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Bilateral JNK activation is a hallmark of interface contractility and promotes elimination of aberrant cells

Deepti Prasad, Katharina Illek, Friedericke Fischer, View ORCID ProfileKathrin Holstein, View ORCID ProfileAnne-Kathrin Classen
doi: https://doi.org/10.1101/2022.06.20.496791
Deepti Prasad
1Hilde-Mangold-Haus, University of Freiburg, Habsburgerstrasse 49, 79104 Freiburg
2Spemann Graduate School of Biology and Medicine (SGBM), University of Freiburg
3Faculty of Biology, University of Freiburg
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Katharina Illek
1Hilde-Mangold-Haus, University of Freiburg, Habsburgerstrasse 49, 79104 Freiburg
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Friedericke Fischer
1Hilde-Mangold-Haus, University of Freiburg, Habsburgerstrasse 49, 79104 Freiburg
3Faculty of Biology, University of Freiburg
4International Max Planck Research School for Immunobiology, Epigenetics, and Metabolism, Freiburg
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Kathrin Holstein
1Hilde-Mangold-Haus, University of Freiburg, Habsburgerstrasse 49, 79104 Freiburg
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Anne-Kathrin Classen
1Hilde-Mangold-Haus, University of Freiburg, Habsburgerstrasse 49, 79104 Freiburg
3Faculty of Biology, University of Freiburg
5CIBSS Centre for Integrative Biological Signalling Studies, University of Freiburg
6BIOSS Centre for Biological Signalling Studies, University of Freiburg
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  • For correspondence: anne.classen@biologie.uni-freiburg.de
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Abstract

Tissue-intrinsic defence mechanisms eliminate aberrant cells from epithelia and thereby maintain the health of developing tissues or adult organisms. 'Interface contractility' comprises one such distinct mechanism that specifically guards against aberrant cells, which undergo inappropriate cell fate and differentiation programs. The cellular mechanisms which facilitate detection and elimination of these aberrant cells are currently unknown. We find that in Drosophila imaginal discs, interface contractility is associated with bilateral JNK activation at the clonal interface of wild type and aberrant cells. Bilateral JNK activation is unique to interface contractility and is not observed in other tissue-intrinsic defence mechanisms, such as cell-cell competition. We find that JNK is activated cell-autonomously by either of the contacting cell types and drives apoptotic elimination of cells at clonal interfaces. Ultimately, JNK interface signalling provides a collective tissue-level mechanism, which ensures elimination of aberrant, misspecified cells that cannot be identified by cell fitness criteria, as in cell-cell competition. Importantly, oncogenic Ras activates interface contractility but evades apoptotic elimination by bilateral JNK activation. Combined, our work establishes bilateral JNK interface signalling and interface apoptosis as a new hallmark of interface contractility, and it highlights how oncogenic mutations evade tumour suppressor function encoded by this tissue-intrinsic surveillance system.

Competing Interest Statement

The authors have declared no competing interest.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY 4.0 International license.
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Posted June 20, 2022.
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Bilateral JNK activation is a hallmark of interface contractility and promotes elimination of aberrant cells
Deepti Prasad, Katharina Illek, Friedericke Fischer, Kathrin Holstein, Anne-Kathrin Classen
bioRxiv 2022.06.20.496791; doi: https://doi.org/10.1101/2022.06.20.496791
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Bilateral JNK activation is a hallmark of interface contractility and promotes elimination of aberrant cells
Deepti Prasad, Katharina Illek, Friedericke Fischer, Kathrin Holstein, Anne-Kathrin Classen
bioRxiv 2022.06.20.496791; doi: https://doi.org/10.1101/2022.06.20.496791

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