delta}p. Here, we apply genomic sequencing technologies to samples from natural populations, obtaining millions of observations of {Delta}p. We estimate natural selection on SNPs in a natural population of yellow monkeyflowers and find extensive evidence for selection through differential male success. We use the SNP-specific fitness estimates to calibrate a population genetic model that predicts observed {Delta}p into the next generation. We find that when male selection favored one nucleotide at a SNP, that nucleotide increased in frequency in the next generation. Since neither observed nor predicted {Delta}p are generally large in magnitude, we developed a novel method called "haplotype matching" to improve prediction accuracy. The method leverages intensive whole genome sequencing of a reference panel (187 individuals) to infer sequence-specific selection in thousands of field individuals sequenced at much lower coverage. This method proved essential to accurately predicting {Delta}p in this experiment and further development may facilitate population genetic prediction more generally.

evolutionary biology↗

broad controls leg imaginal disc morphogenesis in Drosophila via regulation of cell shape changes and remodeling of extracellular matrix

Imaginal disc morphogenesis during metamorphosis in Drosophila melanogaster provides an excellent model to uncover molecular mechanisms by which hormonal signals effect physical changes during development. The broad (br) Z2 isoform encodes a transcription factor required for disc morphogenesis in response to 20-hydroxyecdysone, yet how it accomplishes this remains largely unknown. Here, we show that amorphic br5 mutant discs fail to remodel their basal extracellular matrix (ECM) after puparium formation and do not undergo necessary cell shape changes. RNA sequencing of wild type and mutant leg discs identified 717 genes differentially regulated by br; functional studies reveal that several are required for adult leg formation, particularly those involved in remodeling the ECM. Additionally, br Z2 expression is abruptly shut down at the onset of metamorphosis, and expressing it beyond this time results in failure of leg development during the late prepupal and pupal stages. Taken together, our results suggest that br Z2 is required to drive ECM remodeling, change cell shape, and maintain metabolic activity through the mid prepupal stage, but must be switched off to allow expression of pupation genes. Summary StatementThe Drosophila melanogaster ecdysone-responding transcription factor broad controls morphogenetic processes in leg imaginal discs during metamorphosis through regulation of genes involved in extracellular matrix remodeling, metabolism, and cell shape changes and rearrangements.

developmental biology↗