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中胚层Fgf10b在斑马鱼耳和鳃上神经节原基诱导过程中与其他成纤维细胞生长因子协同作用。

Mesodermal Fgf10b cooperates with other fibroblast growth factors during induction of otic and epibranchial placodes in zebrafish.

作者信息

Maulding Kirstin, Padanad Mahesh S, Dong Jennifer, Riley Bruce B

机构信息

Biology Department, Texas A&M University, College Station, Texas.

出版信息

Dev Dyn. 2014 Oct;243(10):1275-85. doi: 10.1002/dvdy.24119. Epub 2014 Mar 3.

Abstract

BACKGROUND

Vertebrate otic and epibranchial placodes develop in close proximity in response to localized fibroblast growth factor (Fgf) signaling. Although less is known about epibranchial induction, the process of otic induction in highly conserved, with important roles for Fgf3 and Fgf8 reported in all species examined. Fgf10 is also critical for otic induction in mouse, but the only zebrafish ortholog examined to date, fgf10a, is not expressed early enough to play such a role. A second zebrafish ortholog, fgf10b, has not been previously examined.

RESULTS

We find that zebrafish fgf10b is expressed at tailbud stage in paraxial cephalic mesoderm beneath prospective epibranchial tissue, lateral to the developing otic placode. Knockdown of fgf10b does not affect initial otic induction but impairs subsequent accumulation of otic cells. Formation of epibranchial placodes and ganglia are also moderately impaired. Combinatorial disruption of fgf10b and fgf3 exacerbates the deficiency of otic cells and eliminates epibranchial induction entirely. Disruption of fgf10b and fgf24 also strongly reduces, but does not eliminate, epibranchial induction.

CONCLUSIONS

fgf10b participates in a late phase of otic induction and, in combination with fgf3, is especially critical for epibranchial induction.

摘要

背景

脊椎动物的耳基板和鳃后基板在局部成纤维细胞生长因子(Fgf)信号的作用下,在相邻位置发育。尽管对鳃后基板诱导的了解较少,但耳基板诱导过程高度保守,在所有已研究的物种中,Fgf3和Fgf8都发挥着重要作用。Fgf10对小鼠的耳基板诱导也至关重要,但迄今为止所检测的斑马鱼唯一直系同源基因fgf10a,其表达时间不够早,无法发挥这样的作用。斑马鱼的第二个直系同源基因fgf10b,此前尚未被研究过。

结果

我们发现斑马鱼的fgf10b在尾芽期表达于预期鳃后组织下方的轴旁头部中胚层,位于发育中的耳基板外侧。敲低fgf10b并不影响耳基板的初始诱导,但会损害随后耳细胞的积累。鳃后基板和神经节的形成也受到中度损害。fgf10b和fgf3的联合破坏会加剧耳细胞的缺乏,并完全消除鳃后基板诱导。fgf10b和fgf24的破坏也会强烈减少,但不会消除鳃后基板诱导。

结论

fgf10b参与耳基板诱导的后期阶段,并且与fgf3一起,对鳃后基板诱导尤为关键。

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