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据2016年4月23日《中国科学报》报道,中科院生物物理所秦燕研究组与中科院动物所、军事医学科学院以及天津科技大学等合作,构建了全身性mtEF4基因敲除鼠,发现mtEF4基因敲除引起雄性小鼠生殖细胞氧化磷酸化功能受损,从而导致雄性不育。进一步研究发现,mtEF4敲除后,线粒体蛋白质翻译速率增加,但代价是蛋白质“合格率”下降,新生成的蛋白质“寿命”变短。体细胞通过激活mTOR信号
According to a report in the China Science Newspaper on April 23, 2016, the Qin Yan Research Group, Institute of Biophysics, Chinese Academy of Sciences, in collaboration with the Institute of Zoology, the Academy of Military Medical Sciences and Tianjin University of Science and Technology, established a systemic mtEF4 knockout mouse and found that the mtEF4 gene Knockout causes impaired oxidative phosphorylation of germ cells in male mice resulting in male infertility. Further study found that, mtEF4 knockout, mitochondrial protein translation rate increased, but at the expense of protein “pass rate ” decreased, the newly generated protein “life span ” shorter. Somatic cells activate mTOR signaling