Background: Adaptive plasticity is essential for many species to cope with environmental heterogeneity. In particular, developmental plasticity allows organisms with complex life cycles to adaptively adjust the timing of ontogenetic switch points. Size at and time to metamorphosis are reliable fitness indicators in organisms with complex cycles. The physiological machinery of developmental plasticity commonly involves the activation of alternative neuroendocrine pathways, causing metabolic alterations. Nevertheless, we have still incomplete knowledge about how these mechanisms evolve under environments that select for differences in adaptive plasticity. In this study, we investigate the physiological mechanisms underlying divergent degrees of developmental plasticity across Rana temporaria island populations inhabiting different types of pools in northern Sweden.
Methods: In a laboratory experiment we estimated developmental plasticity of amphibian larvae from six populations coming from three different island habitats: islands with only permanent pools, islands with only ephemeral pools, and islands with a mixture of both types of pools. We exposed larvae of each population to either constant water level or simulated pool drying, and estimated their physiological responses in terms of corticosterone levels, oxidative stress, and telomere length.
Results: We found that populations from islands with only temporary pools had a higher degree of developmental plasticity than those from the other two types of habitats. All populations increased their corticosterone levels to a similar extent when subjected to simulated pool drying, and therefore variation in secretion of this hormone does not explain the observed differences among populations. However, tadpoles from islands with temporary pools showed lower constitutive activities of catalase and glutathione reductase, and also showed overall shorter telomeres.
Conclusions: The observed differences are indicative of physiological costs of increased developmental plasticity, suggesting that the potential for plasticity is constrained by its costs. Thus, high levels of responsiveness in the developmental rate of tadpoles have evolved in islands with pools at high but variable risk of desiccation. Moreover, the physiological alterations observed may have important consequences for both short-term odds of survival and long term effects on lifespan.
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http://dx.doi.org/10.1186/s12862-017-1004-1 | DOI Listing |
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School of Pharmacy, Aichi Gakuin University, 1-100 Kusumoto-cho, Chikusa-ku, Nagoya, 464-8650, Japan.
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Department of Biology and Center for Biodiversity and Ecosystem Stewardship, Villanova University, 800 Lancaster Avenue, Villanova, PA, 19085, USA.
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College of Natural Resources and Environment, Northwest A&F University, Yangling, Shaanxi Province, 712100, PR China.
As biodegradable and bio-based plastics increasingly replace conventional plastics, the need for a comprehensive understanding of their ecotoxicity becomes more pressing. This review systematically presents the ecotoxicity of the microplastics (MPs) from different biodegradable plastics and bioplastics on various animals and plants. High doses of polylactic acid (PLA) MPs (10%) have been found to reduce plant nitrogen content and biomass, and affect the accumulation of heavy metals in plants.
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Two distinct lineages, pluripotent epiblast (EPI) and primitive (extra-embryonic) endoderm (PrE), arise from common inner cell mass (ICM) progenitors in mammalian embryos. To study how these sister identities are forged, we leveraged mouse embryonic stem (ES) cells and extra-embryonic endoderm (XEN) stem cells-in vitro counterparts of the EPI and PrE. Bidirectional reprogramming between ES and XEN coupled with single-cell RNA and ATAC-seq analyses showed distinct rates, efficiencies, and trajectories of state conversions, identifying drivers and roadblocks of reciprocal conversions.
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Department of Cellular Neuropathology, Brain Research Institute, Niigata University, Niigata, Japan.
Our brain adapts to the environment by optimizing its function through experience-dependent cortical plasticity. This plasticity is transiently enhanced during a developmental stage, known as the "critical period," and subsequently maintained at lower levels throughout adulthood. Thus, understanding the mechanism underlying critical period plasticity is crucial for improving brain adaptability across the lifespan.
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