bims-micesi Biomed News
on Mitotic cell signalling
Issue of 2022‒03‒13
eleven papers selected by
Valentina Piano
Max Planck Institute of Molecular Physiology


  1. Bioessays. 2022 Mar 08. e2100246
      Correct chromosome segregation in mitosis relies on chromosome biorientation, in which sister kinetochores attach to microtubules from opposite spindle poles prior to segregation. To establish biorientation, aberrant kinetochore-microtubule interactions must be resolved through the error correction process. During error correction, kinetochore-microtubule interactions are exchanged (swapped) if aberrant, but the exchange must stop when biorientation is established. In this article, we discuss recent findings in budding yeast, which have revealed fundamental molecular mechanisms promoting this "swap and stop" process for error correction. Where relevant, we also compare the findings in budding yeast with mechanisms in higher eukaryotes. Evidence suggests that Aurora B kinase differentially regulates kinetochore attachments to the microtubule end and its lateral side and switches relative strength of the two kinetochore-microtubule attachment modes, which drives the exchange of kinetochore-microtubule interactions to resolve aberrant interactions. However, Aurora B kinase, recruited to centromeres and inner kinetochores, cannot reach its targets at kinetochore-microtubule interface when tension causes kinetochore stretching, which stops the kinetochore-microtubule exchange once biorientation is established.
    Keywords:  Dam1 complex; INCENP; Ndc80 complex; aurora B kinase; chromosome biorientation; chromosome segregation; error correction; kinetochore-microtubule interactions
    DOI:  https://doi.org/10.1002/bies.202100246
  2. Mol Biol Cell. 2022 Mar 11. mbcE20090600
      During cell cycle progression in metazoans, the kinetochore is assembled at mitotic onset and disassembled during mitotic exit. Once assembled, the kinetochore complex attached to centromeres interacts directly with the spindle microtubules, the vehicle of chromosome segregation. This reassembly program is assumed to be absent in budding and fission yeast, because most kinetochore proteins are stably maintained at the centromeres throughout the entire cell cycle. Here, we show that the reassembly program of the outer kinetochore at mitotic onset is unexpectedly conserved in the fission yeast Schizosaccharomyces pombe. We identified this behaviour by removing the Rabl chromosome configuration, in which centromeres are permanently associated with the nuclear envelope beneath the spindle pole body during interphase. In addition to having evolutionary implications for kinetochore reassembly, our results aid the understanding of the molecular processes responsible for kinetochore disassembly and assembly during mitotic entry.
    DOI:  https://doi.org/10.1091/mbc.E20-09-0600
  3. BMC Res Notes. 2022 Mar 07. 15(1): 96
      OBJECTIVE: Miscarriages affect 10% of women aged 25-29, and 53% of women over 45. The primary cause of miscarriage is aneuploidy that originated in eggs. The Aurora kinase family has three members that regulate chromosome segregation. Therefore, distinguishing the roles of these isoforms is important to understand aneuploidy etiology. In meiosis, Aurora kinase A (AURKA) localizes to spindle poles, where it binds TPX2. Aurora kinase C (AURKC) localizes on chromosomes, where it replaces AURKB as the primary AURK in the chromosomal passenger complex (CPC) via INCENP binding. Although AURKA compensates for CPC function in oocytes lacking AURKB/C, it is unknown whether AURKA binds INCENP in wild type mouse oocytes. ZINC08918027 (ZC) is an inhibitor that prevents the interaction between AURKB and INCENP in mitotic cells. We hypothesized that ZC would block CPC function of any AURK isoform.RESULTS: ZC treatment caused defects in meiotic progression and spindle building. By Western blotting and immunofluorescence, we observed that activated AURKA and AURKC levels in ZC-treated oocytes decreased compared to controls. These results suggest there is a population of AURKA-CPC in mouse oocytes. These data together suggest that INCENP-dependent AURKA and AURKC activities are needed for spindle bipolarity and meiotic progression.
