Mitochondrial transfer RNA modifications in normal and stressed hematopoiesis

我们产生了造血特异性MTO 1敲除小鼠（vav-iCre：MTO 1 KO），并发现KO小鼠由于严重贫血而具有胚胎致死性。胚胎造血干细胞数量发生了显著变化。红细胞祖细胞分析未显示祖细胞水平的任何缺陷。为了进一步研究机制，我们还产生了他莫昔芬诱导的HSC特异性条件性MTO 1敲除小鼠（Hlf-Cre ERT 2：MTO 1 cKO），并将很快分析这些小鼠。此外，为了研究MTO 1在HSC小生境中的作用，我正在产生小生境特异性MTO 1敲除小鼠（LepR cre：MTO 1 KO）。这些小鼠模型在细胞和分子水平的综合分析将描绘新的作用转移RNA修饰在正常和应激造血。

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.