Abnormal development of zebrafish after knockout and knockdown of ribosomal protein L10a

DOI DOI DOI PDF Web Site ほか1件をすべて表示 一部だけ表示 参考文献29件 オープンアクセス

書誌事項

公開日
2019-12-02
資源種別
journal article
権利情報
  • https://creativecommons.org/licenses/by/4.0
  • https://creativecommons.org/licenses/by/4.0
DOI
  • 10.1038/s41598-019-54544-w
  • 10.60692/7g36n-61q10
  • 10.60692/nbr26-ha882
公開者
Springer Science and Business Media LLC

説明

<jats:title>Abstract</jats:title><jats:p>In this study, to investigate the secondary function of Rpl10a in zebrafish development, morpholino antisense oligonucleotides (MOs) were used to knock down the zebrafish ribosomal protein L10a (<jats:italic>rpl10a</jats:italic>). At 25 hpf (hours post-fertilization), embryos injected with the <jats:italic>rpl10a</jats:italic> MO showed an abnormal morphology, including short bodies, curved tails, and small yolk sac extensions. We observed pigment reductions, edema, larger yolk sacs, smaller eyes and smaller yolk sac extensions at 50 hpf. In addition, reductions in the expression of primordial germ cell (PGC) marker genes (<jats:italic>nanos1</jats:italic> and <jats:italic>vasa</jats:italic>) were observed in <jats:italic>rpl10a</jats:italic> knockdown embryos. A rescue experiment using a <jats:italic>rpl10a</jats:italic> mRNA co-injection showed the recovery of the morphology and red blood cell production similar to wild-type. Moreover, the CRISPR-Cas9 system was used to edit the sequence of <jats:italic>rpl10a</jats:italic> exon 5, resulting in a homozygous 5-bp deletion in the zebrafish genome. The mutant embryos displayed a morphology similar to that of the knockdown animals. Furthermore, the loss of <jats:italic>rpl10a</jats:italic> function led to reduced expression of <jats:italic>gata1</jats:italic>, <jats:italic>hbae3</jats:italic>, and <jats:italic>hbbe1</jats:italic> (erythroid synthesis) and increased <jats:italic>tp53</jats:italic> expression. Overall, the results suggested that Rpl10a deficiency caused delays in embryonic development, as well as apoptosis and anemia, in zebrafish.</jats:p>

収録刊行物

  • Scientific Reports

    Scientific Reports 9 (1), 2019-12-02

    Springer Science and Business Media LLC

参考文献 (29)*注記

もっと見る

関連プロジェクト

もっと見る

詳細情報 詳細情報について

問題の指摘

ページトップへ