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Abstract This article explores the historical development of evolutionary biology-from Natural Theology to the Modern Synthesis (MS)-and the ongoing debate around the Extended Evolutionary Synthesis (EES). Over the past 2,500 years, evolutionary thinking has emerged from the interplay between empirical discoveries and dominant philosophical paradigms. Beginning with Aristotle and Saint Augustine, we trace how Darwin and Wallace introduced a scientific framework grounded in natural mechanisms. In the early 20th century, the MS unified Mendelian genetics and Darwinian selection, forming a gene-centered model of evolution focused on mutations and population dynamics. In recent decades, discoveries in epigenetics, phenotypic plasticity, symbiosis, niche construction, and cultural inheritance have challenged the explanatory scope of MS. The EES seeks to incorporate these processes not by discarding Darwinian principles, but by reinterpreting them through a systems biology lens. This mostly represents a conceptual shift in focus: from linear, gene-driven causality to multilevel, reciprocal, and environmentally embedded dynamics. While gaining traction, the EES has been criticized for its lack of formal models and predictive frameworks, remaining a contested proposal. Ultimately, evolutionary biology continues to evolve as a powerful scientific tradition, driven by humanity’s enduring quest to understand the origins and evolution of life on Earth.

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Abstract A key factor contributing to the success of Darwin and Wallace’s theory of biological evolution by natural selection was its population-level perspective. This conceptual framework was not immediately adopted, largely due to the enduring intuitive appeal of Lamarckian ideas. The development of genetics during the twentieth century provided compelling evidence that effectively excluded Lamarckian mechanisms from the mainstream understanding of evolutionary processes. Some naturalists, however, proposed mechanisms by which environmental factors could influence genotypes in shaping phenotypes, later attributed to chemical modifications of DNA or chromosomal proteins, among others. The field of population epigenetics emerged with the aim of extending the well-established discipline of population genetics by incorporating such phenomena. This review seeks to provide a historical background on this subject and to examine how advances in both contemporary epigenetics and population epigenetics have been achieved, as well as their implications for the study of human diseases, particularly regarding their contribution to the phenomenon of missing heritability. Because there are major taxonomic differences in the transgenerational inheritance of epigenetic modifications, the potential effects of epigenetic architecture on phenotypes of interest also differ, as in the case of mammals and, in particular, humans.

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Abstract Drosophila melanogaster established the candidate-gene paradigm that shaped arthropod evolutionary developmental biology (Evo-Devo) for decades. Genome-wide methods-bulk RNA-seq, single-cell/single-nucleus transcriptomics, chromatin profiling (ATAC-seq, CUT&Tag/CUT&RUN), and 3D genome mapping (Hi-C)-now enable direct interrogation of gene regulatory networks (GRNs) in non-model arthropods. Here we review how these approaches have already uncovered lineage-restricted regulators, resolved cell-type trajectories, and mapped cis-regulatory landscapes across diverse clades. We then take a critical view of their scope and limitations: success depends on high-quality genomes and annotations, careful staging and replication, mitigation of dissociation and ambient-RNA artifacts, and robust cross-species mapping of orthology and cell-type homology. At the regulatory level, linking distal accessible sites to target genes remains a central challenge that often requires integrating chromatin and conformation data with functional perturbations. Progress in this field is further supported by the development and adaptation of enabling tools, such as low-input chemistries (e.g., CUT&Tag), single-nucleus and spatial workflows, and the availability of improved genome assemblies and computational frameworks for multi-omic integration. Ultimately, we argue that the integration of these techniques-especially perturbation with multi-omic data across diverse species-is the key to transforming descriptive regulatory ‘maps’ into a mechanistic understanding of evolution.

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Abstract Metastasis is not a de novo functional module innovation but rather the pathological redeployment of deeply conserved biological programs. Here, we reconstruct the evolutionary landscape of biological functions involved in the early stages of the metastatic cascade, including cell adhesion, extracellular matrix organization (ECM), regulation of metallopeptidase activity, cell junction organization, epithelial-mesenchymal transition (EMT), and cellular extravasation alongside the physiological constraints that suppress them (Metastasis Suppressor Genes). Using phyletic pattern reconstruction of 787 orthologs across 473 Clusters of Orthologous Groups with the Bridge algorithm, we identified a divergence between the evolutionary timelines of metastasis-enabling programs and metastasis suppressors. Our results indicate that the molecular systems associated with the structural capacity for tumor dissemination are evolutionary ancient. ECM organization traces to the Human-Discoba last common ancestor, EMT to Ctenophora, cell adhesion to Sauropsida, and cellular extravasation to Actinopterygii. In contrast, mechanisms responsible for suppressing genomically unstable cells during continuous tissue renewal emerged later, peaking in the vertebrate lineage. These findings support the Serial Atavism Model and suggest that metastasis arises from the progressive erosion of recently evolved regulatory constraints, allowing the reactivation of ancestral cellular programs that predate complex multicellularity.

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Abstract The snakelike phenotype is characterized by limb reduction and body elongation, and independently evolved in several vertebrate lineages. This phenotype is often interpreted as adaptive to fossoriality or use of complex habitats. Limblessness and fossoriality might impose different energetic requirements for locomotion, affecting selective rates on mitochondrial genes. Previous studies identified signals of differential selection in mitochondrial genes of limbless lizards and fossorial rodents. However, it remains unclear which of these factors most intensely shapes mitochondrial genome evolution in Squamata. Amphisbaenia is a key group to answer this question, as it is one of the largest lineages of limbless and fossorial squamates. Here we report a new complete mitochondrial genome of Amphisbaena alba and address the relationships between limblessness and fossoriality in the evolution of mitochondrial genes in Squamata. The full length of the A. alba mitochondrial genome was 16,800 bp (13 protein-coding genes, 22 transfer RNAs, two ribosomal RNAs and the control region). We performed selective tests, allowing different rates for clades with limbless and fossorial species separately. Fossorial species have significant changes in selective rates in more mitochondrial genes than the limbless species, a result suggesting fossoriality as a prevalent factor shaping selective pressures on mitochondrial genes.