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首页> 外文期刊>Journal of cellular biochemistry. >Muscle glycogen synthase isoform is responsible for testicular glycogen synthesis: Glycogen overproduction induces apoptosis in male germ cells
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Muscle glycogen synthase isoform is responsible for testicular glycogen synthesis: Glycogen overproduction induces apoptosis in male germ cells

机译：肌肉糖原合酶同工型负责睾丸糖原的合成：糖原的过量生产诱导雄性生殖细胞凋亡

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Glycogen is the main source of glucose for many biological events. However, this molecule may have other functions, including those that have deleterious effects on cells. The rate-limiting enzyme in glycogen synthesis is glycogen synthase (GS). It is encoded by two genes, GYS1, expressed in muscle (muscle glycogen synthase, MGS) and other tissues, and GYS2, primarily expressed in liver (liver glycogen synthase, LGS). Expression of GS and its activity have been widely studied in many tissues. To date, it is not clear which GS isoform is responsible for glycogen synthesis and the role of glycogen in testis. Using RT-PCR, Western blot and immunofluorescence, we have detected expression of MGS but not LGS in mice testis during development. We have also evaluated GS activity and glycogen storage at different days after birth and we show that both GS activity and levels of glycogen are higher during the first days of development. Using RT-PCR, we have also shown that malin and laforin are expressed in testis, key enzymes for regulation of GS activity. These proteins form an active complex that regulates MGS by poly-ubiquitination in both Sertoli cell and male germ cell lines. In addition, PTG overexpression in male germ cell line triggered apoptosis by caspase3 activation, proposing a proapoptotic role of glycogen in testis. These findings suggest that GS activity and glycogen synthesis in testis could be regulated and a disruption of this process may be responsible for the apoptosis and degeneration of seminiferous tubules and possible cause of infertility.
机译：糖原是许多生物学事件中葡萄糖的主要来源。但是，该分子可能具有其他功能，包括对细胞具有有害作用的那些功能。糖原合成中的限速酶是糖原合酶（GS）。它由两个基因编码，即在肌肉（肌肉糖原合酶，MGS）和其他组织中表达的GYS1和主要在肝脏中表达的肝糖原合酶（LGS）的GYS2。 GS的表达及其活性已在许多组织中得到广泛研究。迄今为止，尚不清楚哪种GS同工型负责糖原合成以及糖原在睾丸中的作用。使用RT-PCR，Western印迹和免疫荧光，我们已经检测到在发育过程中小鼠睾丸MGS的表达，但不是LGS。我们还评估了出生后不同天的GS活性和糖原存储，并且我们发现GS活性和糖原水平在发育的头几天都较高。使用RT-PCR，我们还显示了马林和laforin在睾丸中表达，睾丸是调节GS活性的关键酶。这些蛋白质形成一种活性复合物，可通过支持素细胞和雄性生殖细胞系中的多泛素化作用来调节MGS。此外，雄性生殖细胞系中PTG的过度表达通过caspase3激活触发凋亡，提示糖原在睾丸中具有促凋亡作用。这些发现表明，睾丸中的GS活性和糖原合成可能受到调节，而这一过程的破坏可能是造成曲细精管的细胞凋亡和变性以及不孕的可能原因。

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