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Dormancy and diapause are key adaptations in many organisms, enabling survival of temporarily or seasonally unsuitable environmental conditions. In this review, we examine how our understanding of programmed developmental and metabolic arrest during diapause intersects with the increasing body of knowledge about animal co-development and co-evolution with microorganisms. Host-microbe interactions are increasingly understood to affect a number of metabolic, physiological, developmental, and behavioral traits and to mediate adaptations to various environments. Therefore, it is timely to consider how microbial factors might affect the expression and evolution of diapause in a changing world. We examine how a range of host-microbe interactions, from pathogenic to mutualistic, may have an impact on diapause phenotypes. Conversely, we examine how the discontinuities that diapause introduces into animal host generations can affect the ecology of microbial communities and the evolution of host-microbe interactions. We discuss these issues as they relate to physiology, evolution of development, local adaptation, disease ecology, and environmental change. Finally, we outline research questions that bridge the historically distinct fields of seasonal ecology and host-microbe interactions.
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http://dx.doi.org/10.1086/706078 | DOI Listing |
Philos Trans A Math Phys Eng Sci
September 2025
D-BAUG, ETH Zurich, Zürich 8093, Switzerland.
Biofilms-microbial communities encased in a self-produced extracellular matrix-pose a significant challenge in clinical settings due to their association with chronic infections and antibiotic resistance. Their formation in the human body is governed by a complex interplay of biological and environmental factors, including the biochemical composition of bodily fluids, fluid dynamics, and cell-cell and cell-surface interactions. Improving therapeutic strategies requires a deeper understanding of how host-specific conditions shape biofilm development.
View Article and Find Full Text PDFInfluenza Other Respir Viruses
September 2025
Department of Respiratory, Children's Hospital of Nanjing Medical University, Nanjing, China.
Respiratory syncytial virus (RSV) is one of the leading causes of severe respiratory diseases in children, especially in infants. The immune responses induced by RSV infection are a fairly complex process that can contribute significantly to disease severity. Despite decades of research on RSV, many immune mechanisms remain to be explored.
View Article and Find Full Text PDFNeotrop Entomol
September 2025
Kunming Branch of Yunnan Provincial Tobacco Company, Kunming, China.
Successful biological control requires accurate knowledge of the host preference of the released parasitoid. Telenomus remus Nixon (1973) is an effective parasitoid of Spodoptera frugiperda (J.E.
View Article and Find Full Text PDFCancer Immunol Immunother
September 2025
Department of Thoracic Surgery, Tangdu Hospital, Fourth Military Medical University, Xi'an, 710038, China.
Objective: CircRNAs are involved in cancer progression. However, their role in immune escape in non-small cell lung cancer (NSCLC) remains poorly understood.
Methods: This study employed RIP-seq for the targeted enrichment of circRNAs, followed by Western blotting and RT-qPCR to confirm their expression.
NPJ Biofilms Microbiomes
September 2025
Imperial College Parturition Research Group, Institute of Reproductive and Developmental Biology, Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK.
The mechanisms by which vaginal microbiota shape spontaneous preterm birth (sPTB) risk remain poorly defined. Using electronic clinical records data from 74,913 maternities in conjunction with metaxanomic (n = 596) and immune profiling (n = 314) data, we show that the B blood group phenotype associates with increased risk of sPTB and adverse vaginal microbiota composition. The O blood group associates with sPTB in women who have a combination of a previous history of sPTB, an adverse vaginal microbial composition and pro-inflammatory cervicovaginal milieu.
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