十一氨基转移酶(TET)蛋白质最近被发现是多细胞生物中重要的表观遗传调控因子。啮齿动物中的TET knockdown研究突显出这些蛋白质对大脑的正确发育和功能起着关键作用。哺乳动物中mTET蛋白质和mTET2特别是在白血病和胶质瘤中经常发生突变和失调。因此，我们检查了果蝇(Drosophila melanogaster)幼虫血细胞和成年头部中mTET2在肿瘤发生中的作用。我们的发现显示，突变和野生型mTET2的表达导致成年果蝇普遍表型缺陷和腹部黑色质团的积累。值得注意的是，携带mTET2-R43G突变体的果蝇在mTET2的N-端表现出运动和昼夜节律行为缺陷以及寿命减少。携带催化结构域中的mTET2-R1261C突变，这是一种急性髓性白血病(AML)中常见的突变，影响了血细胞止血功能的变化。使用转录组方法，我们发现在果蝇头部上调免疫基因,这些基因不仅出现在TET2突变体中，而且在野生型mTET2的果蝇中也有发现。此外，抑制mTET2突变体中发现的基因(例如那些参与免疫途径、自噬和转录调节等方面的基因)的表达，导致果蝇存活力、行为和血细胞数的恢复。本研究确定了野生型mTET2与mTET2突变体(催化性与非催化性)的转录组谱，表明TET2在正常中枢神经系统(CNS)功能和先天免疫方面的角色。

Ten-Eleven Translocation (TET) proteins have recently come to light as important epigenetic regulators conserved in multicellular organisms. TET knockdown studies in rodents have highlighted the critical role of these proteins for proper brain development and function. Mutations in mammalian mTET proteins and mTET2 specifically are frequent and deregulated in leukaemia and glioma respectively. Accordingly, we examined the role of mTET2 in tumorigenesis in larval haemocytes and adult heads in Drosophila melanogaster. Our findings showed that expression of mutant and wild type mTET2 resulted in general phenotypic defects in adult flies and accumulation of abdominal melanotic masses. Notably, flies with mTET2-R43G mutation at the N-terminus of mTET2 exhibited locomotor and circadian behavioural deficits, as well as reduced lifespan. Flies with mTET2-R1261C mutation in the catalytic domain, a common mutation in acute myeloid leukaemia (AML), displayed alterations affecting haemocyte haemostasis. Using transcriptomic approach, we identified upregulated immune genes in fly heads that were not exclusive to TET2 mutants but also found in wild type mTET2 flies. Furthermore, inhibiting expression of genes that were found to be deregulated in mTET2 mutants, such as those involved in immune pathways, autophagy, and transcriptional regulation, led to a rescue in fly survival, behaviour, and hemocyte number. This study identifies the transcriptomic profile of wild type mTET2 versus mTET2 mutants (catalytic versus non-catalytic) with indications of TET2 role in normal central nervous system (CNS) function and innate immunity.