Tyrosine phosphorylation-independent nuclear translocation of a Dictyostelium STAT in response to DIF signaling

Tyrosine phosphorylation-independent nuclear translocation of a Dictyostelium STAT in response to DIF signaling
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DOI:
10.1016/s1097-2765(01)00222-2
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发表时间:
2001-04-01
期刊:
影响因子:
16
通讯作者:
Williams, JG
Williams, JG
中科院分区:
生物学1区
文献类型:
--
作者:
Fukuzawa, M;Araki, T;Williams, JG

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我们描述了一个Dictyosteoblast STAT,Dd-STATc,它调节早期发育的速度和终末分化的时间。Dd-STATc还作为阻遏物起作用,其指导不同前茎细胞群中ecmA基因的分级表达。发育中的网骨藻细胞产生一种氯代六苯酮,DIF,它指导前柄细胞分化。当细胞暴露于DIF时,Dd-STATc被酪氨酸磷酸化、二聚化并易位至细胞核。然而,令人惊讶的是,SH 2结构域-磷酸酪氨酸相互作用不是DIF诱导的Dd-STATc核转位所必需的。在这方面,Dd-STATc激活类似于几个最近描述的,非典型的哺乳动物STAT信号传导过程。相反,我们表明,DIF介导的核转位通过位于不同的,N-末端的一半的Dd-STATc分子的序列。
We describe a Dictyostelium STAT, Dd-STATc, which regulates the speed of early development and the timing of terminal differentiation. Dd-STATc also functions as a repressor, which directs graded expression of the ecmA gene in different prestalk cell populations. Developing Dictyostelium cells produce a chlorinated hexaphenone, DIF, which directs prestalk cell differentiation. Dd-STATc is tyrosine phosphorylated, dimerizes, and translocates to the nucleus when cells are exposed to DIF. Surprisingly, however, SH2 domain-phosphotyrosine interaction is not necessary for the DIF-induced nuclear translocation of Dd-STATc. In this respect, Dd-STATc activation resembles several recently described, noncanonical mammalian STAT signaling processes. We show instead that DIF mediates nuclear translocation via sequences located in the divergent, N-terminal half of the Dd-STATc molecule.