Loss of CENP-F Results in Dilated Cardiomyopathy with Severe Disruption of Cardiac Myocyte Architecture
Related Experiment Video
Updated: Feb 10, 2026

A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
Annabelle Manalo1, Alison K Schroer2, Aidan M Fenix1
1Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN, 37232, USA.
Abstract:
Centromere-binding protein F (CENP-F) is a very large and complex protein with many and varied binding partners including components of the microtubule network. Numerous CENP-F functions impacting diverse cellular behaviors have been identified. Importantly, emerging data have shown that CENP-F loss- or gain-of-function has critical effects on human development and disease. Still, it must be noted that data at the single cardiac myocyte level examining the impact of CENP-F loss-of-function on fundamental cellular behavior is missing. To address this gap in our knowledge, we analyzed basic cell structure and function in cardiac myocytes devoid of CENP-F. We found many diverse structural abnormalities including disruption of the microtubule network impacting critical characteristics of the cardiac myocyte. This is the first report linking microtubule network malfunction to cardiomyopathy. Importantly, we also present data demonstrating a direct link between a CENP-F single nucleotide polymorphism (snp) and human cardiac disease. In a proximate sense, these data examining CENP-F function explain the cellular basis underlying heart disease in this genetic model and, in a larger sense, they will hopefully provide a platform upon which the field can explore diverse cellular outcomes in wide-ranging areas of research on this critical protein.
Insights
Centromere-binding protein F (CENP-F) deficiency disrupts cardiac myocyte structure and microtubule networks, leading to cardiomyopathy. A CENP-F single nucleotide polymorphism is linked to human heart disease.
Area of Science:
- Cell Biology
- Genetics
- Cardiovascular Research
Background:
- Centromere-binding protein F (CENP-F) is a large protein with diverse binding partners and cellular functions.
- CENP-F dysfunction impacts human development and disease.
- Data on CENP-F loss-of-function in cardiac myocytes is lacking.
Purpose of the Study:
- To investigate the impact of CENP-F loss-of-function on cardiac myocyte structure and function.
- To identify the cellular basis of heart disease linked to CENP-F.
Main Methods:
- Analysis of cardiac myocytes lacking CENP-F.
- Examination of cell structure and microtubule network integrity.
- Correlation of CENP-F single nucleotide polymorphism (SNP) with human cardiac disease.
Main Results:
- Cardiac myocytes lacking CENP-F exhibit structural abnormalities.
- Disruption of the microtubule network was observed, impacting myocyte characteristics.
- A direct link between a CENP-F SNP and human cardiac disease was established.
- Microtubule network malfunction is linked to cardiomyopathy.
Conclusions:
- CENP-F is crucial for maintaining cardiac myocyte structure and microtubule network integrity.
- CENP-F dysfunction contributes to cardiomyopathy.
- CENP-F SNPs represent a genetic risk factor for human heart disease.
Related Concept Videos
Cardiomyopathy II: Dilated Cardiomyopathy
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cardiomyopathy IV: Restrictive Cardiomyopathy
Line Loss
Line loss impacts power delivery efficiency in a balanced three-phase circuit. The symmetry in such a circuit simplifies the...
Cardiomyopathy V: Interprofessional Care
Cardiomyopathy I: Introduction and Classification

