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首页> 外文期刊>American Journal of Physiology >Steady-state effects of temperature acclimation on the transcriptome of the rainbow trout heart.
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Steady-state effects of temperature acclimation on the transcriptome of the rainbow trout heart.

机译：温度适应对虹鳟心脏转录组的稳态影响。

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摘要

Cold-acclimated (CA) phenotype of trout heart was induced by 4-wk acclimation at 4 degrees C and was characterized by 32.7% increase in relative heart mass and 49.8% increase in ventricular myocyte size compared with warm-acclimated (WA; 18 degrees C) fish (P < 0.001). Effect of temperature acclimation on transcriptome of the rainbow trout heart was examined using species-specific microarray chips containing 1,380 genes. After 4 wk of temperature acclimation, 8.8% (122) of the genes were differently expressed in CA and WA hearts, and most of them (82%) were upregulated in the cold (P < 0.01). Transcripts of genes engaged in protein synthesis and intermediary metabolism were most strongly upregulated, whereas genes contributing to the connective tissue matrix were clearly repressed. Extensive upregulation of the genes coding for ribosomal proteins and translation elongation and initiation factors suggest that the protein synthesis machinery of the trout heart is enhanced in the cold and is an essential part of the compensatory mechanism causing and maintaining the hypertrophy of cardiac myocytes. The prominent depression of collagen genes may be indicative of a reduced contribution of extracellular matrix to the remodeling of the CA fish heart. Temperature-related changes in transcripts of metabolic enzymes suggest that at mRNA level, glycolytic energy production from carbohydrates is compensated in the heart of CA rainbow trout, while metabolic compensation is absent in mitochondria. In addition, the analysis revealed three candidate genes: muscle LIM protein, atrial natriuretic peptide B, and myosin light chain 2, which might be central for induction and maintenance of the hypertrophic phenotype of the CA trout heart. These findings indicate that extensive modification of gene expression is needed to maintain the temperature-specific phenotype of the fish heart.
机译：鳟鱼心脏在4°C的4 wk适应下会产生冷适应（CA）表型，与热适应（WA; 18度）相比，其相对心脏质量增加32.7％，心室心肌细胞大小增加49.8％ C）鱼（P <0.001）使用包含1,380个基因的物种特异性微阵列芯片，研究了温度适应对虹鳟心脏转录组的影响。温度适应4周后，CA和WA心脏中有8.8％（122）个基因差异表达，其中大多数（82％）在寒冷中上调（P <0.01）。参与蛋白质合成和中间代谢的基因的转录物被最强烈地上调，而有助于结缔组织基质的基因被明显抑制。编码核糖体蛋白的基因的广泛上调以及翻译延伸和起始因子表明，鳟鱼心脏的蛋白质合成机制在寒冷时会增强，并且是引起和维持心肌细胞肥大的补偿机制的重要组成部分。胶原基因的显着降低可能表明细胞外基质对CA鱼心脏重塑的贡献减少。代谢酶转录物的温度相关变化表明，在mRNA水平上，CA虹鳟鱼的心脏补偿了碳水化合物产生的糖酵解能，而线粒体则缺乏代谢补偿。此外，该分析还揭示了三个候选基因：肌肉LIM蛋白，心房利钠肽B和肌球蛋白轻链2，这可能是诱导和维持CA鳟鱼心脏肥大表型的关键。这些发现表明，需要维持基因表达的大量修饰，以维持鱼心的温度特异性表型。

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