NAA10 controls osteoblast differentiation and bone formation as a feedback regulator of Runx2

Haejin Yoon, Hye-Lim Kim, Yang-Sook Chun, Dong Hoon Shin, Kyoung-Hwa Lee, Chan Soo Shin, Dong Yeon Lee, Hong-Hee Kim, Zang Hee Lee, Hyun-Mo Ryoo, Mi-Ni Lee, Goo Taeg Oh () and Jong-Wan Park ()
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Haejin Yoon: Seoul National University College of Medicine
Hye-Lim Kim: Seoul National University College of Medicine
Yang-Sook Chun: Seoul National University College of Medicine
Dong Hoon Shin: Seoul National University College of Medicine
Kyoung-Hwa Lee: Seoul National University College of Medicine
Chan Soo Shin: Seoul National University College of Medicine
Dong Yeon Lee: Seoul National University College of Medicine
Hong-Hee Kim: Seoul National University School of Dentistry
Zang Hee Lee: Seoul National University School of Dentistry
Hyun-Mo Ryoo: Seoul National University School of Dentistry
Mi-Ni Lee: Ewha Womans University
Goo Taeg Oh: Ewha Womans University
Jong-Wan Park: Seoul National University College of Medicine

Nature Communications, 2014, vol. 5, issue 1, 1-14

Abstract: Abstract Runt-related transcription factor 2 (Runx2) transactivates many genes required for osteoblast differentiation. The role of N-α-acetyltransferase 10 (NAA10, arrest-defective-1), originally identified in yeast, remains poorly understood in mammals. Here we report a new NAA10 function in Runx2-mediated osteogenesis. Runx2 stabilizes NAA10 in osteoblasts during BMP-2-induced differentiation, and NAA10 in turn controls this differentiation by inhibiting Runx2. NAA10 delays bone healing in a rat calvarial defect model and bone development in neonatal mice. Mechanistically, NAA10 acetylates Runx2 at Lys225, and this acetylation inhibits Runx2-driven transcription by interfering with CBFβ binding to Runx2. Our study suggests that NAA10 acts as a guard ensuring balanced osteogenesis by fine-tuning Runx2 signalling in a feedback manner. NAA10 inhibition could be considered a potential strategy for facilitating bone formation.

Date: 2014
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DOI: 10.1038/ncomms6176

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