Actin and myosin isoforms in aneural and malformed chick hearts.
Although it is generally accepted that actin and myosin isoforms adapt to their functional requirements, the sequence of expression of these proteins in hearts developing abnormally is unknown. In the chick embryo it is possible to change various aspects of heart development without direct manipulation of the cardiovascular system, by removing various regions of the neural crest from early embryos. The neural crest provides both neural (sympathetic and parasympathetic) and ectomesenchymal components to the heart, and selective removal of various areas results in embryos with sympathetically aneural hearts, or persistent truncus arteriosus with or without parasympathetic denervation. Myosin isoform expression was studied in each of these types of hearts using an array of myosin antibodies specific for atrium, ventricle or the conduction system. Myosin expression in experimental hearts was found to follow the normal pattern of development using these antibodies. Actin expression was studied using cDNA probes for the 3' untranslated region of actin mRNA of the alpha-skeletal, alpha-cardiac and beta-actin isoforms. Using slot-blot hybridization analysis, the pattern of actin expression in atrium and ventricle was followed throughout the period of incubation in normal hearts. The pattern of actin expression was found to be abnormal in hearts which were sympathetically aneural and those which had persistent truncus arteriosus combined with parasympathetic denervation. ATPase activity was increased only in atria of hearts with persistent truncus arteriosus. It appears from these experiments that actin isoform expression is influenced in the chick heart by autonomic innervation.
Kirby
M L
ML
Department of Anatomy, Medical College of Georgia, Augusta 30912-2000.
Shimizu
N
N
Gagnon
J
J
Toyofuku
T
T
Kennedy
J
J
Conrad
D C
DC
Zak
R
R
D000199:Actins / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D002642:Chick Embryo; D003714:Denervation; D006321:Heart / Q000294:innervation; D006330:Heart Defects, Congenital / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D009218:Myosins / Q000378:metabolism*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism
D000199:Actins; D012333:RNA, Messenger; D009218:Myosins