Mitochondrial transfer RNA modifications in normal and stressed hematopoiesis

我们建立了造血特异性MTO1基因敲除小鼠(VaV-iCre：MTO1KO)，发现KO小鼠因严重贫血而胚胎死亡。胚胎中的造血干细胞数量发生了明显的变化。红细胞造血祖细胞分析未显示造血祖细胞水平有任何缺陷。为了进一步研究其机制，我们还建立了他莫昔芬诱导的HSC特异性条件性MTO1基因敲除小鼠(HLF-CRE ERT2：MTO1 CKO)，并将很快对这些小鼠进行分析。此外，为了研究MTO1在HSC生态位中的作用，我正在培育生态位特异性MTO1基因敲除小鼠(Lepr cre：MTO1KO)。在细胞和分子水平上对这些小鼠模型的综合分析将描绘出正常和应激造血中新的角色转移RNA修饰。

We generated hematopoiesis specific MTO1 knock out mice (vav-iCre: MTO1 KO) and found that the KO mice was embryonic lethal due to severe anemia. Hematopoietic stem cell population was changed significantly in the embryos. Erythrocyte progenitors analysis did not showed any defect in the progenitor level. To study the mechanisms further, we also generated tamoxifen inducible HSC specific conditional MTO1 knock out mice (Hlf-Cre ERT2: MTO1 cKO) and will analyze these mice very soon. Furthermore, to study the role of MTO1 in HSC niche, i am generating niche specific MTO1 knock out mice (LepR cre: MTO1 KO). Comprehensive analysis of these mouse models at cellular and molecular level will delineate the novel role transfer RNA modifications in normal and stressed hematopoiesis.