Recognizing when and how rapid evolution drives ecological change is fundamental for our understanding of almost all ecological and evolutionary processes such as community assembly, genetic diversification and the stability of communities and ecosystems. Generally, rapid evolutionary change is driven through selection on genetic variation and is affected by evolutionary constraints, such as tradeoffs and pleiotropic effects, all contributing to the overall rate of evolutionary change. Each of these processes can be influenced by the presence of multiple environmental stressors reducing a population's reproductive output. Potential consequences of multistressor selection for the occurrence and strength of the link from rapid evolution to ecological change are unclear. However, understanding these is necessary for predicting when rapid evolution might drive ecological change. Here we investigate how the presence of two stressors affects this link using experimental evolution with the bacterium Pseudomonas fluorescens and its predator Tetrahymena thermophila. We show that the combination of predation and sublethal antibiotic concentrations delays the evolution of anti-predator defence and antibiotic resistance compared with the presence of only one of the two stressors. Rapid defence evolution drives stabilization of the predator-prey dynamics but this link between evolution and ecology is weaker in the two-stressor environment, where defence evolution is slower, leading to less stable population dynamics. Tracking the molecular evolution of whole populations over time shows further that mutations in different genes are favoured under multistressor selection. Overall, we show that selection by multiple stressors can significantly alter eco-evolutionary dynamics and their predictability.
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http://dx.doi.org/10.1038/s41559-018-0701-5 | DOI Listing |
Explor Target Antitumor Ther
November 2024
Division of Pulmonary, Critical Care, and Sleep Disorders Medicine, Department of Medicine, University of Louisville School of Medicine, Louisville, KY 40202, USA.
There has been a rapid expansion of immunotherapy options for non-small cell lung cancer (NSCLC) over the past two decades, particularly with the advent of immune checkpoint inhibitors. Despite the emerging role of immunotherapy in adjuvant and neoadjuvant settings though, relatively few patients will respond to immunotherapy which can be problematic due to expense and toxicity; thus, the development of biomarkers capable of predicting immunotherapeutic response is imperative. Due to the promise of a noninvasive, personalized approach capable of providing comprehensive, real-time monitoring of tumor heterogeneity and evolution, there has been wide interest in the concept of using circulating tumor DNA (ctDNA) to predict treatment response.
View Article and Find Full Text PDFJ Gastrointest Cancer
January 2025
Department of Medical Oncology, Princess Margaret Cancer Centre, Toronto, ON, Canada.
Purpose: Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive malignancy with limited therapeutic options and poor prognosis. Recent advances in targeted therapies have opened new avenues for intervention in PDAC, focusing on key genetic and molecular pathways that drive tumor progression.
Methods: In this review, we provide an overview on advances in novel targeted therapies in pancreatic adenocarcinoma.
Int J Med Inform
December 2024
Department of Hepatobiliary Surgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China. Electronic address:
Background: Solid organ transplantation (SOT) is vital for end-stage organ failure but faces challenges like organ shortage and rejection. Artificial intelligence (AI) offers potential to improve outcomes through better matching, success prediction, and automation. However, the evolution of AI in SOT research remains underexplored.
View Article and Find Full Text PDFBlood
January 2025
South Australian Health & Medical Research Institute, Australia.
One of the most remarkable achievements of the TKI era has been the capacity to induce deep molecular remissions that are sustainable off therapy in chronic myeloid leukemia (CML) patients - treatment-free remission (TFR). TFR was first described in a handful of patients within 3-4 years of imatinib approval. In 2004 TFR was tested in a small French pilot study, followed soon after by the French STIM and Australasian TWISTER studies.
View Article and Find Full Text PDFPLoS Biol
January 2025
Institut de Génétique Humaine, Univ Montpellier, Centre National de la Recherche Scientifique, Montpellier, France.
In many eukaryotes, meiotic recombination occurs preferentially at discrete sites, called recombination hotspots. In various lineages, recombination hotspots are located in regions with promoter-like features and are evolutionarily stable. Conversely, in some mammals, hotspots are driven by PRDM9 that targets recombination away from promoters.
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