論文

査読有り
2015年11月

Mindbomb 2 is dispensable for embryonic development and Notch signalling in zebrafish

BIOLOGY OPEN
  • Shohei Mikami
  • ,
  • Mizuki Nakaura
  • ,
  • Atsuo Kawahara
  • ,
  • Takamasa Mizoguchi
  • ,
  • Motoyuki Itoh

4
11
開始ページ
1576
終了ページ
1582
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1242/bio.014225
出版者・発行元
COMPANY OF BIOLOGISTS LTD

The Mindbomb E3 ubiquitin protein ligase (Mib) family of proteins, Mib1 and Mib2, are RING finger ubiquitin ligases that share specific substrates. Mib1 is known to play essential roles in Notch signalling by ubiquitinating Notch ligands in vivo. Conversely, the functions of Mib2 in vivo are not fully understood, although Mib2 ubiquitinates multiple substrates, including Notch ligands, in vitro. To determine the Notch-dependent and Notch-independent functions of Mib2 in vivo, we generated mutant alleles of zebrafish mib2 using transcription activator-like effector nucleases (TALENs). We found that mib2 homozygous mutants were viable and fertile. Notch-mediated functions, such as early neurogenesis, somitogenesis, and pigment cell development, were not affected in mib2 mutant embryos. The lack of Notch-deficient phenotypes in mib2 mutants was not due to compensation by a mib2 maternal gene product because mib2 maternal-zygotic mutants also did not exhibit a distinct phenotype. We also showed that Mib2 does not redundantly act with Mib1 because the genetic ablation of mib2 neither enhanced mib(tfi91)-null phenotypes nor did it alleviate antimorphic mib(ta52b) phenotypes. Furthermore, the postulated Notch-independent roles of Mib2 in maintaining muscular integrity and N-methyl-D-aspartate receptor (NMDAR) activity were not evident: mib2 mutants did not show phenotypes different from that of the control embryos. These observations suggest that Mib2 is dispensable for embryonic development and does not have redundant functions with Mib1 in Notch signalling at least during early development stages in zebrafish.

Web of Science ® 被引用回数 : 3

リンク情報
DOI
https://doi.org/10.1242/bio.014225
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000365078200024&DestApp=WOS_CPL
URL
http://www.scopus.com/inward/record.url?eid=2-s2.0-84982786702&partnerID=MN8TOARS
URL
http://orcid.org/0000-0002-9475-6495

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