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首页> 外文期刊>Current Biology: CB >Ken & Barbie selectively regulates the expression of a subset of JAK/STAT pathway target genes
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Ken & Barbie selectively regulates the expression of a subset of JAK/STAT pathway target genes

机译：Ken＆Barbie选择性地调节JAK / STAT通路靶基因子集的表达

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摘要

A limited number of evolutionarily conserved signal transduction pathways are repeatedly reused during development to regulate a wide range of processes. Here we describe a new negative regulator of JAK/STAT signaling and identify a potential mechanism by which the pleiotropy of responses resulting from pathway activation is generated in vivo. As part of a genetic interaction screen, we have identified Ken & Barbie (Ken) [1], which is an ortholog of the mammalian proto-oncogene BCL6 [2], as a negative regulator of the JAK/STAT pathway. Ken genetically interacts with the pathway in vivo and recognizes a DNA consensus sequence overlapping that of STAT92E in vitro. Tissue culture-based assays demonstrate the existence of Ken-sensitive and Ken-insensitive STAT92E binding sites, while ectopically expressed Ken is sufficient to downregulate a subset of JAK/STAT pathway target genes in vivo. Finally, we show that endogenous Ken specifically represses JAK/STAT-dependent expression of ventral veins lacking (vvl) in the posterior spiracles. Ken therefore represents a novel regulator of JAK/STAT signaling whose dynamic spatial and temporal expression is capable of selectively modulating the transcriptional repertoire elicited by activated STAT92E in vivo.
机译：有限数量的进化保守信号转导途径可在开发过程中重复使用，以调节广泛的过程。在这里，我们描述了JAK / STAT信号转导的新的负调节器，并确定了一种潜在的机制，通过该机制体内产生了由途径激活引起的反应的多效性。作为遗传相互作用筛选的一部分，我们已将Ken＆Barbie（Ken）[1]（它是哺乳动物原癌基因BCL6的直系同源物）[2]鉴定为JAK / STAT通路的负调节剂。 Ken在体内与该途径进行了遗传相互作用，并在体外识别出一个与STAT92E重叠的DNA共有序列。基于组织培养的测定法证明存在Ken敏感和Ken不敏感的STAT92E结合位点，而异位表达的Ken足以在体内下调JAK / STAT通路靶基因的子集。最后，我们显示内源性Ken特异地抑制了后气孔中缺乏（vvl）的腹静脉的JAK / STAT依赖性表达。因此，Ken代表了JAK / STAT信号传导的新型调节剂，其动态时空表达能够选择性地调节体内活化STAT92E引发的转录谱。

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