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突变体在镰孢菌中 CRE1 逆转了 FRP1 缺失突变体的致病性缺陷。

Mutation of CRE1 in Fusarium oxysporum reverts the pathogenicity defects of the FRP1 deletion mutant.

机构信息

Plant Pathology, Swammerdam Institute for Life Sciences, University of Amsterdam, Science Park 904, 1098 XH Amsterdam, the Netherlands.

出版信息

Mol Microbiol. 2009 Dec;74(5):1100-13. doi: 10.1111/j.1365-2958.2009.06922.x. Epub 2009 Nov 13.

DOI:10.1111/j.1365-2958.2009.06922.x
PMID:19912543
Abstract

The F-box protein Frp1 is required for pathogenicity of Fusarium oxysporum f. sp. lycopersici towards tomato. The Delta frp1 mutant is deficient in expression of genes for cell wall-degrading enzymes (CWDEs) and ICL1, encoding a key enzyme for the assimilation of C2 carbon sources. An explanation for the inability of the Delta frp1 mutant to express these genes may be found in constitutive carbon catabolite repression. Cre1 is the transcriptional repressor in filamentous fungi known to repress several CWDE genes and other genes required for assimilation of non-sugar carbon sources. Here, we demonstrate that Frp1 and Cre1 both control the repression/derepression state of such genes. The replacement of CRE1 with GST::CRE1 resulted in a derepressed phenotype in wild-type background, suggesting that this replacement affects Cre1 function. Strikingly, in the Delta frp1 mutant the replacement of CRE1 with GST::CRE1 restored pathogenicity, growth on ethanol and expression of ICL1 and CWDE genes. A GFP-Cre1 fusion protein is not degraded nor exported out of the nucleus during growth on ethanol, a derepressing carbon source, suggesting that Cre1 is not likely a target of Frp1 for degradation by the proteasome. We conclude that both proteins function together to regulate transcription of carbon source utilization genes.

摘要

F -box 蛋白 Frp1 是尖孢镰刀菌番茄专化型致病性所必需的。Delta frp1 突变体缺乏细胞壁降解酶(CWDE)和 ICL1 的基因表达,ICL1 编码同化 C2 碳源的关键酶。Delta frp1 突变体无法表达这些基因的原因可能在于组成型碳分解代谢物阻遏。Cre1 是丝状真菌中已知的转录阻遏物,可阻遏几种 CWDE 基因和其他同化非糖碳源所需的基因。在这里,我们证明 Frp1 和 Cre1 都控制着这些基因的阻遏/去阻遏状态。用 GST::CRE1 替换 CRE1 在野生型背景下导致去阻遏表型,表明这种替换影响了 Cre1 的功能。引人注目的是,在 Delta frp1 突变体中,用 GST::CRE1 替换 CRE1 恢复了致病性、在乙醇上的生长以及 ICL1 和 CWDE 基因的表达。在乙醇这种去阻遏碳源上生长时,GFP-Cre1 融合蛋白不会被降解或输出细胞核,这表明 Cre1 不太可能是 Frp1 通过蛋白酶体降解的靶标。我们得出结论,这两种蛋白质共同作用调节碳源利用基因的转录。

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