BioEssays最新文献

Because of their interest in medicine, most studies on anesthesia have historically focused on the nervous systems of animals. This has often led to the neglect of the fact that all life forms have the potential to be anesthetized. Anesthetics target proteins, such as four-domain voltage-dependent Na⁺/Ca²⁺ channels (4D-NaV/CaV) and glutamate receptor channels (iGluR/GLR), which have homologs in a wide variety of species. These proteins originate from ancestral channels that predate eukaryotes in the evolutionary process. These channels are evidently so essential for living cells that they are under strong selective pressure. Consequently, the susceptibility of most living organisms to anesthesia has been interpreted as a result of natural selection. Here, we propose an alternative hypothesis that this susceptibility is attributable to an intrinsic weakness in living cells.

Ribosome recycling is a fundamental biological process crucial for cellular health. Defective recycling disrupts ribosome biogenesis and organelle function, particularly in mitochondria, contributing to ribosomopathies, neurodegenerative diseases, and cancer. While not directly linked to human diseases via known genetic mutations, emerging evidence suggests a critical interplay between ribosome recycling and organelle quality control. Impaired ribosome recycling leads to aberrant ribosome production, compromised translational quality control, protein misfolding, and subsequent organelle dysfunction and cellular stress. These cascading defects underscore the critical need for effective ribosome reutilization, especially under stress, as disruptions can cause translational arrest and heightened stress signaling, perturbing cellular homeostasis. Our analyses establish an indirect but significant link between ribosome recycling and human disease, offering new perspectives on how translational fidelity and organelle maintenance converge to support cellular well-being.

Persistent genomic instability compromises cellular viability while also triggers non-cell-autonomous responses that drive dysfunction across tissues, contributing to aging. Recent evidence suggests that DNA damage activates secretory programs, including the release of inflammatory cytokines, damage-associated molecular patterns, and extracellular vesicles, that reshape immune homeostasis, stem cell function, and metabolic balance. Although these responses may initially support tissue integrity and organismal survival, their chronic activation has been associated with tissue degenerative changes and systemic decline. Here, we discuss how nuclear DNA damage responses trigger the activation of cytoplasmic sensing pathways, promote secretory phenotypes, and affect organismal physiology. Targeting DNA damage-driven mechanisms may help buffer harmful systemic responses while preserving regeneration and immune surveillance, offering new ways to delay aging-related decline.

We propose that top-down coercive mechanisms have played a role in the origin and maintenance of the Major Transitions in Evolution (MTE). Top-down coercion has potentially been underappreciated due to the lack of a conceptual framework. Therefore, we provide a formalized top-down coercion framework for the MTE. Our conceptualization of top-down biological coercion is a loss of potential due to a constraint from the top-down. We also present three case studies of coercive top-down mechanisms in the evolution of eukaryotic cells, multicellularity and eusocial insect colonies. The MTE project studies the origin and maintenance of new levels of individuality in the biological hierarchy. Previously, the MTE has been conceived as a bottom-up process. Our coercion framework provides new empirical questions regarding the origin of transitions and helps reframe discussions of fitness in the MTE.

Once considered biochemical oddities, dinucleoside polyphosphates such as diadenosine tetraphosphate (Ap4A) are now recognized as conserved signaling molecules involved in essential cellular processes, including stress response, RNA stability, and proteostasis. To capture recent advances and reignite collaborative efforts in this re-emerging field, the one-day symposium “Dinucleoside Polyphosphates in Cellular Signalling: Function and Evolution Across Life” was held in Marburg on May 27, 2025. The meeting brought together researchers across disciplines and domains of life to share insights into Ap4A's diverse roles—from bacterial virulence and plant signaling to human disease—and showcased powerful new tools for studying its function, laying the groundwork for future discovery and innovation.

Plant stem cell homeostasis is a tightly controlled process governed by a complex network of transcription factors, hormones, signaling molecules, and various environmental factors. Among these, nitric oxide (NO) and redox signaling have emerged as critical regulators. This review examines the multifaceted role of NO in maintaining plant stem cell homeostasis, focusing on its influence through redox dynamics, DNA methylation, and hormonal regulation. We also explore the intricate cross-talk between NO signaling and other key pathways, including environmental stimuli and the target of rapamycin (TOR) pathway, in balancing stem cell maintenance and differentiation within both shoot and root meristems. Additionally, we discuss NO's involvement in post-translational modifications and transcriptional regulation, offering insights into its broader role in plant growth and development.

In this article, onset mechanisms of colorectal cancer and intestinal bowel diseases (IBD) are postulated to involve the aberrant expression/hyper-activation of E-type prostanoid 4 (EP4) receptors. Although prostaglandin E₂ and EP4 receptors are important factors for maintaining colorectal homeostasis, their mediated signaling is also considered to be involved in the etiology of severe intestinal diseases. To prevent uncontrollable activations of EP4 receptors, two safety factors are proposed: butyrate as an external safety factor and interleukin (IL)-4 as an internal safety factor. Thus, for maintaining vulnerable colorectal homeostasis, the levels of EP4 receptors, butyrate, and IL-4 are proposed as an important triad for protecting against development/onset risks of, at least, EP4 receptor-mediated cancer and IBD.

Recently, a fascinating, well-executed, molecular study regarding the direct influence of mitochondrial reactive oxygen species (ROS) formation by the electron transport chain (ETC) on mitochondrial morphology in baker's yeast appeared in PNAS. The findings highlight some very interesting connections between the choice of metabolic substrates, points of entry into the ETC, ROS formation, efficiency of ATP generation, and mitochondrial structures. These reflect both ancient eukaryotic constraints and later specific adaptations of Saccharomyces cerevisiae. However, by not addressing these adaptations, the important wider implications of the article's findings run the risk of being overlooked. There are illuminating connections to the FADH₂/NADH ratio concept and new studies replacing ETC components with yeast counterparts in diverse metazoan cells, which will also be discussed.