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First published online March 8, 2006

Journal of Cell Science 119, 603e (2006)
© The Company of Biologists Limited
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In this issue

Phospholipid arrested at checkpoint


Figure 1

Checkpoints halt the eukaryotic cell cycle at various points if any of the processes needed to complete cell division (e.g. chromosomal segregation) fail. On p. 1005, Zhongmin Alex Ma and colleagues report that the disruption of phospholipid turnover in G1-phase cells is another factor that induces cell-cycle arrest. The turnover of phosphatidylcholine (the major phospholipid in mammalian membranes) is rapid in G1 phase but stops in S phase to allow cells to make enough membrane for their daughters. Turnover of phosphatidylcholine in G1 phase is regulated by the opposing actions of CTP:phosphocholine cytidyltransferase and the group VIA Ca2+-independent phospholipase A2 (iPLA2). The authors show that inhibition of iPLA2 arrests cells in G1 phase and induces accumulation of the tumour suppressor p53 and expression of the cyclin-dependent kinase inhibitor p21cip1. Additional experiments in p53-deficient and p21cip1-deficient cells confirm that inhibition of iPLA2 activates the p53-p21cip1 checkpoint. Thus, conclude the authors, iPLA2 and p53 cooperate to monitor the integrity of membrane phospholipids in G1 phase to ensure cells are well prepared for division.


Related articles in JCS:

Disruption of G1-phase phospholipid turnover by inhibition of Ca2+-independent phospholipase A2 induces a p53-dependent cell-cycle arrest in G1 phase
Xu Hannah Zhang, Chunying Zhao, Konstantin Seleznev, Keying Song, James J. Manfredi, and Zhongmin Alex Ma
JCS 2006 119: 1005-1015. [Abstract] [Full Text]  




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