Two linked hairy/Enhancer of split-related zebrafish genes, her1 and her7, function together to refine alternating somite boundaries.

Two linked hairy/Enhancer of split-related zebrafish genes, her1 and her7, function together to refine alternating somite boundaries.
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DOI:
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发表时间:
2002-08
期刊:
影响因子:
4.6
通讯作者:
C. Henry;M. Urban;Kariena Dill;J. Merlie;M. Page;C. Kimmel;S. Amacher
C. Henry;M. Urban;Kariena Dill;J. Merlie;M. Page;C. Kimmel;S. Amacher
中科院分区:
生物学2区
文献类型:
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作者:
C. Henry;M. Urban;Kariena Dill;J. Merlie;M. Page;C. Kimmel;S. Amacher

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体节的形成,将产生椎骨和肌肉的重复结构,被认为取决于可能涉及Notch途径的分子振荡器。分裂相关[E(spl)]-相关(her或hes)基因的hairy/增强子,Notch信号传导的潜在靶标,已经被认为是分子振荡器的输出。我们已经分离出一种斑马鱼缺陷症,b567,它删除了两个连锁的her基因,her 1和her 7。纯合子b567突变体沿整个胚胎轴有缺陷的体节沿着。注射her 1和her 7(her 1 +7)吗啉代修饰的反义寡核苷酸(MO)的组合phenocopies的b567突变体节表型,表明her 1和her 7是必要的正常体节的形成和缺陷的b567突变胚胎的体节是由于her 1和her 7的缺失。在细胞水平上的分析表明,在her 1 +7缺陷的胚胎体节扩大的前后尺寸。在这些扩大的体节中经常发现弱体节边界,这些体节被更强但不完美的边界所描绘。此外,这些扩大体节的前后极性是混乱的。her 1 MO-注射胚胎和her 7 MO-注射胚胎的分析表明,虽然这些基因在大部分躯干区域具有部分冗余功能,但her 1是正确形成前体节所必需的,her 7是正确形成体节后体节11所必需的。随着时间的推移,体节的发展,我们证明了她的基因是必要的交替强大的体节边界的形成。因此,即使两个潜在的下游组件Notch信号缺乏her 1 +7缺陷的胚胎,体节边界的形式,但这样做的一个半到两个节段的周期。
The formation of somites, reiterated structures that will give rise to vertebrae and muscles, is thought to be dependent upon a molecular oscillator that may involve the Notch pathway. hairy/Enhancer of split related [E(spl)]-related (her or hes) genes, potential targets of Notch signaling, have been implicated as an output of the molecular oscillator. We have isolated a zebrafish deficiency, b567, that deletes two linked her genes, her1 and her7. Homozygous b567 mutants have defective somites along the entire embryonic axis. Injection of a combination of her1 and her7 (her1+7) morpholino modified antisense oligonucleotides (MOs) phenocopies the b567 mutant somitic phenotype, indicating that her1 and her7 are necessary for normal somite formation and that defective somitogenesis in b567 mutant embryos is due to deletion of her1 and her7. Analysis at the cellular level indicates that somites in her1+7-deficient embryos are enlarged in the anterior-posterior dimension. Weak somite boundaries are often found within these enlarged somites which are delineated by stronger, but imperfect, boundaries. In addition, the anterior-posterior polarity of these enlarged somites is disorganized. Analysis of her1 MO-injected embryos and her7 MO-injected embryos indicates that although these genes have partially redundant functions in most of the trunk region, her1 is necessary for proper formation of the anteriormost somites and her7 is necessary for proper formation of somites posterior to somite 11. By following somite development over time, we demonstrate that her genes are necessary for the formation of alternating strong somite boundaries. Thus, even though two potential downstream components of Notch signaling are lacking in her1+7-deficient embryos, somite boundaries form, but do so with a one and a half to two segment periodicity.