Tissue Crowding Induces Caspase-Dependent Competition for Space.

Moreno, Eduardo; Levayer, Romain; Dupont, Carole (2016). Tissue Crowding Induces Caspase-Dependent Competition for Space. Current Biology, 26(5), pp. 670-677. Cell Press 10.1016/j.cub.2015.12.072

[img]
Preview
Text
Levayer et al Curr Bio 2016.pdf - Published Version
Available under License Creative Commons: Attribution-Noncommercial-No Derivative Works (CC-BY-NC-ND).

Download (7MB) | Preview

Regulation of tissue size requires fine tuning at the single-cell level of proliferation rate, cell volume, and cell death. Whereas the adjustment of proliferation and growth has been widely studied [1, 2, 3, 4 and 5], the contribution of cell death and its adjustment to tissue-scale parameters have been so far much less explored. Recently, it was shown that epithelial cells could be eliminated by live-cell delamination in response to an increase of cell density [6]. Cell delamination was supposed to occur independently of caspase activation and was suggested to be based on a gradual and spontaneous disappearance of junctions in the delaminating cells [6]. Studying the elimination of cells in the midline region of the Drosophila pupal notum, we found that, contrary to what was suggested before, Caspase 3 activation precedes and is required for cell delamination. Yet, using particle image velocimetry, genetics, and laser-induced perturbations, we confirmed [ 6] that local tissue crowding is necessary and sufficient to drive cell elimination and that cell elimination is independent of known fitness-dependent competition pathways [ 7, 8 and 9]. Accordingly, activation of the oncogene Ras in clones was sufficient to compress the neighboring tissue and eliminate cells up to several cell diameters away from the clones. Mechanical stress has been previously proposed to contribute to cell competition [ 10 and 11]. These results provide the first experimental evidences that crowding-induced death could be an alternative mode of super-competition, namely mechanical super-competition, independent of known fitness markers [ 7, 8 and 9], that could promote tumor growth.

Item Type:

Journal Article (Original Article)

Division/Institute:

08 Faculty of Science > Department of Biology > Institute of Cell Biology

UniBE Contributor:

Moreno, Eduardo; Levayer, Romain and Dupont, Carole

Subjects:

500 Science > 570 Life sciences; biology

ISSN:

0960-9822

Publisher:

Cell Press

Language:

English

Submitter:

Eduardo Moreno

Date Deposited:

01 Jun 2016 14:51

Last Modified:

10 Sep 2017 13:20

Publisher DOI:

10.1016/j.cub.2015.12.072

PubMed ID:

26898471

BORIS DOI:

10.7892/boris.82411

URI:

https://boris.unibe.ch/id/eprint/82411

Actions (login required)

Edit item Edit item
Provide Feedback