A Zn-finger/FH2-domain containing protein, FOZI-1, acts redundantly with CeMyoD to specify striated body wall muscle fates in the Caenorhabditis elegans postembryonic mesoderm

A Zn-finger/FH2-domain containing protein, FOZI-1, acts redundantly with CeMyoD to specify striated body wall muscle fates in the Caenorhabditis elegans postembryonic mesoderm
复制标题

DOI:
10.1242/dev.02709
复制
发表时间:
2007-01-01
期刊:
影响因子:
4.6
通讯作者:
Liu, Jun
Liu, Jun
中科院分区:
生物学2区
文献类型:
--
作者:
Amin, Nirav M.;Hu, Kejin;Liu, Jun

文献摘要

被引文献

相似文献

脊椎动物的横纹肌发育需要MyoD家族多个成员的冗余功能。无脊椎动物如果蝇和秀丽隐杆线虫在每个生物体中仅含有一个MyoD同源物。早期的观察表明,在这些生物体中,MyoD家族以外的因子可能与MyoD在横纹肌命运规范中冗余地起作用。然而,这些因素的身份仍然难以捉摸。在这里,我们描述了FOZI-1的鉴定和表征,FOZI-1是一种假定的转录因子,与CeMyoD(HLH-1)在C.胚后中胚层。Fozi-1编码一种新的核定位蛋白,其具有转录因子和肌动蛋白结合蛋白的特征基序。我们表明,FOZI-1与CeMyoD在胚后中胚层谱系(M谱系)中具有相同的表达模式,并且fozi-1无效突变体表现出与在M谱系中缺乏CeMyoD的动物中发现的那些相似的M谱系无效缺陷(例如,G.损失一部分M谱系衍生的BWM)。有趣的是,具有降低的CeMyoD水平的fozi-1无效突变体缺乏大多数(如果不是全部的话)M谱系来源的BWM。我们的研究结果表明,FOZI-1和Hox因子MAB-5与CeMyoD在C. elegans胚后中胚层,暗示了C.优美的
Striated muscle development in vertebrates requires the redundant functions of multiple members of the MyoD family. Invertebrates such as Drosophila and Caenorhabditis elegans contain only one MyoD homolog in each organism. Earlier observations suggest that factors outside of the MyoD family might function redundantly with MyoD in striated muscle fate specification in these organisms. However, the identity of these factors has remained elusive. Here, we describe the identification and characterization of FOZI-1, a putative transcription factor that functions redundantly with CeMyoD (HLH-1) in striated body wall muscle (BWM) fate specification in the C. elegans postembryonic mesoderm. fozi-1 encodes a novel nuclear-localized protein with motifs characteristic of both transcription factors and actin-binding proteins. We show that FOZI-1 shares the same expression pattern as CeMyoD in the postembryonic mesodermal lineage, the M lineage, and that fozi-1-null mutants exhibit similar M lineage-null defects to those found in animals lacking CeMyoD in the M lineage ( e. g. loss of a fraction of M lineage-derived BWMs). Interestingly, fozi-1-null mutants with a reduced level of CeMyoD lack most, if not all, M lineage-derived BWMs. Our results indicate that FOZI-1 and the Hox factor MAB-5 function redundantly with CeMyoD in the specification of the striated BWM fate in the C. elegans postembryonic mesoderm, implicating a remarkable level of complexity for the production of a simple striated musculature in C. elegans.