---
title: "Desmoplakin Hinge Enables Rapid, Reversible Conformational Response to Acute Force"
id: "biorxiv-3-the-desmoplakin-hinge-domain-confers-a-reversible-conformational-change-in"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-3-the-desmoplakin-hinge-domain-confers-a-reversible-conformational-change-in"
content_type: "clinical_feed_article"
specialty: "General"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.22.760798v1?rss=1"
published_at: "2026-10-23T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Desmoplakin Hinge Enables Rapid, Reversible Conformational Response to Acute Force
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-3-the-desmoplakin-hinge-domain-confers-a-reversible-conformational-change-in
- **Specialty:** [General](https://medichelpline.com/clinical-feed/general.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.22.760798v1?rss=1)
- **Published At:** 2026-10-23T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- Investigators reported that the head-domain **hinge** of **desmoplakin** mediates a rapid repositioning of the DP tail when cells experience acute uniaxial mechanical stretch. - The repositioning occurs within 30 seconds of applied stretch and reverses when the stretch is released, indicating a dynamic, short-timescale conformational switch rather than a permanent structural change. - Data indicated the hinge-dependent movement correlates with transmission of mechanical force to the desmosomal **cadherins**, consistent with a role for the hinge in buffering tension at the cadherin interface. - The study team observed that deleting or shortening the hinge abolishes the stretch-induced repositioning and compromises desmosome mechanical integrity. - Authors noted that altering the hinge did not affect DP tail repositioning during the calcium-dependent to hyper-adhesive transition, implying distinct mechanisms for adhesive-state changes versus acute force sensing. - The work defines a reversible, hinge-dependent mechanotransduction pathway through which DP senses and relays mechanical force within the **desmosome** and proposes that this mechanism could reduce force impulses on cadherins and contribute to tissue mechanical resilience. - The preprint listed NIH-NIAMS funding; no competing interests were declared. - The source did not report detailed biophysical parameters beyond the 30-second timescale, nor did it provide molecular-resolution structures of the hinge transition in this abstract.
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Dean, [ View ORCID Profile](http://orcid.org/0009-0006-0468-9484)Yen TB Tran, [ View ORCID Profile](http://orcid.org/0009-0007-1551-3318)Samuel C Bartley, [ View ORCID Profile](http://orcid.org/0000-0002-4182-9283)Eunjoo J Lee, [ View ORCID Profile](http://orcid.org/0000-0001-6438-7863)Andrew P Kowalczyk, [ View ORCID Profile](http://orcid.org/0000-0001-6624-177X)Daniel E Conway, [ View ORCID Profile](http://orcid.org/0000-0002-5119-7750)Alexa L Mattheyses doi: https://doi.org/10.64898/2026.10.22.760798 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. Collin M Ainslie 1 University of Alabama at Birmingham; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Collin%2BM%2BAinslie%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Ainslie%20CM&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ACollin%2BM%2BAinslie%2B) * [ORCID record for Collin M Ainslie](http://orcid.org/0000-0002-2043-4223 "Open in new tab") William F. Dean 1 University of Alabama at Birmingham; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=William%2B%2BF.%2BDean%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Dean%20W&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AWilliam%2B%2BF.%2BDean%2B) * [ORCID record for William F. Dean](http://orcid.org/0000-0001-9186-5795 "Open in new tab") Yen TB Tran 1 University of Alabama at Birmingham; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Yen%2BTB%2BTran%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Tran%20YT&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AYen%2BTB%2BTran%2B) * [ORCID record for Yen TB Tran](http://orcid.org/0009-0006-0468-9484 "Open in new tab") Samuel C Bartley 1 University of Alabama at Birmingham; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Samuel%2BC%2BBartley%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Bartley%20SC&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ASamuel%2BC%2BBartley%2B) * [ORCID record for Samuel C Bartley](http://orcid.org/0009-0007-1551-3318 "Open in new tab") Eunjoo J Lee 1 University of Alabama at Birmingham; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Eunjoo%2BJ%2BLee%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Lee%20EJ&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AEunjoo%2BJ%2BLee%2B) * [ORCID record for Eunjoo J Lee](http://orcid.org/0000-0002-4182-9283 "Open in new tab") Andrew P Kowalczyk 2 Penn State College of Medicine; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Andrew%2BP%2BKowalczyk%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Kowalczyk%20AP&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAndrew%2BP%2BKowalczyk%2B) * [ORCID record for Andrew P Kowalczyk](http://orcid.org/0000-0001-6438-7863 "Open in new tab") Daniel E Conway 3 The Ohio State University * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Daniel%2BE%2BConway%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Conway%20DE&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ADaniel%2BE%2BConway%2B) * [ORCID record for Daniel E Conway](http://orcid.org/0000-0001-6624-177X "Open in new tab") Alexa L Mattheyses 1 University of Alabama at Birmingham; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Alexa%2BL%2BMattheyses%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Mattheyses%20AL&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AAlexa%2BL%2BMattheyses%2B) * [ORCID record for Alexa L Mattheyses](http://orcid.org/0000-0002-5119-7750 "Open in new tab") * For correspondence: mattheyses@uab.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.22.760798v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5898007/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.22.760798v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5898007/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.22.760798v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5898007/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.22.760798v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5898007/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Desmosomes provide mechanical integrity to tissues that experience strain, yet how mechanical force is sensed and distributed within the desmosomal plaque remains poorly understood. Here we identify the hinge within the desmoplakin (DP) head domain is required for repositioning the DP tail in response to acute uniaxial mechanical stretch. This repositioning occurs within 30 seconds of applied stretch and reverses with release, indicating a dynamic reversible switch rather than a stable structural transition. We show this hinge-dependent repositioning correlates with the propagation of mechanical force to the desmosomal cadherins, consistent with the hinge's role in buffering tension at the cadherin interface during mechanical loading. Deletion or shortening of the hinge abolishes the stretch-induced response and compromises desmosome mechanical integrity. The repositioning of the DP tail in the calcium-dependent to hyper-adhesive transition was not impacted by alterations to the hinge, demonstrating that DP repositioning due to acute force or adhesive state is mechanistically distinct. Together, these findings define a reversible, hinge-dependent mechanotransduction pathway through which DP senses and relays mechanical force within the desmosome. This mechanism could act as a mechanical buffer by reducing the impulse of forces on the cadherins, and play a central role in mechanical resilience. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared NIH-NIAMS, R01AR072697, NIH-NIAMS, 1F31AR088336 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-NC 4.0 International license](http://creativecommons.org/licenses/by-nc/4.0/). bioRxiv and medRxiv thank the following for their generous financial support: > The Chan Zuckerberg Initiative, Cold Spring Harbor Laboratory, the Sergey Brin Family Foundation, California Institute of Technology, Centre National de la Recherche Scientifique, Fred Hutchinson Cancer Center, Imperial College London, Massachusetts Institute of Technology, Stanford University, The University of Edinburgh, University of Washington, and Vrije Universiteit Amsterdam. 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