Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/86658
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Type: Journal article
Title: JNK signaling is needed to tolerate chromosomal instability
Author: Wong, H.
Shaukat, Z.
Wang, J.
Saint, R.
Gregory, S.
Citation: Cell Cycle, 2014; 13(4):622-631
Publisher: Landes Bioscience
Issue Date: 2014
ISSN: 1538-4101
1551-4005
Statement of
Responsibility: 
Heidi W-S Wong, Zeeshan Shaukat, Jianbin Wang, Robert Saint, and Stephen L Gregory
Abstract: Chromosomal instability (CIN), as a common feature of tumors, represents a potential therapeutic target if ways can be found to specifically cause apoptosis in unstably dividing cells. We have previously shown that if signaling through the JNK pathway is reduced, apoptosis is triggered in models of chromosomal instability induced by loss of the spindle checkpoint. Here we identify components upstream and downstream of JNK that are able to mediate this effect, and test the involvement of p53 and DNA damage in causing apoptosis when JNK signaling is reduced in CIN cells. We show that cell cycle progression timing has a strong effect on the apoptosis seen when JNK signaling is reduced in genetically unstable cells: a shortened G₂ phase enhances the apoptosis, while lengthening G₂ rescues the JNK-deficient CIN cell death phenotype. Our findings suggest that chromosomal instability represents a significant stress to dividing cells, and that without JNK signaling, cells undergo apoptosis because they lack a timely and effective response to DNA damage.
Keywords: Chromosomal instability; JNK; Drosophila; apoptosis; Mad2
Description: Published Online 12 Dec 2013
Rights: © 2014 Landes Bioscience
RMID: 0020135699
DOI: 10.4161/cc.27484
Grant ID: http://purl.org/au-research/grants/nhmrc/525447
http://purl.org/au-research/grants/nhmrc/1027878
Appears in Collections:Molecular and Biomedical Science publications

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