D. Kayo, S.K. Uehara, M.R. Royan, and S. Kanda, “Emerging Perspectives on Gonadotropin Regulation in Vertebrates Revealed by the Discovery of FSH-RH in Teleosts,” Bioessays 47 (2025): e70066. http://doi.org/10.1002/bies.70066.
D. Kayo, S.K. Uehara, M.R. Royan, and S. Kanda, “Emerging Perspectives on Gonadotropin Regulation in Vertebrates Revealed by the Discovery of FSH-RH in Teleosts,” Bioessays 47 (2025): e70066. http://doi.org/10.1002/bies.70066.
The separation of DNA-based processes from cytoplasmic protein synthesis demands precise and effective nuclear import of histones and chromatin regulators. Because histones are highly basic and aggregation-prone, their proper folding, sequestration, and deposition into chromatin depend on coordinated action of histone chaperones and nuclear import receptors. This review summarizes recent advances in understanding the mechanisms of core and linker histone import and chaperoning. Structural and biochemical studies have elucidated how Importin-4/Kap123 mediates nuclear import of H3-H4 heterodimers in concert with ASF1, revealing Importin-4's dual role as both transporter and histone chaperone. Likewise, Importin-9/Kap114 recognizes and imports H2A-H2B heterodimers through a mechanism unusually insensitive to RanGTP, which cooperates with Nap1 for histone release. Finally, new structural analyses of the Importin-β-Importin-7 heterodimer clarify its mode of linker histone H1 import. Together, these studies establish importins as multifunctional factors that couple histone stabilization, protection from aberrant interactions, nuclear import, and targeted delivery for nucleosome assembly. Outstanding questions include how secondary importins, histone modifications, and compartment-specific chaperone dynamics regulate histone trafficking, and whether importins themselves function in nucleosome assembly. Addressing these questions will define how nuclear import integrates with chromatin homeostasis.
Stem cell populations employ cell-intrinsic and niche-mediated mechanisms to preserve long-term self-renewal and regenerative potential. We propose that tumor-initiating cells (TICs) hijack this developmental circuitry to sustain their growth and establish an early immunosuppressive microenvironment during malignant progression. Recent work implicates CXCR4+ tissue-resident macrophages (TRMs) in the mammary gland as a central orchestrator of this process. Conserved CXCL12/CXCR4-AKT-β-catenin signaling links CXCR4+ TRM support of normal mammary stem cells to TIC maintenance, underscoring how developmental niches are exploited in malignancy. During tumorigenesis, aberrant CXCL12 production from tumor-associated fibroblasts promotes the expansion of CXCR4+ TRMs, while CXCR4 signaling enhances ALDH1A2-dependent retinoic acid production, which induces regulatory T cells and thereby suppresses anti-tumor immunity at the earliest stages of tumor development. From this perspective, early immune evasion is not only a hallmark of cancer but also a therapeutic window. Targeting TRMs early in cancer development could delay, or even prevent, malignant initiation. More broadly, we propose that TIC–niche crosstalk constitutes a tractable vulnerability, and that incorporating TRM-directed interventions alongside conventional and immune-based therapies may shift the balance toward durable tumor control.
We review recent multi-omics analyses of the coral heat stress response to explore the generality of the Oxidative Theory of Coral Bleaching (OTCB), which posits that algal symbiont release is the final act of defense by the coral host to survive alga-derived oxidative stress. The OTCB is particularly relevant given that ocean warming, which is accelerating under climate change, has proven devastating for corals, leading to the bleaching phenotype and widespread reef loss. Multi-omics results, in combination with other data, such as genome-wide association studies, support the idea that coral bleaching is a multifactorial response that reflects a wide array of causes and effects and is population-specific under most conditions, with coral ploidy and genotype being critical to bleaching sensitivity. This perspective leverages the location, algal and prokaryotic microbiome, and host genotype-specific aspects of coral resilience to promote a new “personal genomics” approach to coral conservation, analogous to that used in human health.
The cover image is based on the article Where, When, and How? Integrating Spatiotemporal Cues in Cell Division by Luca Cirillo et al., https://doi.org/10.1002/bies.70093.
The Hippo signaling pathway plays a key role in organ size control in normal development and tumorigenesis. While many components of this pathway are well understood, its upstream regulation remains unclear. Among the most enigmatic upstream regulators are the protocadherins Dachsous and Fat. These transmembrane proteins regulate a growth-promoting complex composed of the atypical myosin Dachs, the adaptor protein Dlish, and the palmitoyltransferase Approximated (together termed the core complex). We propose that by default the core complex promotes growth and that Dachsous and Fat, which previously have been thought to act antagonistically, can also function synergistically to repress core complex function and therefore restrict growth. Understanding the molecular mechanisms underlying Dachsous-Fat signaling offers insight into how multicellular organisms precisely control organ size.
Life on Earth has evolved as a series of evolutionary transitions, during which lower-level units merged to form a new and more complex higher-level entity. Besides few canonical examples, many life forms exist for which it remains unclear whether or not they are about to complete the transition. This paucity of mechanistic understanding is likely due to an overemphasis on few model systems and a lack of criteria to compare disparate biological units. Here, we aim at filling this gap by proposing a new framework to classify different forms of biological organization, which considers two fundamental aspects: (i) the physiological component and (ii) the evolutionary component. Categorizing different biological units according to whether and how these aspects are represented yields six types of structural organization. Our framework allows to compare different organizational forms, and, in this way, provide insight into the evolutionary processes giving rise to these arrangements.
In eukaryotic cells, genomic DNA is packaged into chromatin, restricting the access of regulatory proteins and thus regulating key processes such as transcription, replication, recombination, and the repair of DNA. Barrier-to-autointegration factor (BAF) plays key roles in organizing chromatin architecture and nuclear functions. BAF bridges DNA segments and connects them to Lamin A/C and inner nuclear membrane proteins containing the LEM domain, ensuring proper chromatin organization and nuclear envelope assembly and repair. Over the last three decades, multiple structural studies have revealed that BAF dimerizes to bind DNA and shapes higher-order chromatin structure. In this review, we summarize the structural features of BAF in complexes with its binding partners and explore how these interactions contribute to maintaining nuclear integrity and regulating genome function.
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