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White, C. R.

Publications and source records attributed to White, C. R..

7 recordsLinked to original sources

Local adaptation in climate tolerance at a small geographic scale contrasts with broad latitudinal patterns

While climate adaptation is typically quantified across broad gradients, the potential for adaptation to the same environmental variables at small scales is rarely tested. If local-scale environmental heterogeneity can generate patterns of adaptation similar to broad gradients, then we currently underestimate adaptive capacity to global change. We quantified population variation in climate tolerance traits and their plasticity for five populations of Drosophila melanogaster from a 3000-km latitudinal gradient, which we contrasted with eight local populations from an environmentally heterogeneous 600x300km area. Population variation in stress tolerance at the local scale was comparable to that across latitude. Consistent with local adaptation, populations from warmer and drier environments showed greater heat and desiccation tolerance, and populations from more predictable environments showed greater plasticity. Climate adaptation at smaller geographic scales can therefore be comparable to adaptation across broad geographic scales. However, patterns of adaptation often changed across geography, which makes predicting responses to global change challenging.

evolutionary biology↗

Variation in temperature but not diet determines the stability of latitudinal clines in tolerance traits and their plasticity

Latitudinal clines are routinely used as evidence of adaptation across broad climatic gradients. However, if environmental variation influences the strength of latitudinal clines, then clinal patterns will be unstable, and using patterns of adaptation to predict population responses to global change will be difficult. To test whether environmental variation influences latitudinal clines, we sampled five populations of Drosophila melanogaster spanning 3000-km of east coast Australia, and measured stress tolerance (heat, cold and desiccation) and body size on flies that developed in six combinations of temperature (13{degrees}C, 25{degrees}C and 29{degrees}C) and diet (standard and low-calorie) treatments. We found latitudinal clines where populations further from the equator had larger wings, higher cold tolerance and lower heat tolerance. For all traits, temperature determined the strength of latitudinal clines, whereas diet had little influence. Steeper clines often emerged in warmer treatments, created by latitudinal clines in plasticity. In the warmest temperature, higher latitude populations showed larger increases in heat tolerance, larger reductions in desiccation tolerance but smaller decreases in cold tolerance. Heat tolerance was the only trait that supported the climate variability hypothesis and a trade-off between plasticity and tolerance. Environment-dependent latitudinal clines are therefore likely to determine variation in population responses to global change.

evolutionary biology↗

RTN4IP1 is essential for the final stages of mitochondrial complex I assembly and coenzyme Q biosynthesis

A biochemical deficiency of mitochondrial complex I (CI) underlies [~]30% of cases of primary mitochondrial disease, yet the inventory of molecular machinery required for CI assembly remains incomplete. We previously characterised patients with isolated CI deficiency caused by segregating variants in RTN4IP1, encoding a mitochondrial NAD(P)H oxidoreductase. Here, we demonstrate that RTN4IP1 deficiency causes a CI assembly defect in both patient fibroblasts and knockout cells, and report that RTN4IP1 is a bona fide CI assembly factor. Complexome profiling revealed accumulation of unincorporated ND5-module and impaired N-module production. RTN4IP1 patient fibroblasts also exhibited defective coenzyme Q biosynthesis, substantiating this emerging function of RTN4IP1. Thus, our data reveal RTN4IP1 plays an essential role in both the terminal stages of CI assembly and in coenzyme Q metabolism, and that pathogenic RTN4IP1 variants impair both functions in patients with mitochondrial disease.

cell biology↗

Body size shapes song in honeyeaters

Birdsongs are among the most distinctive animal signals. Their evolution is thought to be shaped simultaneously by habitat structure and by the constraints of morphology. Habitat structure affects song transmission and detectability, thus influencing song (the acoustic adaptation hypothesis), while body size and beak size and shape necessarily constrain song characteristics (the morphological constraint hypothesis). Yet, support for the acoustic adaptation and morphological constraint hypotheses remains equivocal, and their simultaneous examination is infrequent. Using a phenotypically diverse Australasian bird clade, the honeyeaters (Aves: Meliphagidae), we compile a dataset consisting of song, environmental, and morphological variables for 163 species and jointly examine predictions of these two hypotheses. Overall, we find that body size constrains song frequency and pace in honeyeaters. Although habitat type and environmental temperature influence aspects of song, that influence is indirect, likely via effects of environmental variation on body size, with some evidence that elevation constrains the evolution of song peak frequency. Our results demonstrate that morphology has an overwhelming influence on birdsong, in support of the morphological constraint hypothesis, with the environment playing a secondary role generally via body size rather than habitat structure. These results suggest that changing body size, a consequence of both global effects such as climate change, and local effects such as habitat transformation, will substantially influence the nature of birdsong.

