Transient knockdown and overexpression reveal a developmental role for the zebrafish enosf1b gene.
Transient knockdown and overexpression reveal a developmental role for the zebrafish enosf1b gene.
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DOI：
10.1186/2045-3701-1-32
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发表时间：
2011-09-26
影响因子：
7.5
通讯作者：
Liu P
中科院分区：
文献类型：
--
作者：
Finckbeiner S;Ko PJ;Carrington B;Sood R;Gross K;Dolnick B;Sufrin J;Liu P
Despite detailed in vivo knowledge of glycolytic enolases and many bacterial non-enolase members of the superfamily, little is known about the in vivo function of vertebrate non-enolase enolase superfamily members (ENOSF1s). Results of previous studies suggest involvement of the β splice form of ENOSF1 in breast and colon cancers. This study used the zebrafish (Danio rerio) as a vertebrate model of ENOSF1β function. Whole mount in situ hybridization (WISH) showed that zebrafish ENOSF1β (enosf1b) is zygotic and expressed ubiquitously through the first 24 hours post fertilization (hpf). After 24 hpf, enosf1b expression is restricted to the notochord. Embryos injected with enosf1b-EGFP mRNA grew slower than EGFP mRNA-injected embryos but caught up to the EGFP-injected embryos by 48 hpf. Embryos injected with ATG or exon 10 enosf1b mRNA-targeting morpholinos had kinked notochords, shortened anterior-posterior axes, and circulatory edema. WISH for ntl or pax2a expression showed that embryos injected with either morpholino have deformed notochord and pronephros. TUNEL staining revealed increased apoptosis in the peri-notochord region. This study is the first report of ENOSF1 function in a vertebrate and shows that ENOSF1 is required for embryonic development. Increased apoptosis following enosf1b knockdown suggests a potential survival advantage for increased ENOSF1β expression in human cancers.
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影响因子：
3.7
作者：
Demuth JP;De Bie T;Stajich JE;Cristianini N;Hahn MW
通讯作者：
Hahn MW
影响因子：
64.8
作者：
DErchia, AM;Gissi, C;Arnason, U
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影响因子：
14.9
作者：
DOLNICK, BJ
通讯作者：
DOLNICK, BJ
DOI：
10.1073/pnas.0406252102
发表时间：
2005-01-11
影响因子：
11.1
作者：
Berghmans, S;Murphey, RD;Look, AT
通讯作者：
Look, AT
影响因子：
56.9
作者：
Dehal, P;Satou, Y;Rokhsar, DS
通讯作者：
Rokhsar, DS