Coronary vessel development is a highly coordinated process during heart formation. Abnormal development and dysfunction of coronary network contribute to majority of heart disease. Understanding molecular mechanisms that regulate coronary formation is critical for preventing and treating the disease. We report here a zebrafish gene-trap vinculin b (vclb) mutant that displays abnormal coronary vessel development among multiple cardiac defects. The mutant has over-proliferated epicardium derived cells and disorganization of coronary vessels, eventually die off at juvenile stages. Mechanistically, vclb deficiency results in release of another cytoskeletal protein Paxillin from the Vclb complex and up-regulation of ERK and FAK phosphorylation in epicardium and endocardium, causing disorganization of endothelial cells and pericytes during coronary vessel development. On the other hand, cardiac muscle development is relatively normal, likely due to redundant function of Vcla, a vinculin paralog that is expressed in the myocardium but not the epicardium. Together, our results reveal a previously unappreciated function of Vinculin in epicardium and endocardium and reinforce a notion that well-balanced FAK activity is essential for coronary vessel development.