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Pespeni, M.

Publications and source records attributed to Pespeni, M..

5 recordsLinked to original sources

Developmental temperature drives distinct transcriptomic responses to acute temperatures and correlated differences in thermal tolerance

Marine invertebrate populations exhibit varying capacities to withstand rising environmental temperatures, but the genetic basis of this differential tolerance remains an important area of investigation. Plasticity can be a valuable tool in the arsenal of an animal trying to maintain physiological function under rapidly changing conditions and can be an important contributor to thermal tolerance. In this work, we characterized the transcriptomic response to elevated developmental temperature, and subsequent acute exposure to two higher temperatures using the widespread and ecologically important copepod, Acartia tonsa. Using a split brood experimental design, we found that copepods that developed at 22{degrees}C had higher upper lethal temperatures compared to those reared at 18{degrees}C, demonstrating developmental plasticity in thermal tolerance. Transcriptomic analyses revealed that developmental temperature strongly influenced gene expression both at baseline and in response to acute thermal stress. Exposure to a moderate heat challenge (28{degrees}C) elicited divergent transcriptional responses between developmental treatments, suggesting developmental preconditioning, whereas exposure to extreme heat (33{degrees}C) triggered a more conserved stress response across groups. Weighted gene co-expression network analysis (WGCNA) identified gene modules associated with upper lethal temperature, highlighting stress response, cellular regulation, and metabolic pathways as key contributors to thermal tolerance. Together, our results reveal how developmental environments shape gene expression patterns and thermal phenotypes, providing insight into the molecular basis of plasticity and potential resilience to climate change.

genomics↗

Geographic Divergence in Population Genomics and Shell Morphology Reveal History of Glacial Refugia in a Coastal Dogwhelk

Studying contemporaneous spatial patterns of genomic diversity can yield important insights into the evolutionary processes that structure populations and shape patterns of adaptation. In contrast to the large number of marine species with planktonic larvae, populations of marine taxa with low dispersal and deep evolutionary divergences offer an opportunity to reveal the phylogeographic histories of marine ecosystems. Here, we constructed a draft genome assembly for the low-dispersing marine dogwhelk, Nucella canaliculata, and studied patterns of genomic diversity and shell morphometrics in 19 populations distributed along [~]1,500 km of the west coast of North America. We observed significant population structure with a strong phylogeographic break at Monterey Bay, which was matched with divergence in shell morphology. Genomic patterns, concomitant with computer simulations, suggest that there were at least two refugial populations during the last glacial maximum that subsequently experienced post-glacial expansion and admixture. Lastly, linking genotype to phenotype, we identified candidate loci underlying variation in shell morphology. These findings demonstrate how high-resolution genomic data reveal the roles of demography, selection, and historical events in shaping the spatial distribution of genetic variation, offering key insights into the processes that structure modern coastal populations and their potential to respond to future climatic changes.

evolutionary biology↗

Precursors of Sea Star Wasting: Immune and Microbial Disruption During Initial Disease Outbreak in Southeast Alaska

Sea Star Wasting Disease (SSW) has devastated sea star populations along the North American Pacific coast since 2013, yet the mechanisms of disease progression, particularly in natural environments, remain unclear. Here we integrate transcriptomic and microbial data from wild Pycnopodia helianthoides sampled across sites affected and unaffected by SSW in southeast Alaska during the initial outbreak recorded in the region in 2016. Individuals exposed to SSW but lacking visible symptoms showed elevated expression of complement system components, pathogen recognition genes, immune regulatory and cell death pathways. Alongside signs of immune activation, genes involved in maintaining extracellular matrix composition, tissue remodeling, and cell adhesion were differentially expressed, indicating early disruption of tissue homeostasis preceding visible wasting symptoms. Gene ontology analysis revealed enrichment of immune response, cell-cell adhesion, response to oxygen levels and nervous system regulatory pathways. Furthermore, network analyses revealed differentially abundant microbes in Exposed individuals--notably Vibrio spp.--were highly correlated with immune response, tissue integrity, stress and detoxification genes in network modules. Together, our findings offer insight into early host-pathogen dynamics in wild populations, underscoring putative links between immune activation and microbial community shifts with the onset of SSW disease.

