A histone H3 lysine 36 trimethyltransferase links Nkx2-5 to Wolf–Hirschhorn syndrome

Keisuke Nimura, Kiyoe Ura (), Hidetaka Shiratori, Masato Ikawa, Masaru Okabe, Robert J. Schwartz and Yasufumi Kaneda ()
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Keisuke Nimura: Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan
Kiyoe Ura: Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan
Hidetaka Shiratori: Developmental Genetics Group, Graduate School of Frontier Biosciences, and,
Masato Ikawa: Genome Information Research Center, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan
Masaru Okabe: Genome Information Research Center, Osaka University, 1-3 Yamada-oka, Suita, Osaka 565-0871, Japan
Robert J. Schwartz: Institute of Bioscience and Technology, Center for Molecular Development and Disease, 2121 West Holcombe Boulevard, Houston, Texas 77030, USA
Yasufumi Kaneda: Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita, Osaka 565-0871, Japan

Nature, 2009, vol. 460, issue 7252, 287-291

Abstract: Transcription factor Nkx2-5 and Wolf-Hirschhorn syndrome Histone H3 trimethylation at lysine 36 (H3K36me3) is associated with actively transcribed regions and has been proposed to provide landmarks for ongoing transcription. Here, an H3K36me3-specific histone methyltransferase Wolf–Hirschhorn syndrome candidate 1 (WHSC1) is shown to function in transcriptional regulation together with developmental transcription factors such as Nkx2-5. Whsc1-deficient mice display growth and developmental defects similar to those seen in WHS patients, and the defects are more severe when Nkx2-5 is also deficient. WHSC1 seems to function together with developmental transcription factors to prevent transcriptional pathophysiologies.

Date: 2009
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DOI: 10.1038/nature08086

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