Non-uniform rates of morphological evolution and evolutionary increases in organismal complexity, captured in metaphors like "adaptive zones", "punctuated equilibrium" and "blunderbuss patterns", require more elaborate explanations than a simple gradual accumulation of mutations. Here we argue that non-uniform evolutionary increases in phenotypic complexity can be caused by a threshold-like response to growing ecological pressures resulting from evolutionary diversification at a given level of complexity. Acquisition of a new phenotypic feature allows an evolving species to escape this pressure but can typically be expected to carry significant physiological costs. Therefore, the ecological pressure should exceed a certain level to make such an acquisition evolutionarily successful. We present a detailed quantitative description of this process using a microevolutionary competition model as an example. The model exhibits sequential increases in phenotypic complexity driven by diversification at existing levels of complexity and a resulting increase in competitive pressure, which can push an evolving species over the barrier of physiological costs of new phenotypic features.
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http://dx.doi.org/10.1371/journal.pcbi.1007388 | DOI Listing |
Semin Cell Dev Biol
December 2024
Institute of Cellular and Organismic Biology, Academia Sinica, Taipei 11529, Taiwan. Electronic address:
The intricate control of collective cell dynamics is crucial for enabling organismic development and tissue regeneration. Despite the availability of various in vitro and in vivo models, studies on tissue-scale cell dynamics and associated emergent properties in living systems remain methodically challenging. Here, we describe key advantages of using the adult zebrafish tailfin (caudal fin) as a robust in vivo model for dissecting millimeter-scale collective cell dynamics during regeneration and wound healing in a complex tissue.
View Article and Find Full Text PDFNew Phytol
December 2024
Department of Biology, University of Kentucky, Lexington, KY, 40506, USA.
The effects of single chromosome number change-dysploidy - mediating diversification remain poorly understood. Dysploidy modifies recombination rates, linkage, or reproductive isolation, especially for one-fifth of all eukaryote lineages with holocentric chromosomes. Dysploidy effects on diversification have not been estimated because modeling chromosome numbers linked to diversification with heterogeneity along phylogenies is quantitatively challenging.
View Article and Find Full Text PDFSci Total Environ
December 2024
Department of Ecology, Evolution, and Organismal Biology, Iowa State University, Ames, IA, USA; Department of Plant Pathology, Entomology and Microbiology, Iowa State University, Ames, IA, USA. Electronic address:
Health and population status of bees is negatively affected by anthropogenic stressors, many of which co-occur in agricultural settings. While pollinator habitat (often involving plantings of native forbs) holds promise to benefit both managed and wild bees, important issues remain unresolved. These include whether conventional, broad-spectrum insecticide use negates these benefits and how non-native, managed honey bees affect wild bees in these areas.
View Article and Find Full Text PDFMed Sci (Paris)
December 2024
Université Paris Cité, CNRS UMR7216, Épigénétique et destin cellulaire, Paris, France.
The development of sequencing technologies and their increased accessibility in clinical services and genetic laboratories have considerably accelerated the identification of genetic variants associated with rare diseases (RDs). Among these, Mendelian disorders of the epigenetic machinery (MDEM) are rare monogenic diseases characterized by the presence of mutations in genes encoding epigenetic regulators that play a key role in organismal development and cellular functions. Loss of function of these regulators is expected to lead to epigenetic modifications that profoundly affect genome expression and cellular identity.
View Article and Find Full Text PDFJ Hered
December 2024
Ohio Biodiversity Conservation Partnership, The Ohio State University, Columbus, Ohio, 43210 USA.
Conservation of threatened species can benefit from an evaluation of genes in the Major Histocompatibility Complex (MHC), whose loci encode proteins that bind pathogens and are often under strong selection to maintain diversity in immune response to diseases. Despite this gene family's importance to disease resistance, little is known about these genes in reptiles including snakes. To address this issue, we assembled and annotated a highly-contiguous genome assembly for the timber rattlesnake (Crotalus horridus), a pit viper which is threatened or endangered in parts of its range, and analyzed this new genome along with three other rattlesnake genomes to characterize snake MHC loci.
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