<i>Setd5</i>, but not <i>Setd2</i>, is indispensable for retinal cell survival and proliferation
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- Toshiro Iwagawa
- Division of Molecular and Developmental Biology, Institute of Medical Science University of Tokyo Japan
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- Ryoko Kawabata
- Division of Molecular and Developmental Biology, Institute of Medical Science University of Tokyo Japan
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- Masaya Fukushima
- Division of Molecular and Developmental Biology, Institute of Medical Science University of Tokyo Japan
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- Hiroshi Kuribayashi
- Division of Molecular and Developmental Biology, Institute of Medical Science University of Tokyo Japan
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- Sumiko Watanabe
- Division of Molecular and Developmental Biology, Institute of Medical Science University of Tokyo Japan
抄録
<jats:p>Trimethylation of histone H3 at lysine 36 (H3K36me3) is associated with active transcription. We used mouse retinal explant cultures and shRNA to investigate the roles of <jats:italic>Setd2</jats:italic> and <jats:italic>Setd5</jats:italic>, which encode H3K36me3 methyltransferases, in retinal development. We found that shSetd5 caused abnormal retinal structures and reduced rods and Müller cells, whereas shSetd2 did not cause any abnormalities. The mutant SETD5 lacking the SET domain failed to reverse the phenotypes observed in the shSetd5‐expressing retinas, while SETD5S1257*, which does not interact with HDAC3 and PAF1 complexes, rescued proliferation, but not apoptosis, induced by shSetd5. Taken together, we found that <jats:italic>Setd5</jats:italic>, but not <jats:italic>Setd2</jats:italic>, is essential for sustaining retinal cell survival and proliferation, and the SET domain of SETD5 is pivotal for both functions.</jats:p>
収録刊行物
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- FEBS Letters
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FEBS Letters 597 (3), 427-436, 2022-11-22
Wiley
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詳細情報 詳細情報について
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- CRID
- 1360017282216904576
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- ISSN
- 18733468
- 00145793
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- データソース種別
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- Crossref
- KAKEN