Forés Marta, Ajuria Leiore, Samper Núria, Astigarraga Sergio, Nieva Claudia, Grossman Rona, González-Crespo Sergio, Paroush Ze'ev, Jiménez Gerardo
Institut de Biologia Molecular de Barcelona-CSIC, Parc Científic de Barcelona, Barcelona, Spain.
Department of Developmental Biology and Cancer Research, IMRIC, The Hebrew University, Jerusalem, Israel.
PLoS Genet. 2015 Jan 8;11(1):e1004902. doi: 10.1371/journal.pgen.1004902. eCollection 2015 Jan.
Receptor Tyrosine Kinase (RTK) signaling pathways induce multiple biological responses, often by regulating the expression of downstream genes. The HMG-box protein Capicua (Cic) is a transcriptional repressor that is downregulated in response to RTK signaling, thereby enabling RTK-dependent induction of Cic targets. In both Drosophila and mammals, Cic is expressed as two isoforms, long (Cic-L) and short (Cic-S), whose functional significance and mechanism of action are not well understood. Here we show that Drosophila Cic relies on the Groucho (Gro) corepressor during its function in the early embryo, but not during other stages of development. This Gro-dependent mechanism requires a short peptide motif, unique to Cic-S and designated N2, which is distinct from other previously defined Gro-interacting motifs and functions as an autonomous, transferable repressor element. Unexpectedly, our data indicate that the N2 motif is an evolutionary innovation that originated within dipteran insects, as the Cic-S isoform evolved from an ancestral Cic-L-type form. Accordingly, the Cic-L isoform lacking the N2 motif is completely inactive in early Drosophila embryos, indicating that the N2 motif endowed Cic-S with a novel Gro-dependent activity that is obligatory at this stage. We suggest that Cic-S and Gro coregulatory functions have facilitated the evolution of the complex transcriptional network regulated by Torso RTK signaling in modern fly embryos. Notably, our results also imply that mammalian Cic proteins are unlikely to act via Gro and that their Cic-S isoform must have evolved independently of fly Cic-S. Thus, Cic proteins employ distinct repressor mechanisms that are associated with discrete structural changes in the evolutionary history of this protein family.
受体酪氨酸激酶(RTK)信号通路通常通过调节下游基因的表达来诱导多种生物学反应。HMG盒蛋白Capicua(Cic)是一种转录抑制因子,其表达会响应RTK信号而下调,从而使RTK能够依赖性地诱导Cic靶标的表达。在果蝇和哺乳动物中,Cic均以两种异构体形式存在,即长异构体(Cic-L)和短异构体(Cic-S),但其功能意义和作用机制尚不清楚。在这里,我们表明果蝇Cic在早期胚胎功能中依赖于Groucho(Gro)共抑制因子,但在发育的其他阶段则不然。这种依赖Gro的机制需要一个短肽基序,该基序是Cic-S特有的,称为N2,它不同于其他先前定义的与Gro相互作用的基序,并且作为一个自主的、可转移的抑制元件发挥作用。出乎意料的是,我们的数据表明N2基序是双翅目昆虫中产生的一种进化创新,因为Cic-S异构体是从祖先的Cic-L型形式进化而来的。因此,缺乏N2基序的Cic-L异构体在早期果蝇胚胎中完全无活性,这表明N2基序赋予Cic-S一种新的依赖Gro的活性,而这种活性在这个阶段是必不可少的。我们认为,Cic-S和Gro的共调节功能促进了现代果蝇胚胎中由躯干RTK信号调节的复杂转录网络的进化。值得注意的是,我们的结果还意味着哺乳动物的Cic蛋白不太可能通过Gro发挥作用,并且它们的Cic-S异构体一定是独立于果蝇Cic-S进化而来的。因此,Cic蛋白采用了不同的抑制机制,这些机制与该蛋白家族进化历史中的离散结构变化相关。