ecology↗

The Variability of Evolvability: Properties of Dynamic Fitness Landscapes Determine How Phenotypic Variability Evolves

The magnitude and shape of phenotypic variation depends on properties of the genotype-to-phenotype (GP) map, which itself can evolve over time. The evolution of GP maps is particularly interesting in variable environments, as GP maps can evolve to bias variation in the direction of past selection, increasing the evolvability of the population over time. However, the degree and manner in which environmental variation shapes GP maps and influences evolutionary dynamics may depend on properties of the fitness landscape. To explore how evolutionary dynamics are affected by variable environments across a wide range of different pairs of fitness landscapes, we evolved GP maps to produce spatial-temporal gene expression patterns that matched two-dimensional patterns generated by different elementary cellular automata (CA) rules. We found remarkable variation in how populations evolved in variable environments. In some cases, changing the environment helped populations find higher fitness peaks; in others, it hindered them. The evolution of evolvability also depended on the fitness landscape pair. In some experiments, the ability to generate adaptive phenotypic variation upon environment change increased over time, while in some others, populations found shared areas between fitness landscapes. On the other hand, environmental variability consistently resulted in higher fitness landscape exploration, average fitness and mutational robustness compared to evolution in static environments, which we hypothesize are tightly connected. In conclusion, work presented here sheds light on important general consequences of environmental variability, while also demonstrating dependency on properties of fitness landscapes, which future research on the evolution of evolvability should consider. Significance statementThe speed and direction of evolution depend on the availability of phenotypic variation. Genotype-to-phenotype maps can over time bias phenotypic variability to more readily produce alternative adaptive phenotypes in fluctuating environments. However, because properties of the fitness landscapes influence evolutionary dynamics, it remains unclear which previously observed dynamics reflect general effects of environmental variability and which are specific to the pair of landscapes used. We found that the height of the fitness peaks discovered, and how the populations became more evolvable, significantly differed across landscape pairs. In contrast, environmental variability consistently increased average fitness and mutational robustness. Thus, future research investigating the inherent consequences of frequent environmental change should be done on a range of dynamic landscapes.

evolutionary biology↗

Epigenetic and evolutionary mechanisms uniquely contribute to rescue from global change

To persist in the geologically unprecedented rates of global change, populations can adapt or acclimate. However, how these mechanisms of resilience interact, particularly the role of epigenetic variation in long-term adaptation, is unknown. To address this gap, we experimentally evolved the foundational marine copepod Acartia tonsa for 25 generations under ocean acidification, warming, their combination, and control conditions then measured epigenomic, genomic, and transcriptomic responses. We observed clear and consistent epigenomic and genomic divergence between treatments, with epigenomic divergence concentrated in genes related to stress response and the regulation of transposable elements. However, epigenetic and genetic changes occurred in different regions of the genome such that regions with significant methylation divergence had 2-2.5 fold lower FST than regions without methylation divergence. This negative relationship between epigenetic and genetic divergence could be driven by local inhibition of one another or distinct functional targets of selection. In contrast, epigenetic divergence was positively linked to gene expression divergence, indicating that epigenetic changes may facilitate phenotypic change. Taken together, these results suggest that unique, complementary genetic and epigenetic mechanisms promote resilience to global change. Significance StatementOrganisms must adapt or acclimate to survive global change, but how these processes interact and the role of epigenetic variation is unknown. To address these gaps, we experimentally evolved the marine copepod Acartia tonsa for 25 generations in global change conditions and measured their genomic, epigenomic, and gene expression responses. We found that both genetic and epigenetic changes contributed to resilience and were inversely related, acting in different regions of the genome. Epigenetic changes were functionally linked to the regulation of stress and transposable elements and correlated with shifts in gene expression. Therefore, the resilience of populations to ongoing global change is driven by the complementary contribution of both genetic and epigenetic mechanisms.

evolutionary biology↗