Author
Listed:
- David Q. Matus
(Duke University
Present address: Department of Biochemistry and Cell Biology, Stony Brook University, Stony Brook, New York 11794, USA)
- Emily Chang
(Duke University
Present address: Johns Hopkins School of Medicine, Baltimore, Maryland 21205, USA)
- Sasha C. Makohon-Moore
(Duke University)
- Mary A. Hagedorn
(Duke University)
- Qiuyi Chi
(Duke University)
- David R. Sherwood
(Duke University)
Abstract
Large gaps in basement membrane (BM) occur during organ remodelling and cancer cell invasion. Whether dividing cells, which temporarily reduce their attachment to BM, influence these breaches is unknown. Here we analyse uterine–vulval attachment during development across 21 species of rhabditid nematodes and find that the BM gap that forms between these organs is always bounded by a non-dividing vulval cell. Through cell cycle manipulation and live cell imaging in Caenorhabditis elegans, we show that actively dividing vulval cells facilitate enlargement of this breach by promoting BM movement. In contrast, targeted cell cycle arrest halts BM movement and limits gap opening. Further, we demonstrate that the BM component laminin accumulates at the BM gap edge and promotes increased integrin levels in non-dividing vulval cells, stabilizing gap position. Together, these studies reveal that cell division can be used as a mechanism to regulate BM breaches, thus controlling the exchange of cells between tissues.
Suggested Citation
David Q. Matus & Emily Chang & Sasha C. Makohon-Moore & Mary A. Hagedorn & Qiuyi Chi & David R. Sherwood, 2014.
"Cell division and targeted cell cycle arrest opens and stabilizes basement membrane gaps,"
Nature Communications, Nature, vol. 5(1), pages 1-13, September.
Handle:
RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5184
DOI: 10.1038/ncomms5184
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