Organisms often modify their environments to their advantage through a process of niche construction. Environments that are improved through positive niche construction can be viewed as a public good. If free riders appear that do not contribute to the shared resource and therefore do not incur any associated costs, the constructed niche may become degraded, resulting in a tragedy of the commons and the extinction of niche constructors. Niche construction can persist if free riders are excluded, for example, if niche constructors monopolize the resource they produce to a sufficient degree. We suggest, however, that the problem of free riders remains because it is possible that nonniche constructors with an enhanced ability to access the resource appear and invade a population of constructors. Using mathematical models we show that positive niche construction can be maintained if it is inextricably linked to a mechanism that makes free riding costly, such as a trait that confers a benefit to only niche constructors. We discuss this finding in terms of genetic interactions and illustrate the principle with a two-locus model. We conclude that positive niche construction can both evolve and be maintained when it has other beneficial effects via pleiotropy. This situation may apply generally to the evolutionary maintenance of cooperation.
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http://dx.doi.org/10.1086/697471 | DOI Listing |
mSystems
January 2025
Zoological Institute, Kiel University, Kiel, Germany.
The microbiomes of host organisms and their direct source environments are closely linked and key for shaping microbial community dynamics. The relationship between these linked dynamics is largely unexplored because source substrates are usually unavailable. To address this current knowledge gap, we employed bacteriovorous nematodes as a unique model system, for which source substrates like rotting apples can be easily collected.
View Article and Find Full Text PDFPhilos Trans R Soc Lond B Biol Sci
January 2025
Centre for Biodiversity and Environment Research, Department of Genetics, Evolution and Environment,, University College London, London WC1E 6BT, UK.
Zoonotic and vector-borne infectious diseases are among the most direct human health consequences of biodiversity change. The COVID-19 pandemic increased health policymakers' attention on the links between ecological degradation and disease, and sparked discussions around nature-based interventions to mitigate zoonotic emergence and epidemics. Yet, although disease ecology provides an increasingly granular knowledge of wildlife disease in changing ecosystems, we still have a poor understanding of the net consequences for human disease.
View Article and Find Full Text PDFPLoS Pathog
January 2025
State Key Laboratory of Resource Insects, Southwest University, Chongqing, China.
Microsporidia are a group of intracellular pathogens that actively manipulate host cell biological processes to facilitate their intracellular niche. Apoptosis is an important defense mechanism by which host cell control intracellular pathogens. Microsporidia modulating host cell apoptosis has been reported previously, however the molecular mechanism is not yet clear.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
National Medical Research Center of Cardiology Named after Academician E.I. Chazov, Moscow 121552, Russia.
Constructing artificial tertiary lymphoid structures (TLSs) opens new avenues for advancing cancer immunotherapy and personalized medicine by creating controllable immune niches. Mesenchymal stromal cells (MSCs) offer an ideal stromal source for such constructs, given their potent immunomodulatory abilities and accessibility. In this study, we explored the potential of adipose-derived MSCs to adopt TLS-supportive phenotypes and facilitate lymphocyte organization.
View Article and Find Full Text PDFCell Tissue Res
December 2024
Cancer Research Institute, School of Basic Medical Sciences, Southern Medical University, Guangzhou, 510515, China.
Blastocyst complementation can potentially generate a rodent model with humanized nasopharyngeal epithelium (NE) that supports sustained Epstein-Barr virus (EBV) infection, enabling comprehensive studies of EBV biology in nasopharyngeal carcinoma. However, during this process, the specific gene knockouts required to establish a developmental niche for NE remain unclear. We performed bioinformatics analyses and generated Foxa1 mutant mice to confirm that Foxa1 disruption could potentially create a developmental niche for NE.
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