The stress responsive gene ankrd1a is dynamically regulated during skeletal muscle development and upregulated following cardiac injury in border zone cardiomyocytes in adult zebrafish

• Published in: Gene 2021-08, Vol.792, p.145725-145725, Article 145725
• Main Authors: Boskovic, Srdjan, Marín Juez, Rubén, Stamenkovic, Nemanja, Radojkovic, Dragica, Stainier, Didier YR, Kojic, Snezana
• Format: Article
• Language: English
• Subjects: Cryoinjury; Exercise; Reporter line; Slow muscle fibers
• ISSN: 0378-1119; 1879-0038
• DOI: 10.1016/j.gene.2021.145725

•TgBAC(ankrd1a:EGFP) is expressed in the developing zebrafish slow muscle.•Exercise induces cardiac expression of TgBAC(ankrd1a:EGFP).•ankrd1a is upregulated after cardiac injury.•TgBAC(ankrd1a:EGFP) is upregulated in injury border zone cardiomyocytes. Ankyrin repeat domain 1 (ANKRD1) is a functionally pleiotropic protein found in the nuclei and sarcomeres of cardiac and skeletal muscles, with a proposed role in linking myofibrilar stress and transcriptional regulation. Rapid upregulation of its expression in response to both physiological and pathological stress supports the involvement of ANKRD1 in muscle tissue adaptation and remodeling. However, the exact role of ANKRD1 remains poorly understood. To begin to investigate its function at higher resolution, we have generated and characterized a TgBAC(ankrd1a:EGFP) zebrafish line. This reporter line displays transgene expression in slow skeletal muscle fibers during development and exercise responsiveness in adult cardiac muscle. To better understand the role of Ankrd1a in pathological conditions in adult zebrafish, we assessed ankrd1a expression after cardiac ventricle cryoinjury and observed localized upregulation in cardiomyocytes in the border zone. We show that this expression in injured hearts is recapitulated by the TgBAC(ankrd1a:EGFP) reporter. Our results identify novel expression domains of ankrd1a and suggest an important role for Ankrd1a in the early stress response and regeneration of cardiac tissue. This new reporter line will help decipher the role of Ankrd1a in striated muscle stress response, including after cardiac injury.