Cell growth and/or proliferation may require the reprogramming of metabolic pathways, whereby a switch from oxidative to glycolytic metabolism diverts glycolytic intermediates towards anabolic pathways. Herein, we identify a novel role for TRIM32 in the maintenance of glycolytic flux mediated by biochemical interactions with the glycolytic enzymes Aldolase and Phosphoglycerate mutase. Loss of Drosophila TRIM32, encoded by thin (tn), shows reduced levels of glycolytic intermediates and amino acids. This altered metabolic profile correlates with a reduction in the size of glycolytic larval muscle and brain tissue. Consistent with a role for metabolic intermediates in glycolysis-driven biomass production, dietary amino acid supplementation in tn mutants improves muscle mass. Remarkably, TRIM32 is also required for ectopic growth - loss of TRIM32 in a wing disc-associated tumor model reduces glycolytic metabolism and restricts growth. Overall, our results reveal a novel role for TRIM32 for controlling glycolysis in the context of both normal development and tumor growth.

中文翻译：

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果蝇TRIM32与糖酵解酶共同促进细胞生长。

细胞生长和/或增殖可能需要重新编程代谢途径，从而从氧化代谢转变为糖酵解代谢会将糖酵解中间体转移至合成代谢途径。在本文中，我们确定了TRIM32在维持糖酵解通量中的新作用，该糖酵解通量是由与糖酵解酶醛缩酶和磷酸甘油酸突变酶的生化相互作用介导的。的损失果蝇TRIM32，由编码薄（TN） ，示出了降低的糖酵解中间体和氨基酸的水平。这种改变的代谢特征与糖酵解幼虫肌肉和脑组织的大小减少有关。与糖酵解驱动的生物质生产中代谢中间体的作用，TN中膳食氨基酸的补充突变体改善肌肉质量。值得注意的是，异位生长也需要TRIM32-在与翼盘相关的肿瘤模型中TRIM32的缺失会降低糖酵解代谢并限制其生长。总的来说，我们的结果揭示了TRIM32在正常发育和肿瘤生长的背景下控制糖酵解的新作用。