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, 294 (30), 11382-11390

Dissecting the Mechanisms of Cell Division


Dissecting the Mechanisms of Cell Division

Joseph Y Ong et al. J Biol Chem.


Cell division is a highly regulated and carefully orchestrated process. Understanding the mechanisms that promote proper cell division is an important step toward unraveling important questions in cell biology and human health. Early studies seeking to dissect the mechanisms of cell division used classical genetics approaches to identify genes involved in mitosis and deployed biochemical approaches to isolate and identify proteins critical for cell division. These studies underscored that post-translational modifications and cyclin-kinase complexes play roles at the heart of the cell division program. Modern approaches for examining the mechanisms of cell division, including the use of high-throughput methods to study the effects of RNAi, cDNA, and chemical libraries, have evolved to encompass a larger biological and chemical space. Here, we outline some of the classical studies that established a foundation for the field and provide an overview of recent approaches that have advanced the study of cell division.

Keywords: cancer; cell cycle; cell division; chemical biology; classical genetics; computational biology; genomics; post-translational modification (PTM); protein structure; proteomics.

Conflict of interest statement

The authors declare that they have no conflicts of interest with the contents of this article


Figure 1.
Figure 1.
Overview of approaches used to dissect the mechanisms of cell division. Multiple approaches have been used to dissect the mechanisms of cell division, including genetic, proteomic, chemical, structural, and computational approaches. Figure contains the structure of the MIND complex from Kluyveromyces lactis (84) (Protein Data Bank code 5T58 (127), created using the NGL Viewer (128)). Examples of Plk1-interacting proteins are Bub1 (129), Cdh1 (130), and Chk2 (131). Examples of PLK1 substrates are FOXM1 (8), Cdc25C (132), p150Glued (133), Myt1 (134), and Wee1 (45).

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