Cardiac performance in the zebrafish breakdance mutant

被引:71
作者
Kopp, R
Schwerte, T
Pelster, B [1 ]
机构
[1] Univ Innsbruck, Inst Zool & Immunol, A-6020 Innsbruck, Austria
[2] Univ Innsbruck, Ctr Mol Biosci, A-6020 Innsbruck, Austria
关键词
Breakdance mutation; cardiac activity; temperature; development; cardiac arrhythmia; zebrafish; Danio rerio;
D O I
10.1242/jeb.01620
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
In the Tubingen screen a break-dance mutant of zebrafish (bre) was described as an arrhythmia, in which the ventricle beats only with every second atrial contraction (2:1 rhythm). Surprisingly, a careful analysis of the effect of the breakdance mutation on cardiac performance of the zebrafish during development between 3 d.p.f. and 14 d.p.f revealed that homozygous bre mutants did not always show the 2:1 rhythm. Cardiac activity was continuously recorded for a period of 20 min in each larva, and during this period we observed that heart rate randomly switched between the 2:1 rhythm and a 1:1 rhythm. Furthermore, at 28 degrees C and at 31 degrees C the expression of the 2:1 rhythm decreased with development. At 31 degrees C this was in part due to a significantly reduced survival rate of mutants beyond 4 d.p.f. Besides development, temperature had a marked effect on the expression of the 2:1 rhythm, and during the first days of development the expression of the 2:1 rhythm was significantly higher at elevated incubation temperatures. By contrast, in the 2:1 beating heart ventricular contraction rate was about 80 beats min(-1) throughout development irrespective of the temperature, and even in the 1:1 rhythm mutants showed a significant bradycardia at all three temperatures (25 degrees C, 28 degrees C or 31 degrees C). Compared to wild-type animals, cardiac output was significantly lower in bre mutants. Pressure traces recorded in the ventricle of mutants revealed a prolonged relaxation phase, indicating that the second pacemaker current could not be conveyed to the ventricle (AV-block). This phenotype is comparable to the human Long QT Syndrome, an arrhythmia caused by a modification of an ion channel involved in cardiac repolarization. The bradycardia and the modified temperature sensitivity of heart rate suggested that the activity of the pacemaker cells was also affected by this mutation.
引用
收藏
页码:2123 / 2134
页数:12
相关论文
共 37 条
[1]  
Alexander J, 1998, DEV GENET, V22, P288, DOI 10.1002/(SICI)1520-6408(1998)22:3<288::AID-DVG10>3.0.CO
[2]  
2-2
[3]  
Alexander J, 1999, HEART DEV, P91
[4]   Defective ''pacemaker'' current (I-h) in a zebrafish mutant with a slow heart rate [J].
Baker, K ;
Warren, KS ;
Yellen, G ;
Fishman, MC .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1997, 94 (09) :4554-4559
[5]   O2 consumption and heart rate in developing zebrafish (Danio rerio):: influence of temperature and ambient O2 [J].
Barrionuevo, WR ;
Burggren, WW .
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 1999, 276 (02) :R505-R513
[6]   α1H mRNA in single skeletal muscle fibres accounts for T-type calcium current transient expression during fetal development in mice [J].
Berthier, C ;
Monteil, A ;
Lory, P ;
Strube, C .
JOURNAL OF PHYSIOLOGY-LONDON, 2002, 539 (03) :681-691
[7]  
BURGGREN WW, 1994, CARDIOSCIENCE, V5, P183
[8]  
Chen Jau-Nian, 1997, P7
[9]  
Chen JN, 1996, DEVELOPMENT, V123, P293
[10]   DEVELOPMENTAL TEMPERATURE SELECTIVELY REGULATES A VOLTAGE-ACTIVATED POTASSIUM CURRENT IN DROSOPHILA [J].
CHOPRA, M ;
SINGH, S .
JOURNAL OF NEUROBIOLOGY, 1994, 25 (02) :119-126