The Ufm1-activating enzyme Uba5 is indispensable for erythroid differentiation in mice

Kanako Tatsumi, Harumi Yamamoto-Mukai, Ritsuko Shimizu, Satoshi Waguri, Yu-Shin Sou, Ayako Sakamoto, Choji Taya, Hiroshi Shitara, Takahiko Hara, Chin Ha Chung, Keiji Tanaka, Masayuki Yamamoto () and Masaaki Komatsu ()
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Kanako Tatsumi: Protein Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Kamikitazawa 2-1-6
Harumi Yamamoto-Mukai: Tohoku University Graduate School of Medicine
Ritsuko Shimizu: Tohoku University Graduate School of Medicine
Satoshi Waguri: Fukushima Medical University School of Medicine, 1 Hikarigaoka, Fukushima 960-1295, Japan.
Yu-Shin Sou: Protein Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Kamikitazawa 2-1-6
Ayako Sakamoto: Protein Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Kamikitazawa 2-1-6
Choji Taya: Laboratory of Mouse Models for Human Heritable Diseases, Tokyo Metropolitan Institute of Medical Science, Kamikitazawa 2-1-6
Hiroshi Shitara: Laboratory of Mouse Models for Human Heritable Diseases, Tokyo Metropolitan Institute of Medical Science, Kamikitazawa 2-1-6
Takahiko Hara: Stem Cell Project, Tokyo Metropolitan Institute of Medical Science, Kamikitazawa 2-1-6
Chin Ha Chung: School of Biological Science, Seoul National University
Keiji Tanaka: Protein Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Kamikitazawa 2-1-6
Masayuki Yamamoto: Tohoku University Graduate School of Medicine
Masaaki Komatsu: Protein Metabolism Project, Tokyo Metropolitan Institute of Medical Science, Kamikitazawa 2-1-6

Nature Communications, 2011, vol. 2, issue 1, 1-7

Abstract: Abstract Post-translational protein modifications are systems designed to expand restricted genomic information through functional conversion of target molecules. Ubiquitin-like post-translational modifiers regulate numerous cellular events through their covalent linkages to target protein(s) by an enzymatic cascade analogous to ubiquitylation consisting of E1 (activating), E2 (conjugating) and E3 (ligating) enzymes. In this study, we report the essential role of Uba5, a specific activating enzyme for the ubiquitin-like modifier, Ufm1, in erythroid development. Mice lacking Uba5 exhibited severe anaemia, followed by death in utero. Although Uba5 was dispensable for the production of erythropoietin, its genetic loss led to impaired development of megakaryocyte and erythroid progenitors from common myeloid progenitors. Intriguingly, transgenic expression of Uba5 in the erythroid lineage rescued the Uba5-deficient embryos from anaemia and prolonged their survival, demonstrating the importance of Uba5 in cell-autonomous erythroid differentiation. Our results suggest that one of the ubiquitin-like protein modification systems, the Ufm1 system, is involved in the regulation of haematopoiesis.

Date: 2011
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DOI: 10.1038/ncomms1182

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