Key result
The Sema3a-CreERT2 knock-in mouse line specifically targets Purkinje fibres in the adult heart, labeling approximately 1% of cardiomyocytes, with fate determination occurring in the perinatal stage.
Absolute Event Rate: 1.02% vs 0%
The Sema3a-CreERT2 mouse line provides a specific genetic tool for targeting Purkinje fibres, enabling future studies on the ventricular conduction system and arrhythmias.
Provides genetic tool for murine Purkinje studies; leaves open translation to human conduction disorders.
The maintenance of the heart rhythm and the conduction of excitatory signals require changing excitatory signals via electrical activity and coordination by communication between working and conductive cardiomyocytes. Understanding how the ventricular conduction system is established provides novel insights into the pathophysiological progress of cardiac arrhythmias. However, the major hurdle in this field is the lack of a specific genetic tool that targets the Purkinje fibres of the ventricular conduction system and no other types of cardiomyocytes or coronary vessels. Here, we generated a Sema3a-CreERT2 knock-in mouse line to test its specificity for genetically labelled Purkinje fibres. We found that Sema3a was expressed in the subendocardial layer of the trabecular myocardium in the embryonic heart and was restricted to the Purkinje fibres in the adult heart. A fate mapping study based on the Sema3a-CreERT2 line revealed that the Sema3a+ cardiomyocytes were restricted to the fate of Purkinje fibres in the perinatal but not the embryonic stage. Collectively, our study provides a new genetic tool, i.e., Sema3a-CreERT2, for studying the molecular mechanisms that regulate the function of Purkinje fibres.
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Li et al. (2018) studied this question. Sema3a-CreERT2 knock-in vs. Wild-type littermates or un-induced controls was evaluated on Percentage of cardiomyocytes labelled with Sema3a-CreERT2; R26-tdTomato in adult mouse hearts. The Sema3a-CreERT2 knock-in mouse line specifically targets Purkinje fibres in the adult heart, labeling approximately 1% of cardiomyocytes, with fate determination occurring in the perinatal stage.
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