Molecular cloning, characterization, and tissue distribution of c-Myc from blood clam Tegillarca granosa and its role in cadmium-induced stress response.

Molecular cloning, characterization, and tissue distribution of c-Myc from blood clam Tegillarca granosa and its role in cadmium-induced stress response.
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DOI:
10.1016/j.gene.2022.146611
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发表时间:
2022-05
期刊:
影响因子:
3.5
通讯作者:
Defeng Zhao;Min Li;Guo-qiang Xiao;Jianshe Zhang;Shuangshuang Teng
Defeng Zhao;Min Li;Guo-qiang Xiao;Jianshe Zhang;Shuangshuang Teng
中科院分区:
生物学3区
文献类型:
--
作者:
Defeng Zhao;Min Li;Guo-qiang Xiao;Jianshe Zhang;Shuangshuang Teng

文献摘要

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镉(Cd)污染对血蛤泥蚶(tegillarca granosa, T。在中国东海沿海地区。血蛤对镉胁迫反应和解毒的分子机制尚不清楚。在本研究中,全长t。首次克隆到granosac-Myc (Tgc-Myc) cDNA。全长3063 bp的cDNA由一个129 bp的5 ‘未翻译区(UTR)、一个1746 bp的3 ’未翻译区和一个1188 bp的开放阅读框组成,编码395个氨基酸残基的预测蛋白。预测得到的蛋白分子量为44.9 kDa,等电点为6.82。预测的蛋白含有一个n端转激活域和一个c端碱性螺旋-环-螺旋亮氨酸拉链域,这是c-Myc蛋白的保守功能域。Tgc-Myc在血蛤中组织分布广泛,在鳃和肝胰腺中表达量最高。东海沿海地区主要重金属污染物Cd暴露可诱导鳃组织中Tgc-Myc表达。Tgc-Myc基因敲低导致cd污染海水中养殖的血蛤多种应激反应/解毒基因表达减少。Tgc-Myc敲低也导致igf1r表达降低,igf1r是一种促进细胞增殖的原癌基因。这些结果表明,Tgc-Myc调节cd诱导的血蛤应激反应和解毒。Tgc-Myc的上调可以作为一种方法,产生具有增强解毒反应的菌株,从而降低重金属积累。
Cadmium (Cd) pollution threatens the cultivation of the blood clamTegillarca granosa(T. granosa) in coastal regions of the East China Sea. The molecular mechanisms regulating Cd stress response and detoxification in blood clams are largely unclear. In the present study, the full-lengthT. granosac-Myc (Tgc-Myc) cDNA was cloned for the first time. The 3063-bp cDNA consisted of a 129-bp 5′ untranslated region (UTR), a 1746-bp 3′ UTR, and a 1188-bp open reading frame encoding a predicted protein of 395 amino acid residues. The predicted protein had a calculated molecular weight of 44.9 kDa and an estimated isoelectric point of 6.82. The predicted protein contained an N-terminal transactivation domain and a C-terminal basic helix-loop-helix leucine zipper domain, which are conserved functional domains of c-Myc proteins. Tgc-Myc showed broad tissue distribution in blood clams, with the highest expression detected in the gill and hepatopancreas. Exposure to Cd, a major heavy metal pollutant in coastal regions of the East China Sea, induced Tgc-Myc expression in gill tissues. Tgc-Myc knockdown led to reduced expression of a variety of stress response/detoxification genes in blood clams cultivated in Cd-contaminated seawater. Tgc-Myc knockdown also led to decreased expression ofIGF1R, a proto-oncogene that promotes cell proliferation. These findings indicated that Tgc-Myc regulates Cd-induced stress response and detoxification in blood clams. The upregulation of Tgc-Myc may serve as an approach to generate strains with an enhanced detoxification response and consequently a low heavy metal buildup.