As a fundamental biological principle, genomic information is typically transmitted vertically from parent to offspring. Occasionally, however, genetic material is transferred horizontally between species. Transposable elements (TEs) are frequently involved in such horizontal transfer (HT), possibly due to their ability to move in genomes. HT has been particularly well-studied in Drosophila melanogaster , a key model organism for evolutionary and ecological research. Recent studies have revealed that HT triggered the invasion of 12 different TEs in the D. melanogaster genome over the past 200 years. This finding challenges our traditional view of genome evolution, suggesting that TE invasions may not only be isolated events that can be ignored as rare exceptions but could represent recurrent events that continuously reshape genomes. In this review, we trace the history of how these 12 invasions were discovered and outline the lines of evidence supporting them. We also discuss the potential evolutionary consequences of these TE invasions, including their roles in adaptation, genome evolution, speciation, and extinction risk. Finally, we highlight open questions and directions for future research. In particular, it will be essential to test whether other organisms also exhibit similarly high rates of recent TE invasions and to assess whether human activity triggered the high rate of invasions.
For over a century, biologists have used test tubes and petri dishes to investigate life. By studying bacteria in laboratory conditions, generations of scientists have amassed a wealth of biological knowledge. However, simple experimental systems remove complexity, leading us to question how our knowledge translates to the natural world. Approaches combining microfluidics and molecular biology have made rapid progress, filling this gap by reintroducing experimental complexity. In our review, we highlight how microfluidics has shifted and enhanced our understanding of several core molecular microbiology processes. In Section 1, we follow the journey of bacterial cells as they colonize surfaces, emphasizing that this is not a linear process. In Section 2, we explore how the interplay of physical, chemical, and biological features impacts surface-attached communities. Along the way, we highlight how using microfluidics captures bacterial behavior that classical approaches overlook, often revealing unexpected and counterintuitive outcomes.
Dicer has long been viewed as the RNAse III enzyme that generates small regulatory RNAs to drive RNA interference (RNAi) machinery and posttranscriptional gene silencing. However, a growing body of evidence reveals that Dicer's functional landscape extends far beyond its canonical role in the cytoplasmic RNAi pathway. In this review, we delineate the classical, RNAse III-dependent small RNA processing activities from an expanding set of noncanonical functions in which Dicer operates independently of RNAi outputs. We highlight emerging principles that underlie these functions, including structural and regulatory principles, with a focus on nuclear functions, posttranslational regulation, and noncanonical substrates. We then explore how Dicer intersects with genome integrity pathways, transcriptional programs, and cellular response to DNA damage. Finally, we propose an integrated conceptual framework in which Dicer acts as a multifunctional regulator of chromatin architecture and genome stability, as we consider how perturbations of these pathways contribute to disease.
Meiosis is a specialized cell division essential for sexual reproduction, generating haploid gametes through two consecutive nuclear divisions following a single round of DNA replication. During an extended meiotic prophase I, chromosomes undergo elaborate rearrangements, such as pairing, synapsis, and recombination, culminating in crossovers that physically link homologs for accurate segregation. Errors in these processes cause aneuploidy, a leading contributor to infertility, miscarriage, and congenital disorders. These chromosomal events must be precisely coordinated with cell cycle transitions through signaling pathways involving cell cycle and DNA damage checkpoint kinases, as well as ubiquitin-mediated regulation. These pathways control the timing and levels of programmed DNA double-strand breaks, monitor synapsis and crossover formation, and enforce surveillance checkpoints that eliminate defective cells. This review examines how signaling networks orchestrate chromosome dynamics during meiotic prophase, highlighting conserved principles and organism-specific adaptations that ensure faithful genetic transmission across generations.
Multicellularity necessitated the evolution of cellular diversity and specialization, yet across organisms, the retention of cellular plasticity within defined physiological contexts is a recurring principle. Here, we examine early-diverging metazoans to reevaluate the evolutionary logic of stemness. Rather than viewing stem cells as exceptional, we argue that cellular plasticity represents a deeply conserved attribute of early life. The ability of cells to remain responsive, multipotent, and regenerative under ecological or physiological contexts challenges the notion of cellular identity. We integrate evidence across three layers: evolutionary origins of cellular plasticity, systemic physiological axes that govern stem cell behavior, and metabolic and epigenetic mechanisms that execute fate decisions. This synthesis reveals that stemness is not a default cellular state but a licensed state, permitted when organism-level physiological signals align with local tissue demands. Within this framework, regeneration, age-associated decline, and cancer emerge as evidence of how effectively systemic governance regulates cellular plasticity across multicellular life.
