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The editorial in the journal "Biomedicines" discusses the recent advances in cellular senescence, highlighting its role in health, disease, and aging. The text explores various aspects of senescence, such as the impact of long non-coding RNAs, ion channels, metabolic states, extracellular vesicles, and mitochondrial reactive oxygen species. It also delves into the therapeutic potential of targeting senescence and the interplay between cellular senescence and circadian regulation. The editorial emphasizes the need for interdisciplinary collaboration and innovative technologies to further understand the complexities of senescence. [Extracted from the article]

Whole-chromosome aneuploidy is a major feature of cancer genomes, yet its role in tumour development remains controversial (1,2). This contrasts with chromosome breaks and rearrangements, which are known to produce [...], The involvement of whole-chromosome aneuploidy in tumorigenesis is the subject of debate, in large part because of the lack of insight into underlying mechanisms. Here we identify a mechanism by which errors in mitotic chromosome segregation generate DNA breaks via the formation of structures called micronuclei. Whole-chromosome-containing micronuclei form when mitotic errors produce lagging chromosomes. We tracked the fate of newly generated micronuclei and found that they undergo defective and asynchronous DNA replication, resulting in DNA damage and often extensive fragmentation of the chromosome in the micronucleus. Micronuclei can persist in cells over several generations but the chromosome in the micronucleus can also be distributed to daughter nuclei. Thus, chromosome segregation errors potentially lead to mutations and chromosome rearrangements that can integrate into the genome. Pulverization of chromosomes in micronuclei may also be one explanation for 'chromothripsis' in cancer and developmental disorders, where isolated chromosomes or chromosome arms undergo massive local DNA breakage and rearrangement.

The amino acid sequence of the CAMP cohemolysin, Cam, from Riemerella anatipestifer exhibits high homology to those of O-sialoglycoprotein endopeptidases, suggesting that the cohemolysin is a sialoglycoprotease. The cohemolysin gene, cam, is confined to a 1026-basepair open reading frame and encodes a 37 kilodalton molecular size protein.

Abstract Accurate transmission of chromosomes from parent to progeny cell requires assembly of a bipolar spindle. Centrosomes (spindle pole body in yeast) are critical for the biogenesis of this complex mitotic apparatus since they confer bipolarity on the spindle and serve as the site of microtubule polymerization. In each division cycle, the centrosome is duplicated and the sister-centrosomes move away from each other, forming the two poles of the spindle. While the structure and the duplication of centrosomes have been investigated extensively, the understanding of the control of their segregation remains scant. Recent findings are beginning to yield insights into the regulation of centrosome segregation in yeast and its link to the mitotic kinase.

Antimicrotubule agents are commonly utilised as front-line therapies against several malignancies, either by themselves or as combination therapies. Cell-based studies have pinpointed the anti-proliferative basis of action to be a consequence of perturbation of microtubule dynamics leading to sustained activation of the spindle assembly checkpoint, prolonged mitotic arrest and mitotic cell death. However, depending on the biological context and cell type, cells may take an alternative route besides mitotic cell death via a process known as mitotic slippage. Here, mitotically arrested cells 'slip' to the next interphase without undergoing proper chromosome segregation and cytokinesis. These post-slippage cells in turn have two main cell fates, either cell death or a G1 arrest ensuing in senescence. In this review, we take a look at the factors determining mitotic cell death vs mitotic slippage, post-slippage cell fates and accompanying features and their consequences for antimicrotubule drug treatment outcomes. [ABSTRACT FROM AUTHOR]