BioEssays最新文献

To an external observer, the goal of cell division is evident from the very shape of the duplicated chromosomes. Cells, however, cannot see—they must proceed by groping in the dark, searching for their own DNA—and a series of sophisticated spatial mechanisms enables them to align and segregate their genetic material. Spatial organization is only part of the challenge: cell division is also a race against time—spending too little or too much time in mitosis can be equally detrimental to cell survival. Dividing cells must not only coordinate the movement of often dozens of chromosomes but must do so with precise timing. Yet, chromosome segregation occurs with remarkable accuracy. In this review, we highlight the role of mitotic chromosomes as a platform to integrate spatial and temporal cues to ensure their successful segregation.

Flow cytometry is a versatile analytical technology for measuring physical and molecular characteristics of individual cells or particles in suspension. The technology has had its greatest impact in immunology, enabling the identification and quantification of rare cell populations within complex mixtures, but applications span diverse biological systems including hematopoietic cells, microorganisms, cultured cells, plant cells, gametes, and disaggregated tissues. Target molecules are typically identified using fluorophore-conjugated antibodies, though alternative labeling strategies exist. A key advantage of flow cytometry is the ability to physically isolate cells of interest for downstream applications such as culture, genomic analysis, or functional studies. The field has undergone substantial evolution from conventional filter-based polychromatic systems to spectral cytometry platforms that capture full emission spectra, enabling higher-parameter analyses and more flexible panel design. This review examines current capabilities and limitations of flow cytometry technology, with emphasis on recent advances in spectral detection, quantitative standardization, and computational analysis. We discuss remaining technical challenges and explore emerging opportunities for innovation in excitation systems, detector technology, and integration with artificial intelligence-based analysis platforms. Addressing these challenges will be essential for cytometry to continue driving biological discovery and clinical applications in the coming decades.

How cells repair oxidative damage to DNA has been studied for over 60 years. Recent evidence confirms that the base excision repair (BER) machinery not only acts to restore an intact double DNA helix by replacing oxidized bases, but under some circumstances, BER goes awry, generating double-strand breaks and provoking chromosome fragmentation. This fragmentation can lead to extensive genomic rearrangements that correlate with oncogenesis. Whether the BER factors suppress or promote DNA damage depends on multiple parameters: the nature of the damage, the clustering of modified bases, the pathway of BER chosen, and chromatin remodelers. Recent data leading to this unexpected role for BER are reviewed here.

Human immunodeficiency virus type 1 (HIV-1) possesses an envelope enriched with a specific set of host plasma membrane (PM) lipids, a composition that is critical for viral infectivity. Virus budding is initiated by the binding of the viral Gag protein to phosphatidylinositol-4,5-bisphosphate (PI(4,5)P₂) located in the inner leaflet of the PM. However, the mechanism by which inner leaflet-associated Gag protein contributes to the enrichment of specific outer leaflet lipids, such as sphingomyelin (SM) and cholesterol (Chol), remains poorly understood. Visualization of endogenous lipids using specific lipid probes and advanced microscopy has revealed that Gag multimerization reorganizes SM- and Chol-rich lipid domains in a curvature-dependent manner. To further elucidate the molecular mechanisms underlying Gag-induced selective lipid enrichment across the bilayer, two potential scenarios are discussed: one involving interdigitation and the other involving Chol enrichment through flip-flop. These models are considered in the context of existing literature describing the distribution and interactions of SM, PI(4,5)P₂, and Chol within the PM.

Cutaneous wound repair is tightly regulated by numerous signaling pathways that coordinate a multiphased response. The repair process includes a proliferative phase that forms granulation tissue at the wound base and re-epithelialization of the wound surface. Two of the signaling pathways that regulate the proliferative phase are Wnt/β-catenin and Notch, stimulating the proliferation of keratinocytes and fibroblasts, respectively. While ephrin–Eph signaling pathways also induce keratinocyte proliferation, their contribution to cutaneous wound repair is less defined. In distal limb wounds on horses, the proliferative phase is often characterized by the formation of excessive granulation tissue that delays healing by impeding keratinocyte migration from the wound margin. Comparison of normal and aberrant healing makes distal limb horse wounds well-suited for defining molecular mechanisms that regulate repair during the proliferative phase and identifying targets that promote healthy wound healing. We hypothesize that ephrin–Eph signaling pathways that stimulate keratinocyte proliferation provide an unexplored but effective target for accelerating re-epithelialization in distal limb wounds of the horse. As re-epithelialization is a key to physiologic healing in many mammals, we further hypothesize that ephrin–Eph signaling pathways offer targets for enhanced wound repair in humans.

Most vertebrate genes are split up into exons and introns, with exons being spliced together to make mRNA. Many of the proteins involved in splicing, called splicing factors, exert concentration-dependent effects on gene expression through post-transcriptional modification of mRNAs. These include the serine/arginine-enriched (SR) proteins that have essential roles in normal development and physiology. All SR proteins (and many other splicing factors) regulate their own expression levels, often using negative feedback pathways involving alternative splicing of “poison exons” (PEs), which lead to mRNA degradation. The PEs within SR protein genes are encoded by ultra-conserved genome sequences, suggesting they have been under extreme selective pressure despite not encoding protein sequences. Here, we discuss the hypothesis that PEs enable rapid switches in SR protein concentrations, yet prevent these splicing regulators from increasing to toxic levels that cause cell death or interfere with cell function. This hypothesis is based on analysis of an ultra-conserved PE in the TRA2B gene during male meiosis. Distinct roles for this TRA2B PE in different tissues further predict cell type-specific effects on development and physiology that will need to be experimentally detected using animal models.