Genetic compensation: A phenomenon in search of mechanisms

被引:590
作者
El-Brolosy, Mohamed A. [1 ]
Stainier, Didier Y. R. [1 ]
机构
[1] Max Planck Inst Heart & Lung Res, Dept Dev Genet, Bad Nauheim, Germany
关键词
LEUCINE-ZIPPER KINASE; TAU-ANTISENSE OLIGONUCLEOTIDES; OPEN READING FRAMES; DOSAGE COMPENSATION; NONCODING RNAS; FUNCTIONAL REDUNDANCY; TRANSLATIONAL CONTROL; BRAIN-DEVELOPMENT; MAMMALIAN-CELLS; MESSENGER-RNAS;
D O I
10.1371/journal.pgen.1006780
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Several recent studies in a number of model systems including zebrafish, Arabidopsis, and mouse have revealed phenotypic differences between knockouts (i.e., mutants) and knockdowns (e.g., antisense-treated animals). These differences have been attributed to a number of reasons including off-target effects of the antisense reagents. An alternative explanation was recently proposed based on a zebrafish study reporting that genetic compensation was observed in egfl7 mutant but not knockdown animals. Dosage compensation was first reported in Drosophila in 1932, and genetic compensation in response to a gene knockout was first reported in yeast in 1969. Since then, genetic compensation has been documented many times in a number of model organisms; however, our understanding of the underlying molecular mechanisms remains limited. In this review, we revisit studies reporting genetic compensation in higher eukaryotes and outline possible molecular mechanisms, which may include both transcriptional and posttranscriptional processes.
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页数:17
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