MISP: The missing link between extracellular matrix and astral microtubules

Nain, Amrinder S.; Cimini, Daniela

doi:10.4161/cc.25171

Cited by 3 publications

(4 citation statements)

References 8 publications

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“…Interestingly, in addition to nucleoporins, 19 non‐nucleoporin NUP88‐associated proteins were identified to associate with cell cycle or mitotic cell cycle processes, suggesting a critical involvement of NUP88 interactome in cell cycle control. Moreover, among the cell cycle‐related proteins, we confirmed the interaction between NUP88 and MISP and found that NUP88 overexpression blocks MISP phosphorylation, which has been reported to be critical for mitotic spindle positioning and accurate chromosome segregation (Maier et al, ; Nain and Cimini, ; Zhu et al, ).…”

Section: Discussionsupporting

confidence: 68%

“…In this group of proteins, MISP (mitotic interactor and substrate of Plk1) was identified as a NUP88‐binding protein with a high enrichment fold (=17.6). Interestingly, recent studies from independent groups have shown that MISP is required for spindle positioning and accurate chromosome segregation, and that phostphorylation of MISP is critical for its function (Maier et al, ; Nain and Cimini, ; Zhu et al, ). Moreover, this protein was also found to be an actin‐binding protein (Kumeta et al, ), which is consistent with our observation that NUP88 associates with MISP in the insoluble fraction (Fig.…”

Section: Resultsmentioning

confidence: 99%

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Multiple biological processes may be associated with tumorigenesis under NUP88‐overexpressed condition

Zhao

2016

Genes Chromosomes & Cancer

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Overexpression of the nucleoporin NUP88 has been observed in a large number of tumors and has been experimentally proven to promote tumorigenesis. However, the mechanism underlying the tumor-promoting activity of overexpressed NUP88 is not clear. To investigate the potential pathways that drive tumorigenesis under NUP88 overexpressed condition, we applied a proteomic approach to identify NUP88-associated proteins at a subcellular compartment level. Gene ontology analysis revealed significant associations between NUP88 interactome and biological processes that are related to nuclear transport, RNA processing, cell cycle progression, metabolic regulation, and viral infection. Moreover, we found that NUP88 interacts with MISP, a mitotic interactor and substrate of PLK1. Interestingly, NUP88 overexpression blocks MISP phosphorylation, which is known to be critical for normal spindle formation and accurate chromosome segregation during mitosis. In conclusion, our data for the first time provide a global view of biological processes that may drive tumorigenesis under NUP88 overexpressed condition, revealing a biological effect of NUP88-MISP interaction. Furthermore, identification of NUP88-associated proteins provides a valuable database for future studies. © 2016 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 68%

Section: Resultsmentioning

confidence: 99%

Multiple biological processes may be associated with tumorigenesis under NUP88‐overexpressed condition

Zhao

2016

Genes Chromosomes & Cancer

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“…During mitosis, cortical actins line the plasma membrane all over the cortex, and retraction fibers, composed of actin filaments, maintain the cellsubstrate adhesions (13). The extracellular matrix linked to the retraction fibers form as the cell rounds up and can control spindle positioning via forces that are transmitted through the plasma membrane (13,14). Inside the plasma membrane, spindle positioning is believed to be directed by interactions between the plus-end of astral microtubules that originate from the spindle poles and an evolutionarily conserved cortical machinery, the Gαi-LGN-NuMA ternary complex, which exerts a pulling force on them (15)(16)(17)(18).…”

Section: J O U R N a L P R E -P R O O Fmentioning

confidence: 99%

“…Spindle positioning requires the actin cytoskeleton and retraction fibers to control mitotic centrosome positioning (13,47). Mitotic actindependent pulling forces initiate from retraction fibers that link rounded mitotic cells to sites of cell matrix adhesion (13,14,48,49). Interactions between the plus-end of astral microtubules and the cortical Gαi-LGN-NuMA ternary complex generates cortical spindle-pulling forces (15)(16)(17)(18).…”

Section: 1r Depletion Induces Mitotic Arrest and Its Interaction With Numa Promotes The Stability Of Astral Microtubules And The Associatmentioning

confidence: 99%

Multifunctional protein 4.1R regulates the asymmetric segregation of Numb during terminal erythroid maturation

Huang

et al. 2021

Journal of Biological Chemistry

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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A guide to classifying mitotic stages and mitotic defects in fixed cells

Baudoin

Cimini

2018

Chromosoma

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Cell division is fundamental to life and its perturbation can disrupt organismal development, alter tissue homeostasis, and cause disease. Analysis of mitotic abnormalities provides insight into how certain perturbations affect the fidelity of cell division and how specific cellular structures, molecules, and enzymatic activities contribute to the accuracy of this process. However, accurate classification of mitotic defects is instrumental for correct interpretation of data and formulation of new hypotheses. In this article, we provide guidelines for identifying specific mitotic stages and for classifying normal and deviant mitotic phenotypes. We hope this will clarify confusion about how certain defects are classified and help investigators avoid misnomers, misclassification, and/or misinterpretation, thus leading to a unified and standardized system to classify mitotic defects.

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MISP: The missing link between extracellular matrix and astral microtubules

Cited by 3 publications

References 8 publications

Multiple biological processes may be associated with tumorigenesis under NUP88‐overexpressed condition

Multiple biological processes may be associated with tumorigenesis under NUP88‐overexpressed condition

Multifunctional protein 4.1R regulates the asymmetric segregation of Numb during terminal erythroid maturation

A guide to classifying mitotic stages and mitotic defects in fixed cells

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