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Kif11-haploinsufficient oocytes reveal spatially differential requirements for chromosome biorientation in the spindle

ABSTRACT: Kif11-haploinsufficient oocytes reveal spatially differential requirements for chromosome biorientation in the spindle

PROVIDER: PRJNA1198919 | ENA |

REPOSITORIES: ENA

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Kif11-haploinsufficient oocytes reveal spatially differential requirements for chromosome biorientation in the spindle

Project description:Bipolar spindle assembly and chromosome biorientation are prerequisites for chromosome segregation during cell division. The kinesin motor KIF11 (also widely known as Eg5) drives spindle bipolarization by sliding antiparallel microtubules bidirectionally, elongating a spherical spindle into a bipolar-shaped structure in acentrosomal oocytes. During meiosis I, this process stretches homologous chromosome pairs, establishing chromosome biorientation at the spindle equator. The quantitative requirement for KIF11 in acentrosomal spindle bipolarization and homologous chromosome biorientation remains unclear. Here, using a genetic strategy to modulate KIF11 expression levels, we show that Kif11 haploinsufficiency impairs spindle elongation, leading to the formation of a partially bipolarized spindle during meiosis I in mouse oocytes. While the partially bipolarized spindle allows chromosome stretching in the inner region of its equator, it fails to do so in the outer region, where merotelic kinetochore-microtubule attachments are favored to form. These findings demonstrate the necessity of biallelic functional Kif11 for bipolar spindle assembly in acentrosomal oocytes and reveal a spatially differential requirement for homologous chromosome biorientation within the spindle.

2025-07-01 | GSE284383 | GEO

Kif11-haploinsufficient oocytes reveal spatially differential requirements for chromosome biorientation.

Project description: Not available

| S-EPMC12457643 | biostudies-literature

Kif11-haploinsufficient oocytes reveal spatially differential requirements for chromosome biorientation

Project description: Not available

| S-SCDT-10_1038-S44319-025-00539-W | biostudies-other

KIF11 and its inhibitor SB-743921 inhibit acute myeloid leukaemia (AML) by blocking the cell cycle

Project description:Acute myeloid leukaemia (AML) is a highly heterogeneous haematological malignancy with limited prognostic improvement despite evolving therapeutic strategies.KIF11 is a member of the kinesin family and a microtubule-associated motility protein that plays a key role in spindle dynamics during cellular mitosis and is overexpressed in leukaemias including AML. Studies have shown that inhibition of KIF11 leads to spindle pole collapse, which prevents chromosome segregation and leads to cell death; this identifies KIF11 as a potential therapeutic target.SB-743921, a novel selective inhibitor of KIF11, has shown anti-tumour activity in a variety of cancers, including breast, lung, and cholangiocarcinoma. Our study shows that SB-743921 can effectively inhibit the proliferation of AML cells and induce cell cycle arrest, thereby hindering tumour growth. In vitro experiments showed that SB-743921 exhibited significant cytotoxicity against several AML cell lines, and its IC50 value indicated that these cells were very sensitive to SB-743921. Further in vivo studies in AML mouse models treated with SB-743921 showed that the drug significantly delayed tumour progression while prolonging survival with minimal toxic side effects. In addition, RNA sequencing analysis showed that SB-743921 inhibited tumour cell proliferation by down-regulating key signalling pathways, including MYC, E2F and G2M. These findings suggest that KIF11 plays a crucial role in the onset and progression of AML. As its inhibitor, SB-743921 has significant anti-tumour effects and is an innovative targeted agent for the treatment of AML. This discovery provides new insights into potential clinical applications for the treatment of this challenging malignancy.