    Keywords:  Aurora kinase; Chromosomal passenger complex; Meiosis; Oocyte
    DOI:  https://doi.org/10.1186/s13104-022-05987-4
  4. Cells. 2022 Mar 03. pii: 875. [Epub ahead of print]11(5):
      The recent discovery demonstrating that the leakage of cathepsin B from mitotic lysosomes assists mitotic chromosome segregation indicates that lysosomal membrane integrity can be spatiotemporally regulated. Unlike many other organelles, structural and functional alterations of lysosomes during mitosis remain, however, largely uncharted. Here, we demonstrate substantial differences in lysosomal proteome, lipidome, size, and pH between lysosomes that were isolated from human U2OS osteosarcoma cells either in mitosis or in interphase. The combination of pharmacological synchronization and mitotic shake-off yielded ~68% of cells in mitosis allowing us to investigate mitosis-specific lysosomal changes by comparing cell populations that were highly enriched in mitotic cells to those mainly in the G1 or G2 phases of the cell cycle. Mitotic cells had significantly reduced levels of lysosomal-associated membrane protein (LAMP) 1 and the active forms of lysosomal cathepsin B protease. Similar trends were observed in levels of acid sphingomyelinase and most other lysosomal proteins that were studied. The altered protein content was accompanied by increases in the size and pH of LAMP2-positive vesicles. Moreover, mass spectrometry-based shotgun lipidomics of purified lysosomes revealed elevated levels of sphingolipids, especially sphingomyelin and hexocylceramide, and lysoglyserophospholipids in mitotic lysosomes. Interestingly, LAMPs and acid sphingomyelinase have been reported to stabilize lysosomal membranes, whereas sphingomyelin and lysoglyserophospholipids have an opposite effect. Thus, the observed lysosomal changes during the cell cycle may partially explain the reduced lysosomal membrane integrity in mitotic cells.
    Keywords:  cell cycle; lipidome; lysosomal leakage; lysosome; mitosis
    DOI:  https://doi.org/10.3390/cells11050875
  5. Int J Mol Sci. 2022 Feb 22. pii: 2422. [Epub ahead of print]23(5):
      Young sex chromosomes possess unique and ongoing dynamics that allow us to understand processes that have an impact on their evolution and divergence. The genus Silene includes species with evolutionarily young sex chromosomes, and two species of section Melandrium, namely Silene latifolia (24, XY) and Silene dioica (24, XY), are well-established models of sex chromosome evolution, Y chromosome degeneration, and sex determination. In both species, the X and Y chromosomes are strongly heteromorphic and differ in the genomic composition compared to the autosomes. It is generally accepted that for proper cell division, the longest chromosomal arm must not exceed half of the average length of the spindle axis at telophase. Yet, it is not clear what are the dynamics between males and females during mitosis and how the cell compensates for the presence of the large Y chromosome in one sex. Using hydroxyurea cell synchronization and 2D/3D microscopy, we determined the position of the sex chromosomes during the mitotic cell cycle and determined the upper limit for the expansion of sex chromosome non-recombining region. Using 3D specimen preparations, we found that the velocity of the large chromosomes is compensated by the distant positioning from the central interpolar axis, confirming previous mathematical modulations.
    Keywords:  Silene; central interpolar axis; chromosome velocity; sex chromosomes; sister chromatid division
    DOI:  https://doi.org/10.3390/ijms23052422
  6. Open Biol. 2022 Mar;12(3): 210389
      CENP-E is a large kinesin motor protein which plays pivotal roles in mitosis by facilitating chromosome capture and alignment, and promoting microtubule flux in the spindle. So far, it has not been possible to obtain active human CENP-E to study its molecular properties. Xenopus CENP-E motor has been characterized in vitro and is used as a model motor; however, its protein sequence differs significantly from human CENP-E. Here, we characterize human CENP-E motility in vitro. Full-length CENP-E exhibits an increase in run length and longer residency times on microtubules when compared to CENP-E motor truncations, indicating that the C-terminal microtubule-binding site enhances the processivity when the full-length motor is active. In contrast with constitutively active human CENP-E truncations, full-length human CENP-E has a reduced microtubule landing rate in vitro, suggesting that the non-motor coiled-coil regions self-regulate motor activity. Together, we demonstrate that human CENP-E is a processive motor, providing a useful tool to study the mechanistic basis for how human CENP-E drives chromosome congression and spindle organization during human cell division.
    Keywords:  CENP-E; kinetochore; microtubule; mitosis; motility; motor
    DOI:  https://doi.org/10.1098/rsob.210389
  7. Front Cell Dev Biol. 2022 ;10 838928
      Proper partitioning of replicated sister chromatids at each mitosis is crucial for maintaining cell homeostasis. Errors in this process lead to aneuploidy, a condition in which daughter cells harbor genome imbalances. Importantly, aneuploid cells often experience DNA damage, which in turn could drive genome instability. This might be the product of DNA damage accumulation in micronuclei and/or a consequence of aneuploidy-induced replication stress in S-phase. Although high levels of genome instability are associated with cell cycle arrest, they can also confer a proliferative advantage in some circumstances and fuel tumor growth. Here, we review the main consequences of chromosome segregation errors on genome stability, with a special focus on the bidirectional relationship between aneuploidy and DNA damage. Also, we discuss recent findings showing how increased genome instability can provide a proliferation improvement under specific conditions, including chemotherapeutic treatments.
