---
title: "MYH11 tail variants alter SMII filament dynamics and impair vascular smooth muscle mechanics"
id: "biorxiv-4-disease-associated-myh11-tail-variants-disrupt-vascular-smooth-muscle-myosin-ii"
canonical_url: "https://medichelpline.com/clinical-feed/biorxiv-4-disease-associated-myh11-tail-variants-disrupt-vascular-smooth-muscle-myosin-ii"
content_type: "clinical_feed_article"
specialty: "Cardiology"
source_name: "bioRxiv (Biomedical Preprints)"
source_url: "https://www.biorxiv.org/content/10.64898/2026.10.22.760788v1?rss=1"
published_at: "2026-10-23T12:00:00.000Z"
evidence_level: "Verified Feed"
license: "CC-BY-NC-4.0 / Informational Use"
---
# MYH11 tail variants alter SMII filament dynamics and impair vascular smooth muscle mechanics
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/biorxiv-4-disease-associated-myh11-tail-variants-disrupt-vascular-smooth-muscle-myosin-ii
- **Specialty:** [Cardiology](https://medichelpline.com/clinical-feed/cardiology.md)
- **Primary Source:** bioRxiv (Biomedical Preprints)
- **Source URL:** [Original Journal Publication](https://www.biorxiv.org/content/10.64898/2026.10.22.760788v1?rss=1)
- **Published At:** 2026-10-23T12:00:00.000Z
- **Evidence Rating:** Verified Feed
## Executive GIST (TL;DR)
- The study visualized two human **MYH11** tail variants in living vascular smooth muscle cells (**VSMC**): a pathogenic K1256del and a variant of uncertain significance, A1839V. - Investigators reported that both variants reduced assembly of **smooth muscle myosin II (SMII)** filaments and lowered VSMC contractile output, but the degree of disruption differed between variants. - The A1839V variant largely retained filamentous organization and showed partial agonist-induced filament stabilization, suggesting an intermediate cellular phenotype rather than complete loss of function. - The K1256del variant caused severe disruption of filament architecture: the cohort showed reduced focal adhesion organization, increased SMII network flow, and faster filament exchange dynamics. - K1256del abolished the normal filament stabilization response to induced contraction; the study team observed no agonist-triggered stabilization in those cells. - Data indicated that failure of SMII filament stabilization is a plausible cellular mechanism linking **MYH11** variation to impaired VSMC mechanics and vessel wall dysfunction. - Authors noted that live-cell phenotyping can discriminate variant-specific defects in contractile machinery and proposed this functional approach as a scalable complement to genetic classification for variant prioritization. - The source did not report in vivo experiments, clinical endpoints, patient treatment details, or therapeutic interventions; those remain unaddressed in the preprint.
## Clinical Analysis & Structured Key Points
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Milewicz, [ View ORCID Profile](http://orcid.org/0000-0001-9951-1318)Patrick W Oakes, [ View ORCID Profile](http://orcid.org/0000-0003-0633-4928)Jordan Beach doi: https://doi.org/10.64898/2026.10.22.760788 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. Sasha K Demeulenaere 1 Loyola University Chicago; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Sasha%2BK%2BDemeulenaere%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Demeulenaere%20SK&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ASasha%2BK%2BDemeulenaere%2B) Margaret A Bennett 1 Loyola University Chicago; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Margaret%2BA%2BBennett%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Bennett%20MA&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AMargaret%2BA%2BBennett%2B) Hiral Patel 1 Loyola University Chicago; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Hiral%2BPatel%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Patel%20H&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AHiral%2BPatel%2B) Gregory Aubert 1 Loyola University Chicago; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Gregory%2BAubert%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Aubert%20G&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AGregory%2BAubert%2B) Dianna M. Milewicz 2 The University of Texas Health Science Center at Houston * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Dianna%2B%2BM.%2BMilewicz%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Milewicz%20D&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3ADianna%2B%2BM.