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秀丽隐杆线虫 T 盒因子 MLS-1 需要与 Groucho 共抑制因子相互作用来特化子宫肌。

The Caenorhabditis elegans T-box factor MLS-1 requires Groucho co-repressor interaction for uterine muscle specification.

机构信息

Department of Biological Sciences, Laboratory for Molecular Biology, University of Illinois at Chicago, Chicago, Illinois, United States of America.

出版信息

PLoS Genet. 2011 Aug;7(8):e1002210. doi: 10.1371/journal.pgen.1002210. Epub 2011 Aug 11.

Abstract

T-box proteins are conserved transcription factors that play crucial roles in development of all metazoans; and, in humans, mutations affecting T-box genes are associated with a variety of congenital diseases and cancers. Despite the importance of this transcription factor family, very little is known regarding how T-box factors regulate gene expression. The Caenorhabditis elegans genome contains 21 T-box genes, and their characterized functions include cell fate specification in a variety of tissues. The C. elegans Tbx1 sub-family member MLS-1 functions during larval development to specify the fate of non-striated uterine muscles; and, in mls-1 mutants, uterine muscles are transformed to a vulval muscle fate. Here we demonstrate that MLS-1 function depends on binding to the Groucho-family co-repressor UNC-37. MLS-1 interacts with UNC-37 via a conserved eh1 motif, and the MLS-1 eh1 motif is necessary for MLS-1 to specify uterine muscle fate. Moreover, unc-37 loss-of-function produces uterine muscle to vulval muscle fate transformation similar to those observed in mls-1 mutants. Based on these results, we conclude that MLS-1 specifies uterine muscle fate by repressing target gene expression, and this function depends on interaction with UNC-37. Moreover, we suggest that MLS-1 shares a common mechanism for transcriptional repression with related T-box factors in other animal phyla.

摘要

T 盒蛋白是保守的转录因子,在所有后生动物的发育中发挥着关键作用;而在人类中,影响 T 盒基因的突变与多种先天性疾病和癌症有关。尽管这个转录因子家族非常重要,但对于 T 盒因子如何调节基因表达,我们知之甚少。秀丽隐杆线虫基因组包含 21 个 T 盒基因,其特征功能包括在各种组织中细胞命运的特化。秀丽隐杆线虫 Tbx1 亚家族成员 MLS-1 在幼虫发育过程中发挥作用,特化非横纹子宫肌的命运;而在 mls-1 突变体中,子宫肌被转化为阴道肌命运。在这里,我们证明 MLS-1 的功能取决于与 Groucho 家族共抑制因子 UNC-37 的结合。MLS-1 通过保守的 eh1 基序与 UNC-37 相互作用,并且 MLS-1 eh1 基序对于 MLS-1 特化子宫肌命运是必需的。此外,unc-37 功能丧失会导致子宫肌向阴道肌命运的转变,类似于 mls-1 突变体中观察到的情况。基于这些结果,我们得出结论,MLS-1 通过抑制靶基因的表达来特化子宫肌命运,并且这种功能依赖于与 UNC-37 的相互作用。此外,我们认为 MLS-1 与其他动物门中相关 T 盒因子的转录抑制具有共同的机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8117/3154951/6d234e5dbe8a/pgen.1002210.g001.jpg

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