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一种新型Myb同源物通过诱导腺苷酸环化酶表达启动盘基网柄菌发育。

A novel Myb homolog initiates Dictyostelium development by induction of adenylyl cyclase expression.

作者信息

Otsuka H, Van Haastert P J

机构信息

Department of Biochemistry, University of Groningen, 9747 AG Groningen, The Netherlands.

出版信息

Genes Dev. 1998 Jun 1;12(11):1738-48. doi: 10.1101/gad.12.11.1738.

Abstract

Dictyostelium development is induced by starvation. The adenylyl cyclase gene ACA is one of the first genes expressed upon starvation. ACA produces extracellular cAMP that induces chemotaxis, aggregation, and differentiation in neighboring cells. Using insertional mutagenesis we have isolated a mutant that does not aggregate upon starvation but is rescued by adding extracellular cAMP. Sequencing of the mutated locus revealed a new gene, DdMYB2, whose product contains three Myb repeats, the DNA-binding motif of Myb-related transcription factors. Ddmyb2-null cells show undetectable levels of ACA transcript and no cAMP production. Ectopic expression of ACA from a constitutive promotor rescues differentiation and morphogenesis of Ddmyb2-null mutants. The results suggest that development in Dictyostelium starts by starvation-mediated DdMyb2 activation, which induces adenylyl cyclase activity producing the differentiation-inducing signal cAMP.

摘要

盘基网柄菌的发育由饥饿诱导。腺苷酸环化酶基因ACA是饥饿时最早表达的基因之一。ACA产生细胞外cAMP,诱导相邻细胞的趋化性、聚集和分化。利用插入诱变,我们分离出一个突变体,该突变体在饥饿时不聚集,但通过添加细胞外cAMP得以挽救。对突变位点的测序揭示了一个新基因DdMYB2,其产物包含三个Myb重复序列,这是Myb相关转录因子的DNA结合基序。Ddmyb2基因缺失的细胞显示ACA转录本水平无法检测到,且不产生cAMP。从组成型启动子异位表达ACA可挽救Ddmyb2基因缺失突变体的分化和形态发生。结果表明,盘基网柄菌的发育始于饥饿介导的DdMyb2激活,其诱导腺苷酸环化酶活性产生诱导分化的信号cAMP。

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