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Inhibition of Cdk Activity02:34

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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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KIF11 Inhibition Induces Retinopathy Progression by Affecting Photoreceptor Cell Ciliogenesis and Cell Cycle

Yue Xu1,2, Jie Chen1,2, Xin-Yao Wang1,2

  • 1Department of Cell Biology and Genetics, The School of Basic Medical Sciences, Fujian Medical University, Fuzhou, Fujian, 350122, China.

Advanced Biology
|February 17, 2025
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Summary

Microcephaly with chorioretinopathy, lymphedema, or impaired intellectual development (MCLMR) is linked to KIF11 gene defects. KIF11 inhibition in mice caused retinal defects and vision loss, revealing its role in cilia formation and cell division.

Keywords:
KIF11centrosomesphotoreceptor cellsprimary ciliumretinopathy

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Area of Science:

  • Genetics
  • Developmental Biology
  • Ophthalmology

Background:

  • Microcephaly with chorioretinopathy, lymphedema, or impaired intellectual development (MCLMR) is a rare autosomal dominant disorder.
  • Kinesin-5 (KIF11) is a major causative gene for MCLMR, crucial for mitosis.
  • The precise cellular mechanisms of MCLMR pathogenesis are not fully understood.

Purpose of the Study:

  • To investigate the cellular and molecular mechanisms underlying KIF11 loss-of-function in MCLMR.
  • To explore the role of KIF11 in retinal development and primary cilia formation.

Main Methods:

  • Generation of KIF11-inhibition mouse models.
  • Analysis of retinal development, photoreceptor cilia, and mitotic processes in mouse embryos.

Main Results:

  • KIF11 inhibition led to retinal developmental defects, including rosettes, ciliary alterations, and vision loss.
  • KIF11 is essential for the formation, organization, and maintenance of primary cilia in photoreceptor cells.
  • KIF11 inhibition induced monopolar spindles, mitotic arrest, tetraploidy, and apoptotic cell death in developing mouse embryos.

Conclusions:

  • Loss-of-function of KIF11 contributes to retinopathy in MCLMR through impaired cilia function and disrupted mitosis.
  • KIF11 plays a critical role in retinal development and photoreceptor cell integrity.