evolutionary biology↗

Metabolic scaling has diversified among species, despite an evolutionary constraint within species

Metabolic rate scales disproportionally with body mass, such that the energetic cost of living is relatively lower in larger organisms. Theory emphasises the importance of fixed physical constraints on metabolic scaling, yet empirical data are lacking with which to assess how evolutionary processes (e.g. mutation, drift, selection) contribute to the observed variation in metabolic scaling across the tree of life. Using a large-scale quantitative genetic study of growth in cockroaches, we show that ontogenetic metabolic scaling is evolutionarily constrained due to an absence of additive genetic variation in juvenile metabolic rate and mass. Using a phylogenetic analysis, we also show that ontogenetic metabolic scaling is more similar among closely related species than among distant relatives, suggesting that the constraints on metabolic scaling are subject to change during lineage diversification. Our results are consistent with growing evidence that there is strong stabilising selection on combinations of mass and metabolic rate within species.

physiology↗

Control of Staphylococcus aureus quorum sensing by a membrane-embedded peptidase

Gram-positive bacteria process and release small peptides or \"pheromones\" that act as signals for the induction of adaptive traits including those involved in pathogenesis. One class of small signaling pheromones is the cyclic auto-inducing peptides (AIPs), which regulate expression of genes that orchestrate virulence and persistence in a range of microbes including Staphylococci, Listeria, Clostridia, and Enterococci. In a genetic screen for Staphylococcus aureus secreted virulence factors, we identified a S. aureus mutant containing an insertion in gene SAUSA300_1984 (mroQ), which encodes a putative membrane-embedded metalloprotease. A {Delta}mroQ mutant exhibits impaired induction of TLR2-dependent inflammatory responses from macrophages, but elicits greater production of the inflammatory cytokine IL-1{beta} and is attenuated in a murine skin and soft tissue infection model. The {Delta}mroQ mutant phenocopies a S. aureus mutant containing a deletion of the accessory gene regulatory system (Agr), wherein both strains have significantly reduced production of secreted toxins and virulence factors, but increased surface Protein A abundance. The Agr system controls virulence factor gene expression in S. aureus through sensing accumulation of AIP via the histidine kinase AgrC and response regulator AgrA. We provide evidence to suggest that MroQ acts within the Agr pathway to facilitate optimal processing or export of AIP for signal amplification through AgrC/A and induction of virulence factor gene expression. Mutation of MroQ active site residues significantly reduces AIP signaling and attenuates virulence. Altogether, this work identifies a new component of the Agr quorum sensing circuit that is critical for the production of S. aureus virulence factors.

microbiology↗

A widespread thermodynamic effect, but maintenance of biological rates through space across life’s major domains

For over a century, temperature compensation (maintenance of biological rates with changing temperatures) has remained controversial. An alternative idea, that fitness is greater at higher temperatures (the thermodynamic effect), has gained increasing traction, and is being used to understand large-scale biodiversity responses to environmental change. Yet evidence in favour of each of these contrasting hypotheses continues to emerge. In consequence, the fundamental nature of organismal thermal responses and its implications remain unresolved. Here we investigate these ideas explicitly using a global dataset of 619 observations of four categories of organismal performance, spanning 14 phyla and 403 species. In agreement with both hypotheses, we show a positive relationship between the temperature of maximal performance rate (Topt) and environmental temperature (Tenv) for all traits. Next we demonstrate that relationships between Tenv and the temperature of maximal performance rate (Umax) are rarely significant and positive, as expected if a thermodynamic effect predominates. By contrast, a positive relationship between Topt and Umax is always present, but markedly weaker than theoretically predicted. These outcomes demonstrate that while some form of thermodynamic effect exists, ample scope is present for biochemical and physiological adaptation to thermal environments in the form of temperature compensation.

ecology↗