2025-08-19 | GSE291010 | GEO

Kif11-haploinsufficient oocytes reveal spatially differential requirements for chromosome biorientation in the spindle

Project description: Not available

| S-BIAD1946 | bioimages

19S proteasome loss regulates mitotic spindle assembly through a ubiquitin-independent degradation mechanism

Project description:During regulated protein degradation, the 26S proteasome recognizes ubiquitinated substrates through its 19S particle and then degrades them in its 20S enzymatic core. Despite this close interdependency between proteasome subunits, we demonstrate that knockouts from different proteasome subcomplexes result in distinct cellular phenotypes. In particular, depletion of 19S PSMD lid proteins, but not that of other proteasome subunits, prevents bipolar spindle assembly during mitosis. Despite decreased ubiquitin-mediated protein degradation in PSMD knockouts, we find that the monopolar spindle phenotype is instead caused by the aberrant degradation of the kinesin motor protein KIF11. We show that KIF11 degradation occurs through the 20S proteasome in a ubiquitin-independent manner upon loss of 19S proteins and that the resulting alterations in spindle forces lead to the unique monopolar phenotype. Thus, the presence of the 19S particle ensures proper spindle formation by restraining ubiquitin-independent degradation.

2025-06-24 | PXD065357 | Pride

Association of maternal mRNA with the spindle in mouse oocytes

Project description:The oocytes of many species, both invertebrate and vertebrate, contain a large collection of localized determinants in the form of proteins and translationally inactive maternal mRNAs. However, it is unknown whether mouse oocytes contain localized MmRNA determinants and what mechanisms might be responsible for their control. We collected intact MII oocytes, enucleated MII oocyte cytoplasts (with the spindle removed), and spindle-chromosome complexes which had been microsurgically removed. RNA was extracted, amplified, labeled, and applied to microarrays to determine if any MmRNA determinants were localized to the SCC. We used microarrays to determine whether maternal mRNAs in mouse oocytes are enriched in the meiotic spindle

2013-11-06 | E-GEOD-46875 | biostudies-arrayexpress

Natural product target identification of wheldone as a KIF11 inhibitor in ovarian cancer using the DiffPOP (Differential Protein Precipitation) method

Project description:Wheldone, a fungal metabolite, was identified as a cytotoxic compound in high-grade serous ovarian cancer (HGSOC). Wheldone triggered caspase 3/7–dependent apoptosis and reduced migration, invasion, and spheroid growth. Wheldone was also capable of triggering apoptosis in chemoresistant HGSOC models. Wheldone caused significant downregulation of HNRNPD expression, a DNA repair protein, and increased DNA damage that could be blocked by N-acetyl-L-cysteine. In vivo, wheldone displayed minimal toxicity but was rapidly cleared from circulation, despite in vitro metabolic stability. Wheldone treatment in vivo did not demonstrate significant reduction in tumor burden. Therefore, in order to overcome these liabilities, it was necessary to find the protein target of wheldone so that modifications can be made to improve the drug-like characteristics of the compound. Using the drug-target interaction proteomics method, DiffPOP (differential precipitation of proteins), wheldone was found to act as an inhibitor of KIF11, a motor protein essential for mitotic spindle formation. An ATPase biochemical cell-free assay confirmed direct binding and functional inhibition of KIF11. Wheldone resulted in G2/M arrest and downstream regulation of mitotic proteins such as TPX2, AURKA, and phospho-histone H3. Proteomics analysis after treatment of wheldone in four different HGSOC cancer cell lines all supported changes consistent with mitotic spindle assembly disruption. Further, KIF11 was one of only 13 proteins upregulated in all four cell lines treated. Overall, wheldone represents a promising lead compound for targeting KIF11 in chemoresistant ovarian cancer, with future studies needed to improve its pharmacokinetics and delivery.

2026-05-25 | PXD070302 | Pride

The targeted genes of KIF11 of PLC8024 cell after drug treatment

Project description:We found that KIF11 played an inportant role in PLC8024 apoptosis after drug treatment

2025-12-04 | GSE294035 | GEO

KIF11 immunoprecipitates from control and RAB11 knockdown CACO2 cells

Project description:We want to determine the protein networks that are associated with KIF11 in the presenceor absence of Rab11 in Caco2 cells. We performed immunoprecipitation against KIF11 using an anti-KIF11 antibody in control and Rab11 knockdown Caco2 cells In addition, we included samples of no antibody control to assess background binding.

2023-06-05 | PXD042335 | Pride

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