RNT-1, the C-elegans homologue of mammalian RUNX transcription factors, regulates body size and male tail development
RNT-1, the C-elegans homologue of mammalian RUNX transcription factors, regulates body size and male tail development
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DOI：
10.1016/j.ydbio.2004.07.029
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发表时间：
2004-10-15
影响因子：
2.7
通讯作者：
Ahnn, J
中科院分区：
文献类型：
--
作者：
Ji, YJ;Nam, S;Ahnn, J
rnt-1基因是秀丽隐杆线虫中唯一与哺乳动物RUNX基因同源的基因。一些分子生物学证据表明，RUNX蛋白与Smads相互作用和合作，Smads是转化生长因子-β（TGF-β）信号介导剂。然而，RUNX参与TGF-β信号传导尚未得到任何遗传证据的支持。Sma/ Mab TGF β信号通路在C.已知秀丽线虫调节身体长度和雄性尾巴的发育。rnt-1（ok 351）突变体显示出在Sma/Mab途径突变体中观察到的特征表型，即它们具有小的体型和射线缺陷。此外，RNT-1还能与C.线虫和含有rnt-1（ok 351）突变和已知Sma/Mab途径基因突变的双突变动物在异常表型中显示协同作用。此外，lon-1（e185）突变体在长表型方面对rnt-1（ok 351）突变体具有上位性，这表明lon-1确实是rnt-1的下游靶标。我们的数据表明，RNT-1功能上与SMA-4蛋白合作，以调节身体的大小和雄性尾巴的发展，在C。优雅(C)2004爱思唯尔公司All rights reserved.
The rnt-1 gene is the only Caenorhabditis elegans homologue of the mammalian RUNX genes. Several lines of molecular biological evidence have demonstrated that the RUNX proteins interact and cooperate with Smads, which are transforming growth factor-beta (TGF-beta) signal mediators. However, the involvement of RUNX in TGF-beta signaling has not yet been supported by any genetic evidence. The Sma/ Mab TGF-beta signaling pathway in C. elegans is known to regulate body length and male tail development. The rnt-1(ok351) mutants show the characteristic phenotypes observed in mutants of the Sma/Mab pathway, namely, they have a small body size and ray defects. Moreover, RNT-1 can physically interact with SMA-4 which is one of the Smads in C. elegans, and double mutant animals containing both the rnt-1(ok351) mutation and a mutation in a known Sma/Mab pathway gene displayed synergism in the aberrant phenotypes. In addition, lon-1(e185) mutants was epistatic to rnt-1(ok351) mutants in terms of long phenotype, suggesting that lon-1 is indeed downstream target of rnt-1. Our data reveal that RNT-1 functionally cooperates with the SMA-4 proteins to regulate body size and male tail development in C. elegans. (C) 2004 Elsevier Inc. All rights reserved.