Trends in Cell Biology最新文献

Cellular communication through the dissemination of signal molecules is vital for tissue organisation and homeostasis. The mechanisms of signal spreading can include binding-protein-assisted transport, long membrane protrusions known as cytonemes, and exovesicles. Recent research indicates that cytonemes and exovesicles can not only transport ligands but also facilitate the regulated distribution of receptors, thereby enabling signal transduction in cells lacking endogenous receptors. This mechanism allows non-responsive cells to temporarily acquire the ability to respond to specific ligands. This review explores our understanding of ligand and receptor dispersal, offering fresh insights into the fundamental concept of cellular competence. Notably, these findings may have significant implications for diseases and their associated therapeutic targets, highlighting the urgency and importance of this research area.

Ferroptosis is an iron-dependent cell death pathway that, until recently, has been considered to be dependent on autophagy. However, recent studies have reported conflicting results, raising the question about which cell contexts determine the roles of autophagy in ferroptosis. This opinion article addresses this question by summarizing the contexts and/or diseases in which autophagy is a driver or suppressor of ferroptosis. The execution of ferroptosis depends on levels of (labile) iron, unsaturated (phospho)lipids and free radicals. We propose that the cell context in which these three factors and/or their upstream pathways are differentially regulated dictates whether autophagy positively or negatively regulates ferroptosis.

This article reviews public science communication (SC) in Latin America, highlighting advances and challenges. It emphasizes the need to foster inclusive policies, interdisciplinary approaches, and effective evaluation to enhance public engagement, address social inequalities, and foster informed decision-making. Improving this field would strengthen science-society relationships, benefiting both professional communicators and scientific communities.

Glycosylphosphatidylinositol (GPI)-anchored proteins (APs) regulate numerous biological processes through interaction with signaling effectors at the cell surface. As a unique feature, GPI-APs can be released from their anchors by multi-pass GPI-specific phospholipases (types A2, C, and D) to impact signaling networks, phenotype, and cell fate; however, many questions remain outstanding. Here, we discuss and expand our current understanding of the distinct GPI-specific phospholipases, their substrates, effector pathways, and emerging physiological roles, with a focus on the six-transmembrane ecto-phospholipases GDE2 (GDPD5) and GDE3 (GDPD2). We provide structural insight into their AlphaFold-predicted inner workings, revealing how transmembrane (TM) domain plasticity may enable GPI-anchor binding and hydrolysis. Understanding lipolytic cleavage of GPI-APs adds a new dimension to their signaling capabilities and biological functions.

Endothelial cells (ENCs) and epithelial cells (EPCs) form monolayers whose barrier function is critical for the maintenance of physiological processes and extremely sensitive to mechanical cues. Computational models have emerged as powerful tools to elucidate how mechanical cues impact the behavior of these monolayers in health and disease. Herein, the importance of mechanics in regulating ENC and EPC monolayer behavior is established, highlighting similarities and differences in various biological contexts. Concurrently, computational approaches and their importance in accelerating mechanobiology studies are discussed, emphasizing their limitations and suggesting future directions. The aim is to inspire further synergies between cell biologists and modelers, which are crucial for accelerating cell mechanobiology research.

The efficacy and safety of chimeric antigen receptor (CAR) T cell therapy is still inconclusive in solid tumor treatment. Recently, nanotechnology has emerged as a potent strategy to reshape CAR-T cell therapy with promising outcomes. This review aims to discuss the significant potential of nano-engineered CAR-T cell therapy in addressing existing challenges, including CAR-T cell engineering evolution, tumor microenvironment (TME) modulation, and precise CAR-T cell therapy (precise targeting, monitoring, and activation), under the main consideration of clinical translation. It also focuses on the growing trend of technological convergence within this domain, such as mRNA therapeutics, organoids, neoantigen, and artificial intelligence. Moreover, safety management of nanomedicine is seriously emphasized to facilitate clinical translation.

RNA localization and local translation are widespread phenomena that play key roles in a plethora of cellular processes ranging from embryo patterning to general cellular functions. The traditional paradigm assigns localization elements to cis-acting RNA sequences which assemble into complexes that regulate mRNA transport and translation, and the mRNA is generally transported while remaining translationally silent. However, recent evidence has shown that the nascent protein can also play an essential role in RNA localization and can enable polysomes to control their own transport and be delivered where and when they are needed. Two such examples are reviewed: translation factories and centrosomal mRNAs. Their comparison highlights the key role of cotranslational interactions in the spatiotemporal control of protein synthesis and protein fate.

Aging is characterized by progressive structural and functional decline, driven partially by epigenetic alterations. While changes in DNA methylation, histone modifications, and chromatin accessibility are well studied, the role of three-dimensional chromatin organization in aging remains underexplored. Advances in chromosome conformation capture technologies have revealed hierarchical chromatin structures, including compartments, topologically associating domains (TADs), and chromatin loops, which are crucial for gene regulation. Emerging evidence suggests that aging changes these structures, leading to altered gene expression and cellular dysfunction. This review summarizes recent findings on age-associated chromatin reorganization, highlighting its impact on transcription and nuclear architecture. It also compares the roles of 3D chromatin organization in aging and senescence, highlighting shared and distinct features in these biological contexts.

Cells are constantly exposed to various stresses, including nutrient deprivation and genotoxic stress, which dynamically interact with cellular sensing pathways to influence metabolism, gene expression, and homeostasis. The integration of nutrient-sensing mechanisms and DNA damage response pathways is critical in cancer progression. While individual processes are well-characterized, their cross-regulatory mechanisms are just beginning to emerge. Deciphering the interplay between nutrient stress and DNA damage is crucial for elucidating the mechanisms underlying cellular responses to stress and developing therapeutic strategies for various diseases, including cancer. This review highlights the relationship between nutrient stress and DNA damage, especially its underlying sensing pathway and cell fate determination.

Polo-like kinase 1 (PLK1) phosphorylates a plethora of different substrates to regulate key cell cycle processes that include, among others, mitotic entry, chromosome condensation, nuclear envelope breakdown, centrosome maturation, spindle assembly and chromosome biorientation, cytokinesis, and the deposition of the specialized centromere histone CENP-A. Addressing the exact spatial and temporal control of PLK1 activity in these processes and its dynamic interplay with protein phosphatases that counteract mitotic phosphorylation, most notably PP1 and PP2A, has proven especially puzzling. In this review, we focus on the main unknowns in the area of human PLK1 regulation, exploring more specifically an emerging concept that master docking sites, including newly discovered noncanonical motifs, trigger initial local activation of PLK1 that promotes subsequent localized spreading of phosphorylation.