%2BMilewicz%2B) Patrick W Oakes 1 Loyola University Chicago; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Patrick%2BW%2BOakes%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Oakes%20PW&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3APatrick%2BW%2BOakes%2B) * [ORCID record for Patrick W Oakes](http://orcid.org/0000-0001-9951-1318 "Open in new tab") Jordan Beach 1 Loyola University Chicago; * [Find this author on Google Scholar](https://www.biorxiv.org/lookup/google-scholar?link_type=googlescholar&gs_type=author&author%5B0%5D=Jordan%2BBeach%2B "Open in new tab") * [Find this author on PubMed](https://www.biorxiv.org/lookup/external-ref?access_num=Beach%20J&link_type=AUTHORSEARCH "Open in new tab") * [Search for this author on this site](https://www.biorxiv.org/search/author1%3AJordan%2BBeach%2B) * [ORCID record for Jordan Beach](http://orcid.org/0000-0003-0633-4928 "Open in new tab") * For correspondence: jbeach1@luc.edu * [Abstract](https://www.biorxiv.org/content/10.64898/2026.10.22.760788v1)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_art/node:5898025/1) * [Info/History](https://www.biorxiv.org/content/10.64898/2026.10.22.760788v1.article-info)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_info/node:5898025/1) * [Metrics](https://www.biorxiv.org/content/10.64898/2026.10.22.760788v1.article-metrics)[](https://www.biorxiv.org/panels_ajax_tab/article_tab_metrics/node:5898025/1) * [Supplementary material](https://www.biorxiv.org/content/10.64898/2026.10.22.760788v1.supplementary-material)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_data/node:5898025/1) * [ Preview PDF](https://www.biorxiv.org/content/10.64898/2026.10.22.760788v1.full.pdf+html)[](https://www.biorxiv.org/panels_ajax_tab/biorxiv_tab_pdf/node:5898025/1) ![Loading](https://www.biorxiv.org/sites/all/modules/contrib/panels_ajax_tab/images/loading.gif) ## Abstract Smooth muscle myosin II (SMII), encoded by MYH11, is the principal motor driving vascular smooth muscle cell (VSMC) contraction. How disease-associated MYH11 variants alter SMII behavior in living cells remains poorly understood. We directly visualized two human MYH11 tail variants in VSMCs: pathogenic K1256del and a variant of uncertain significance A1839V, identified in a patient with severe aortoiliac aneurysmal disease. Both variants reduced SMII filament assembly and VSMC contractile output, but with distinct severity. A1839V predominantly retained filamentous organization and displayed partial agonist-induced stabilization, consistent with an intermediate cellular phenotype. In contrast, K1256del severely disrupted filament architecture and behavior, including reduced focal adhesion organization, increased SMII network flow and accelerated filament exchange. Furthermore, K1256del abolished the filament stabilization response to induced contraction. These findings identify failure of SMII filament stabilization as a cellular mechanism linking MYH11 variation to impaired VSMC mechanics. More broadly, they show that direct live-cell phenotyping can distinguish variant-specific defects in the contractile machinery, providing a scalable functional strategy to complement genetic classification and prioritize MYH11 variants for deeper mechanistic and in vivo study. ### Competing Interest Statement The authors have declared no competing interest. ## Funder Information Declared National Institutes of Health, https://ror.org/01cwqze88, R35-GM138183, R01-GM148644, F30-HL178288, S10OD034431 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-ND 4.0 International license](http://creativecommons.org/licenses/by-nc-nd/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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[ Download PDF](https://www.biorxiv.org/content/10.64898/2026.10.22.760788v1.full.pdf) Print/Save Options [Download PDF](https://www.biorxiv.org/content/biorxiv/early/2026/10/23/2026.10.22.760788.full.pdf)Full Text & In-line FiguresXML [More Info](https://www.biorxiv.org/about/FAQ#PrintOptions "More Information on Print/Save Options") [Supplementary Material ](https://www.biorxiv.org/content/10.64898/2026.10.22.760788v1.supplementary-material) [ Email](https://www.biorxiv.org/ "Email this Article") [ Share](https://www.biorxiv.org/) Disease-associated MYH11 tail variants disrupt vascular smooth muscle myosin II filament dynamics and cell mechanics Sasha K Demeulenaere, Margaret A Bennett, Hiral Patel, Gregory Aubert, Dianna M. Milewicz, Patrick W Oakes, Jordan Beach bioRxiv 2026.10.22.760788; doi: https://doi.org/10.64898/2026.10.22.760788 This article is a preprint and has not been certified by peer review [[what does this mean?](https://www.biorxiv.org/about/FAQ#unrefereed)]. 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