At the latest stages of their cell cycle, cells carry out crucial processes for the correct segregation of their genetic and cytoplasmic material. In this work, we provide evidence demonstrating that the cell cycle arrest of some MEN (mitosis exit network) mutants in the anaphase-telophase transition is bypassed. In addition, the ability of cdc15 diploid mutant strains to develop non-septated chains of cells, supported by nuclear division, is shown. This phenotype is also displayed by haploid cdc15 mutant strains when cell lysis is prevented by osmotic protection, and shared by other MEN mutants. By contrast, anaphase-telophase arrest is strictly observed in double MEN-FEAR (fourteen early anaphase release) mutants. In this context, the overexpression of a FEAR component, SPO12, in a MEN mutant background enhances the ability of MEN mutants to bypass cell cycle arrest. Taken together, these data suggest a critical role of Cdc15 and other MEN proteins in cytokinesis, allowing a new model for their cellular function to be proposed.
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Ann N Y Acad Sci
January 2025
Department of Biology, University of Kentucky, Lexington, Kentucky, USA.
Spiny mice (Acomys spp.) are warm-blooded (homeothermic) vertebrates whose ability to restore missing tissue through regenerative healing has coincided with the evolution of unique cellular and physiological adaptations across different tissue types. This review seeks to explore how these bizarre rodents deploy unique or altered injury response mechanisms to either enhance tissue repair or fully regenerate excised tissue compared to closely related, scar-forming mammals.
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First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China.
Sunitinib is a first-line targeted therapy for patients with renal cell carcinoma (RCC), but resistance represents a significant obstacle to the treatment of advanced and metastatic RCC. Metabolic reprogramming is a characteristic of RCC, and changes in metabolic processes might contribute to resistance to sunitinib. Here, we identified MTHFD2, a mitochondrial enzyme involved in one-carbon metabolism, as a critical mediator of sunitinib resistance in RCC.
View Article and Find Full Text PDFG3 (Bethesda)
January 2025
Department of Biology, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.
Evidence suggests that increases in ploidy have occurred frequently in the evolutionary history of organisms and can serve adaptive functions to specialized somatic cells in multicellular organisms. However, the sudden multiplication of all chromosome content may present physiological challenges to the cells in which it occurs. Experimental studies have associated increases in ploidy with reduced cell survival and proliferation.
View Article and Find Full Text PDFMol Biol Rep
January 2025
Department of Molecular Biology Vadi Kampüsü, Istanbul Atlas University, Anadolu Cd., No 40, Kağıthane, Istanbul, 34408, Turkey.
Background: Modulation of protein synthesis according to the physiological cues is maintained through tight control of Eukaryotic Elongation Factor 2 (eEF2), whose unique translocase activity is essential for cell viability. Phosphorylation of eEF2 at its Thr56 residue inactivates this function in translation. In our previous study we reported a novel mode of post-translational modification that promotes higher efficiency in T56 phosphorylation.
View Article and Find Full Text PDFMol Neurobiol
January 2025
Translational Oncology Laboratory, Department of Zoology, Hansraj College, Delhi University, New Delhi, 110007, India.
This review explores the current understanding and recent advancements in neuroblastoma, one of the most common extracranial solid pediatric cancers, accounting for ~ 15% of childhood cancer-related mortality. The hallmarks of NBL, including angiogenesis, metastasis, apoptosis resistance, cell cycle dysregulation, drug resistance, and responses to hypoxia and ROS, underscore its complex biology. The tumor microenvironment's significance in disease progression is acknowledged in this study, along with the pivotal role of cancer stem cells in sustaining tumor growth and heterogeneity.
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