Evidence map›Paper›PMID 40490973›Full record

ArticleBiology of the cell2025

An Auxin Inducible Degradation System to Study Mklp2 Functions in MDCK Epithelial Cells.

Morgane Rodriguez, Valérie Simon, Bénédicte Delaval, Benjamin Vitre

Abstract read
In one paragraph

Article in Biology of the cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

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4 · The record

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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors.

Morgane RodriguezCentre de Recherche en Biologie cellulaire de Montpellier, Univ Montpellier, CNRS, Montpellier, France.
Valérie SimonCentre de Recherche en Biologie cellulaire de Montpellier, Univ Montpellier, CNRS, Montpellier, France.
Bénédicte DelavalCentre de Recherche en Biologie cellulaire de Montpellier, Univ Montpellier, CNRS, Montpellier, France.
Benjamin VitreCentre de Recherche en Biologie cellulaire de Montpellier, Univ Montpellier, CNRS, Montpellier, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The auxin inducible degradation (AID) system, which allows for rapid and inducible degradation of a protein of interest, is an efficient technology to study protein function in cells. This system proves particularly useful to study cellular motors that can be involved in different mechanisms depending on the cell cycle stage. Mitotic kinesin-like protein 2 (Mklp2) is a member of the kinesin-6 family involved in intracellular trafficking both in interphase and mitosis. In mitosis, at anaphase onset, it relocates the chromosomal passenger complex (CPC), from the chromatin to the spindle midzone and equatorial cortex. Inhibition or knockdown of Mklp2 therefore leads to CPC re-localization defects and cytokinesis failure. Existing tools used to study Mklp2 functions in cells, including antibodies, siRNA, and small molecule inhibitors, allowed the identification of the general function of Mklp2 in mitosis. However, these tools induce different intermediate phenotypes during the course of mitosis, highlighting the need for an alternative Mklp2 perturbation approach. We report here a new tool to study the discrete localization of endogenous Mklp2 at different stages of the cell cycle combined with an AID tag that allows the study of the kinesin with high specificity, high efficiency, and high temporal resolution in MDCK (Madin-Darby canine kidney) epithelial cells. We show that upon auxin treatment, the acute and rapid degradation of Mklp2 results in delayed re-localization of CPC component Aurora-B to the spindle midzone during anaphase, cytokinesis failure, and cell binucleation. We validate the specificity of the system by rescuing Mklp2 expression and reversing the phenotypes. Overall, this new tool facilitates the study of endogenous Mklp2 localization and function at specific stages of the cell cycle and offers a highly specific method for exploring its roles in a nontransformed mammalian model cell line widely used to study epithelial organization and dynamics.

Indexed as

Epithelial CellsIndoleacetic AcidsKinesinsAnimalsDogsMadin Darby Canine Kidney CellsMitosisProteolysisIndoleacetic AcidsKinesins

Identifiers

PMID40490973
PMCPMC12149487

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.