BioEssays最新文献

The brain's vast cellular diversity and complex developmental programs have long inspired neuroscientists' efforts to understand its organization and function. Recent advances in single-cell RNA sequencing (scRNA-seq) have transformed this field, enabling the characterization of neural and glial cell types with unprecedented resolution. This had allowed us to better understand the developmental trajectories and functional specialization of cell types across multiple model organisms, from zebrafish and fruit flies, to mice and humans, but also to address the mechanisms underlying neural disease progression.

Research in molecular cell biology has typically been focused on identifying specific genes and proteins responsible for cellular phenomena. However, it is increasingly recognized that the function of many biomolecules is variable and context dependent, raising the question if specific components can adequately explain cellular mechanisms. Philosophers of biology have proposed an alternative perspective known as process ontology, posing that not objects or molecules, but processes are the fundamental units of living systems. Process ontology is gaining popularity in biological theory, but remains challenging to integrate into scientific practice. Here, we assess the applicability of the process perspective in the context of a concrete biological system, namely polarization in budding yeast. We identify relevant processes in yeast polarization at different timescales and examine how these processes affect our understanding of polarity. Using this case study, we demonstrate how the processual perspective evokes new kinds of scientific questions and provide concrete pointers for incorporating processual thought into cell biological research.

How does the brain prioritize competing drives like hunger, sleep, and mating? In Drosophila, the neuropeptide SIFamide (SIFa) has emerged as a central coordinator of these behavioral states. This commentary synthesizes recent findings, highlighting the study by Velazquez et al., which reveals that SIFa receptor signaling regulates sleep and feeding in a time-of-day-specific manner to maintain energy homeostasis. We further discuss how SIFa modulates reproductive behavior through synaptic plasticity in male-specific GABAergic neurons. Anatomically, SIFa neurons act as an integration hub, receiving convergent circadian and metabolic inputs to bias downstream circuits. We propose that the SIFa system serves as a master conductor, orchestrating adaptive behavioral decisions based on internal physiological needs.

Diseases due to mutations in essential molecules can involve tissues functioning in very different environments, with some in mechanically active environments. Diseases arising from mutations in a single molecule, such as the CFTR in cystic fibrosis exhibit varied clinical phenotypes. The lung cells expressing mutations in CFTR are functioning in the mechanically active environment of the lung, but these mutations may also play an adverse role in the cardiovascular system. Similarly, Marfan syndrome arises from mutations in an extracellular matrix (ECM) molecule, fibrillin-1 and this molecule is also involved in tissues operating in very mechanically active environments. Thus, there is the potential for genetic variants with or without clinical symptoms individually to interact in the same individual to exhibit a unique interdependent phenotype involving disruption of the "Cell-ECM" relationship. Although the clinical phenotypes for the CFTR and fibrillin-1 individually are rare, both molecules are known to each have >500 mutations. This may be one example of a molecular pair that could uniquely interact, influencing cell function. This article will discuss this premise and address the potential basis for complementarity using CFTR and fibrillin-1 as examples.

Collective cell migration is fundamental to developmental processes and disease progression. Despite extensive study, the field lacks a unifying framework for how collective cells initiate and terminate their migration. While these processes have traditionally been explained for individual cell migration by epithelial‒mesenchymal transition (EMT) and mesenchymal‒epithelial transition (MET), these models do not fully recapitulate the complex features of collective cell migration. In this review, I explore the distinct mechanisms by which groups of cells initiate and terminate collective migration, highlighting in vivo examples such as gastrulation and neural crest formation in vertebrates, lateral line migration in zebrafish, and tracheal branch and border cell migration in Drosophila. I also discuss collective cell migration in cancer metastasis. I focus on how the initiation and termination of collective migration are regulated, emphasizing the regulatory pathways and unique features. Clarifying these mechanisms will guide hypothesis-driven discovery and inform strategies to modulate collective cell behaviors in development, regeneration, and metastasis.

The Cambrian Explosion is often seen as a singular event requiring an explanation. In fact, it is better represented as a cascade of linked events, each with numerous causes. The iconic middle Cambrian fauna, represented by sites such as the Burgess Shale, is a culmination of several phases of increases in taxonomic diversity and morphological complexity. I focus on an often-overlooked increase in complexity that took place in a limited number of phyla in parallel after the main "explosion". This increase in morphological complexity and disparity was facilitated by an increase in the complexity of the central nervous system, which in itself was a selective response to the ecological complexity of the biosphere, which had been increasing from the late Ediacaran. Genetic regulatory components that contributed to an increasingly differentiated and regionalized central nervous system were developmentally co-opted to increase the differentiation and complexity of additional organ systems. This process took place convergently in arthropods, mollusks, and annelids at different times throughout the Cambrian and, later in the Ordovician, also in vertebrates.

Fluorescence microscopy is essential in modern cell biology but remains constrained by photobleaching, autofluorescence, and the intrinsic quantum yields of emitters. Metal-enhanced fluorescence (MEF) is a photophysical phenomenon in which interactions between luminescent species and metal nanostructures markedly increase emission, enabling a route to brighter, high-contrast, noninvasive bioimaging by reshaping photophysical pathways without modifying fluorophore chemistry. This review translates MEF fundamentals into an experimental playbook for biologists, distinguishing MEF mechanisms and explaining how distance, spectral overlap, and nanoparticle morphology govern whether emission is boosted or quenched. We synthesize recent live-cell applications—using gold and silver nanoparticles—to illustrate gains in signal-to-noise at lower excitation power, improved photostability, and opportunities where small-molecule dyes often suffer low quantum yield, and provide practical guidelines for pairing dyes with metal nanostructures to lower the barrier to adopting MEF in cellular imaging.