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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Selenoprotein TRXR-1 and GSR-1 are essential for removal of old cuticle during molting in Caenorhabditis elegans
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Selenoprotein TRXR-1 and GSR-1 are essential for removal of old cuticle during molting in Caenorhabditis elegans

机译：硒蛋白线虫的蜕皮过程中硒蛋白TRXR-1和GSR-1是必不可少的

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摘要

Selenoproteins, in particular thioredoxin reductase, have been implicated in countering oxidative damage occurring during aging but the molecular functions of these proteins have not been extensively investigated in different animal models. Here we demonstrate that TRXR-1 thioredoxin reductase, the sole selenoprotein in Caenorhabditis elegans, does not protect against acute oxidative stress but functions instead together with GSR-1 gluta-thione reductase to promote the removal of old cuticle during molting. We show that the oxidation state of disulfide groups in the cuticle is tightly regulated during the molting cycle, and that when trxr-1 and gsr-1 function is reduced, disulfide groups in the cuticle remain oxidized. A selenocysteine-to-cysteine TRXR-1 mutant fails to rescue molting defects. fuerthermore, worms lacking SELB-1, the C. elegans homolog of Escherichia coli SelB or mammalian EFsec, a translation elongation factor known to be specific for selenocysteine in £. coli, fail to incorporate selenocysteine, and display the same phenotype as those lacking trxr-1. Thus, TRXR-1 function in the reduction of old cuticle is strictly selenocysteine dependent in the nematode. Exogenously supplied reduced gluta-thione reduces disulfide groups in the cuticle and induces apolysis, the separation of old and new cuticle, strongly suggesting that molting involves the regulated reduction of cuticle components driven by TRXR-1 and GSR-1. Using dauer larvae, we demonstrate that aged worms have a decreased capacity to molt, and decreased expression of GSR-1. Together, our results establish a function for the selenoprotein TRXR-1 and GSR-1 in the removal of old cuticle from the surface of epidermal cells.
机译：硒蛋白，特别是硫氧还蛋白还原酶，已被认为可抵抗衰老过程中发生的氧化损伤，但尚未在不同的动物模型中广泛研究这些蛋白的分子功能。在这里，我们证明TRXR-1硫氧还蛋白还原酶是秀丽隐杆线虫中的唯一硒蛋白，不能防御急性氧化应激，而是与GSR-1谷胱甘肽还原酶一起起作用，以促进蜕皮过程中旧表皮的去除。我们表明，在蜕皮周期中，表皮中的二硫基团的氧化状态受到严格调节，并且当trxr-1和gsr-1的功能降低时，表皮中的二硫基团仍然被氧化。硒代半胱氨酸到半胱氨酸的TRXR-1突变体无法挽救蜕皮缺陷。此外，蠕虫缺乏SELB-1，即大肠杆菌SelB的秀丽隐杆线虫同源物或哺乳动物EFsec，后者是已知对硒代半胱氨酸具有特异性的翻译延伸因子。大肠埃希菌，不能掺入硒代半胱氨酸，并且表现出与缺乏trxr-1相同的表型。因此，TRXR-1在减少旧表皮中的功能严格依赖于线虫中的硒代半胱氨酸。外源供应的还原性谷氨硫酮减少了表皮中的二硫键基团并诱导了溶融作用，即新旧表皮的分离，强烈表明蜕皮涉及TRXR-1和GSR-1驱动的表皮成分的调节还原。使用道尔幼虫，我们证明了老化的蠕虫的蜕皮能力下降，而GSR-1的表达下降。在一起，我们的结果建立了硒蛋白TRXR-1和GSR-1在从表皮细胞表面清除旧表皮的功能。

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    Joergen Stenvall; Juan Carlos Fierro-Gonzalez; Peter Swoboda; Karunakar Saamarthy; Qing Cheng; Briseida Cacho-Valadez; Elias S. J. Arner; Olof P. Persson; Antonio Miranda-Vizuete; Simon Tuck;

  • 作者单位

    Department of Molecular Biology , Umea University, SE-901 87 Umea, Sweden,Umea Center for Molecular Medicine, Umea University, SE-901 87 Umea, Sweden;

    Karolinska Institute, Department of Biosciences and Nutrition, Soedertoern University College, School of Life Sciences, SE-14157 Huddinge, Sweden;

    Karolinska Institute, Department of Biosciences and Nutrition, Soedertoern University College, School of Life Sciences, SE-14157 Huddinge, Sweden,Karolinska Institute Center for Biosciences at NOVUM, Department of Biosciences and Nutrition, Halsovagen 7, SE-141 83 Huddinge, Sweden;

    Umea Center for Molecular Medicine, Umea University, SE-901 87 Umea, Sweden;

    Division of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolinska Institute, SE-171 77 Stockholm, Sweden;

    Centro Andaluz de Biologia del Desarrollo (CABD-CSIC), Departmento de Fisiologia, Anatomia y Biologfa Celular, Universidad Pablo de Olavide, E-41013 Sevilla, Spain;

    Division of Biochemistry, Department of Medical Biochemistry and Biophysics, Karolinska Institute, SE-171 77 Stockholm, Sweden;

    Department of Molecular Biology , Umea University, SE-901 87 Umea, Sweden,Max Planck Institute for Plant Breeding Research, Carl-von-Linne-Weg 10, D-50829 Cologne, Germany;

    Centro Andaluz de Biologia del Desarrollo (CABD-CSIC), Departmento de Fisiologia, Anatomia y Biologfa Celular, Universidad Pablo de Olavide, E-41013 Sevilla, Spain,Instituto de Biomedicina de Sevilla, Hospital Universitario Virgen del Rocio/CSIC/Universidad de Sevilla, E-41013 Sevilla, Spain;

    Umea Center for Molecular Medicine, Umea University, SE-901 87 Umea, Sweden;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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