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The role of non‐muscle myosin II in early chick morphogenesis
Author(s) -
Hoang My,
ChuLaGraff Quynh
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.557.4
Subject(s) - myosin , embryonic heart , verapamil , actin , heartbeat , chemistry , biophysics , microbiology and biotechnology , biology , anatomy , biochemistry , calcium , embryonic stem cell , gene , organic chemistry , computer security , computer science
Cardiac looping, a highly conserved feature of vertebrate embryonic heart development, comprises of two phases: c‐looping and s‐looping. This process involves the transformation of the relatively straight heart tube into a distinct c‐shaped, then an s‐shaped loop. A previous study indicated that contraction involving muscle myosin and non‐muscle myosin II plays a minor role in the bending component of the first phase of cardiac looping, c‐looping. Here, we investigated whether myosin‐based contraction was necessary for the second phase of cardiac looping, s‐looping. We treated whole, cultured chick embryos with Verapamil, an L‐type channel inhibitor, to block actin‐myosin binding. Verapamil treatment induced heartbeat cessation, cardiac swelling, abnormal actin distribution, and unsuccessful s‐looping. Using Y‐27632, a ROCK inhibitor, to directly inhibit myosin‐based contractions, we showed that cardiac swelling was not a physical constraint that hindered s‐looping. Y‐27632 treated embryos experienced sustained heartbeat, growth retardation, and arrested s‐looping. We will further quantify the levels of non‐myosin and other proteins in the Rho‐ROCK signaling pathway to determine the mechanism that mediates s‐looping.