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Plant Signal Behav. 2016 Oct 2;11(10):e1238547.

Cytokinesis defect in BY-2 cells caused by ATP-competitive kinase inhibitors.

Author information

1
a Graduate School of Science, Nagoya University, Furo-cho , Chikusa-ku, Nagoya, Aichi , Japan.
2
b Division of Biological Science, Graduate School of Science, Nagoya University, Furo-cho , Chikusa-ku, Nagoya, Aichi , Japan.
3
c Higashiyama Live-Holonics Project, ERATO, JST, Furo-cho , Chikusa-ku, Nagoya, Aichi , Japan.
4
d Institute of Transformative Bio-Molecules (ITbM), Nagoya University, Furo-cho , Chikusa-ku, Nagoya, Aichi , Japan.

Abstract

Cytokinesis is last but not least in cell division as it completes the formation of the two cells. The main role in cell plate orientation and expansion have been assigned to microtubules and kinesin proteins. However, recently we reported severe cytokinesis defect in BY-2 cells not accompanied by changes in microtubules dynamics. Here we also confirmed that distribution of kinesin NACK1 is not the cause of cytokinesis defect. We further explored inhibition of the cell plate expansion by ATP-competitive inhibitors. Two different inhibitors, 5-Iodotubercidin and ML-7 resulted in a very similar phenotype, which indicates that they target same protein cascade. Interestingly, in our previous study we showed that 5-Iodotubercidin treatment affects concentration of actin filaments on the cell plate, while ML-7 is inhibitor of myosin light chain kinase. Although not directly, it indicates importance of actomyosin complex in plant cytokinesis.

KEYWORDS:

5-Iodotubercidin; actomyosin role in plant cytokinesis; Haspin kinase; ML-7; cytokinesis defect; inhibition of the cell plate expansion; kinesin NACK1

PMID:
27662076
PMCID:
PMC5257169
DOI:
10.1080/15592324.2016.1238547
[Indexed for MEDLINE]
Free PMC Article

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