2018 Fiscal Year Annual Research Report
Mitochondrial transfer RNA modifications in normal and stressed hematopoiesis
Project/Area Number |
18K16124
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Research Institution | Kumamoto University |
Principal Investigator |
FAKRUDDIN MD 熊本大学, 国際先端医学研究機構, 特定事業研究員 (20816475)
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Project Period (FY) |
2018-04-01 – 2019-03-31
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Keywords | mitochondria / tRNA modification / Hematopoiesis |
Outline of Annual Research Achievements |
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.
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