    Keywords:  aneuploidy; cancer; chromosomal instability; genome instability; mitotic errors
    DOI:  https://doi.org/10.3389/fcell.2022.838928
  8. Cells. 2022 Feb 24. pii: 786. [Epub ahead of print]11(5):
      Centrosomes nucleate and anchor microtubules and therefore play major roles in spindle formation and chromosome segregation during mitosis. Duplication of the centrosome occurs, similar to DNA, only once during the cell cycle. Aberration of the centrosome number is common in human tumors. At the core of centriole duplication is the conserved polo-like kinase 4, Plk4, and two structural proteins, STIL and Sas-6. In this review, I summarize and discuss developments in our understanding of the first steps of centriole duplication and their regulation.
    Keywords:  Plk4; centriole disengagement; centriole duplication; centrosome
    DOI:  https://doi.org/10.3390/cells11050786
  9. Exp Cell Res. 2022 Mar 05. pii: S0014-4827(22)00088-X. [Epub ahead of print]414(1): 113095
      Kinesin-14 KIFC1 regulates spindle assembly and centrosome clustering in diverse organisms during cell division. KIFC1 proteins are essential for spindle assembly and chromosome alignment in mitosis. However, the roles and mechanisms of KIFC1 proteins in male spermatocytes remain largely unknown. In this study, we reveal that KIFC1 proteins mainly accumulate at the centrosomes and central spindle in mouse spermatocytes both in vitro and in vivo. We utilize two KIFC1 specific inhibitors, AZ82 and CW069, for the inhibition of KIFC1 in mouse spermatogenic cells and cultured GC-2 spd(ts) cells. We find that KIFC1 inhibition results in the increase of spermatocytes with micronuclei, the disorganization of the meiotic spindles, and the formation of multiple centrosomes. Furthermore, we demonstrate that KIFC1 inhibition leads to spindle defects, chromosome misalignment and the formation of aneuploidy in cultured GC-2 spd(ts) cells. In this study, we reveal that KIFC1 proteins are critical for centrosome maintenance and chromosome stability in mouse spermatocytes.
    Keywords:  Centrosome; Chromosome; KIFC1; Meiosis; Microtubule; Spermatocyte
    DOI:  https://doi.org/10.1016/j.yexcr.2022.113095
  10. Future Sci OA. 2022 Mar;8(3): FSO778
      Bringing to a halt the cell cycle in mitosis and interfering with its normal progression is one of the most successful anti-cancer strategies used nowadays. Classically, several kinds of anti-cancer drugs like taxanes and vinca alkaloids directly inhibit microtubules during cell division. These drugs exhibit serious side effects, most importantly, severe peripheral neuropathies. Alternatively, KSP inhibitors are grasping a lot of research attention as less toxic mitotic inhibitors. In this review, we track the medicinal chemistry developmental stages of KSP inhibitors. Moreover, we address the challenges that are faced during the development of KSP inhibitor therapy for cancer and future insights for the latest advances in research that are directed to find active KSP inhibitor drugs.
    Keywords:  Eg5; KIF11; KSP; filanesib; ispinesib; kinesin spindle protein; litronesib; monastrol
    DOI:  https://doi.org/10.2144/fsoa-2021-0116
  11. Dev Dyn. 2022 Mar 11.
      BACKGROUND: Cohesinopathies is a term that refers to/covers rare genetic diseases caused by mutations in the cohesin complex proteins. The cohesin complex is a multi-protein complex that facilitates different aspects of cell division, gene transcription, DNA damage repair and chromosome architecture. Shugoshin proteins prevent the cohesin complex from premature dissociation from chromatids during cell division. Patients with a homozygous missense mutation in SGO1, which encodes for Shugoshin1, have problems with normal pacing of the heart and gut.RESULTS: To study the role of shugoshin during embryo development, we mutated the zebrafish sgo1 gene. Homozygous sgo1 mutant embryos display various phenotypes related to different organs, including a reduced heart rate accompanied by reduced cardiac function. In addition, sgo1 mutants are vision-impaired as a consequence of structurally defective and partially non-functional photoreceptor cells. Furthermore, the sgo1 mutants display reduced food intake and early lethality.
    CONCLUSION: We have generated a zebrafish model of Sgo1 that showed its importance during organ development and function. This article is protected by copyright. All rights reserved.
    Keywords:  Sgo1; cohesinopathy; heart defect; retinal defect; shugoshin; zebrafish
    DOI:  https://doi.org/10.1002/dvdy.468