Key result
Strong Lifeact-GFP expression in cardiomyocytes disrupted F-actin filament organization, leading to pericardial edema and early embryonic lethality in transgenic zebrafish.
Why the study?
To investigate the effect of Lifeact-GFP on heart development and evaluate its application for studying cardiomyopathy in transgenic zebrafish.
High levels of Lifeact-GFP expression in transgenic zebrafish cardiomyocytes disrupt F-actin organization and cause early embryonic lethality, highlighting the need to carefully evaluate transgenic models for probe-induced artifacts.
Lifeact-GFP is a frequently used molecular probe to study F-actin structure and dynamic assembly in living cells. In this study, we generated transgenic zebrafish models expressing Lifeact-GFP specifically in cardiac muscles to investigate the effect of Lifeact-GFP on heart development and its application to study cardiomyopathy. The data showed that transgenic zebrafish with low to moderate levels of Lifeact-GFP expression could be used as a good model to study contractile dynamics of actin filaments in cardiac muscles in vivo. Using this model, we demonstrated that loss of Smyd1b, a lysine methyltransferase, disrupted F-actin filament organization in cardiomyocytes of zebrafish embryos. Our studies, however, also demonstrated that strong Lifeact-GFP expression in cardiomyocytes was detrimental to actin filament organization in cardiomyocytes that led to pericardial edema and early embryonic lethality of zebrafish embryos. Collectively, these data suggest that although Lifeact-GFP is a good probe for visualizing F-actin dynamics, transgenic models need to be carefully evaluated to avoid artifacts induced by Lifeact-GFP overexpression.
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Xu et al. (2021) studied Cardiomyopathy. Lifeact-GFP overexpression vs. Low-expressing transgenic zebrafish or wildtype was evaluated on F-actin filament organization and cardiac function. Strong Lifeact-GFP expression in cardiomyocytes disrupted F-actin filament organization, leading to pericardial edema and early embryonic lethality in transgenic zebrafish.
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