Item type |
itemtype_ver1(1) |
公開日 |
2023-07-27 |
タイトル |
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タイトル |
Forced expression of α2,3-sialyltransferase IV rescues impaired heart development in α2,6-sialyltransferase I-deficient medaka |
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言語 |
en |
著者 |
Omoto, Takayuki
Wu, Di
Maruyama, Emi
Tajima, Katsue
Hane, Masaya
Sato, Chihiro
Kitajima, Ken
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アクセス権 |
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アクセス権 |
open access |
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アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
権利 |
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言語 |
en |
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権利情報 |
© 2023. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ |
キーワード |
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主題Scheme |
Other |
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主題 |
α2,6-sialyltransferase |
キーワード |
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主題Scheme |
Other |
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主題 |
α2,3-sialyltransferase |
キーワード |
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主題Scheme |
Other |
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主題 |
Heart development |
キーワード |
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主題Scheme |
Other |
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主題 |
Medaka |
内容記述 |
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内容記述タイプ |
Abstract |
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内容記述 |
Sialic acids (Sias) are often linked to galactose (Gal) residues by α2,6- and α2,3-linkages in glycans of glycoproteins. Sias are indispensable for vertebrate development, because organisms deficient in some enzymes in the Sia synthetic pathway are lethal during the development. However, it remains unknown if the difference of Siaα2,6Gal or α2,3Gal linkage has a critical meaning. To find a clue to understand significance of the linkage difference at the organism level, medaka was used as a vertebrate model. In embryos, Siaα2,6Gal epitopes recognized by Sambucus nigra lectin (SNA) and Siaα2,3Gal epitopes recognized by Maackia amurensis lectin (MAA) were enriched in the blastodisc and the yolk sphere, respectively. When these lectins were injected in the perivitelline space, SNA, but not MAA, impaired embryo body formation at 1 day post-fertilization (dpf). Most Siaα2,6Gal epitopes occurred on N-glycans owing to their sensitivity to peptide:N-glycanase. Of knockout-medaka (KO) for either of two β-galactoside:α2,6-sialyltransferase genes, ST6Gal I and ST6Gal II, only ST6Gal I–KO showed severe cardiac abnormalities at 7–16 dpf, leading to lethality at 14–18 dpf. Interestingly, however, these cardiac abnormalities of ST6Gal I–KO were rescued not only by forced expression of ST6Gal I, but also by that of ST6Gal II and the β-galactoside:α2,3-sialyltransferase IV gene (ST3Gal IV). Taken together, the Siaα2,6Gal linkage synthesized by ST6Gal I are critical in heart development; however, it can be replaced by the linkages synthesized by ST6Gal II and ST3Gal IV. These data suggest that sialylation itself is more important than its particular linkage for the heart development. |
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言語 |
en |
出版者 |
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出版者 |
Elsevier |
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言語 |
en |
言語 |
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言語 |
eng |
資源タイプ |
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資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
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資源タイプ |
journal article |
出版タイプ |
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出版タイプ |
AM |
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出版タイプResource |
http://purl.org/coar/version/c_ab4af688f83e57aa |
関連情報 |
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関連タイプ |
isVersionOf |
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識別子タイプ |
DOI |
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関連識別子 |
https://doi.org/10.1016/j.bbrc.2023.01.010 |
収録物識別子 |
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収録物識別子タイプ |
PISSN |
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収録物識別子 |
0006-291X |
書誌情報 |
en : Biochemical and Biophysical Research Communications
巻 649,
p. 62-70,
発行日 2023-03-15
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ファイル公開日 |
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日付 |
2024-03-15 |
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日付タイプ |
Available |