Divergent cis-regulatory evolution underlies the convergent loss of sodium channel expression in electric fish

被引:8
作者
LaPotin, Sarah [1 ,6 ]
Swartz, Mary E. [2 ]
Luecke, David M. [3 ]
Constantinou, Savvas J. [3 ,4 ]
Gallant, Jason R. [3 ,4 ]
Eberhart, Johann K. [2 ]
Zakon, Harold H. [1 ,5 ]
机构
[1] Univ Texas Austin, Dept Neurosci, Austin, TX 78712 USA
[2] Univ Texas Austin, Dept Mol Biosci, Austin, TX 78712 USA
[3] Michigan State Univ, Dept Integrat Biol, E Lansing, MI 48824 USA
[4] Michigan State Univ, Ecol Evolut & Behav Program, E Lansing, MI 48824 USA
[5] Univ Texas Austin, Dept Integrat Biol, Austin, TX 78712 USA
[6] Univ Utah, Dept Human Genet, Salt Lake City, UT 84112 USA
基金
美国国家科学基金会; 美国国家卫生研究院;
关键词
SKELETAL-MUSCLE; GENE; MUTATION; ORGAN;
D O I
10.1126/sciadv.abm2970
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
South American and African weakly electric fish independently evolved electric organs from muscle. In both groups, a voltage-gated sodium channel gene independently lost expression from muscle and gained it in the electric organ, allowing the channel to become specialized for generating electric signals. It is unknown how this voltage-gated sodium channel gene is targeted to muscle in any vertebrate. We describe an enhancer that selectively targets sodium channel expression to muscle. Next, we demonstrate how the loss of this enhancer, but not trans-activating factors, drove the loss of sodium channel gene expression from muscle in South American electric fish. While this enhancer is also altered in African electric fish, key transcription factor binding sites and enhancer activity are retained, suggesting that the convergent loss of sodium channel expression from muscle in these two electric fish lineages occurred via different processes.
引用
收藏
页数:7
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