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PLoS One. 2016 Mar 9;11(3):e0151251. doi: 10.1371/journal.pone.0151251. eCollection 2016.

Wound-Induced Polyploidization: Regulation by Hippo and JNK Signaling and Conservation in Mammals.

Author information

1
Department of Embryology, Carnegie Institution for Science, Howard Hughes Medical Institute, 3250 San Martin Dr., Baltimore, MD 21218, United States of America.
2
Wilmer Eye Institute, Johns Hopkins School of Medicine, 400 N. Broadway, Baltimore, MD 21231, United States of America.

Abstract

Tissue integrity and homeostasis often rely on the proliferation of stem cells or differentiated cells to replace lost, aged, or damaged cells. Recently, we described an alternative source of cell replacement- the expansion of resident, non-dividing diploid cells by wound-induced polyploidization (WIP). Here we show that the magnitude of WIP is proportional to the extent of cell loss using a new semi-automated assay with single cell resolution. Hippo and JNK signaling regulate WIP; unexpectedly however, JNK signaling through AP-1 limits rather than stimulates the level of Yki activation and polyploidization in the Drosophila epidermis. We found that polyploidization also quantitatively compensates for cell loss in a mammalian tissue, mouse corneal endothelium, where increased cell death occurs with age in a mouse model of Fuchs Endothelial Corneal Dystrophy (FECD). Our results suggest that WIP is an evolutionarily conserved homeostatic mechanism that maintains the size and synthetic capacity of adult tissues.

PMID:
26958853
PMCID:
PMC4784922
DOI:
10.1371/journal.pone.0151251
[Indexed for MEDLINE]
Free PMC Article

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