Abstract
Drosophila melanogaster, a classical genetic model organism, is widely used in the field of research on cardiac development and pathophysiological changes. Drosophila Lmpt, a LIM domain protein, is highly homologous to the vertebrate Fhl2. Fhl2 mutations cause heart failure, but the molecular mechanism is still unclear. Firstly, we prepared Lmpt polyclonal antibody and detected the expression of endogenous Lmpt in Drosophila muscle tissue and myocardial tissue, suggested Lmpt may play a role in Drosophila heart tissue. Secondly, We constructed Lmpt knockout drosophila by CRISPR/Cas9 system, the Lmpt knockout homozygous were lethal in embryonic stage, and showed absence and disorder of myocardial cells, indicated that Drosophila Lmpt regulates heart development. Thirdly, we found that the expression of Lmpt was down-regulated in dmef2 knockdown Drosophila. Lastly, Lmpt interacted with Mlp84B. We speculated that Drosophila Lmpt might participate in cardiac development through the dmef2-Lmpt/Mlp84B molecular pathway. This research provides a foundation and points out a new direction for the functional study of Lmpt in heart tissue.
