The transcription factor VpCRZ1 is required for fruiting body formation and pathogenicity in Valsa pyri
The transcription factor VpCRZ1 is required for fruiting body formation and pathogenicity in Valsa pyri
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DOI：
10.1016/j.micpath.2016.02.018
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发表时间：
2016-06-01
影响因子：
3.8
通讯作者：
Dou, Daolong
中科院分区：
文献类型：
--
作者：
He, Feng;Zhang, Xiong;Dou, Daolong
梨腐烂病是梨和苹果腐烂病的主要病原菌。迄今为止，其细胞发育和致病性知之甚少。在这项研究中，梨弧菌钙/钙调神经磷酸酶依赖性转录因子CRZ 1（VpCRZ 1）的鉴定和功能。Delta VpCRZ 1突变体表现出受损的致病性，不再能够形成子实体。有趣的是，该突变体还表现出增强的色素沉积和对细胞壁扰动剂（包括SDS、刚果红和荧光钙白色（CFW））的增强的抗性。与野生型相比，Δ VpCRZ 1突变体中刚果红抗性基因（VpRCR 1和VpRCR 2）和几丁质合成酶基因（VpCHS 2和VpCHS 6）的表达水平上调。此外，我们发现VpCRZ 1：eGFP融合蛋白定位于细胞核中的Ca 2+依赖的方式类似于其在其他真菌中的同源物，VpFKS 1，VpPMC 1，VpPMC 2，VpPMR 1，和VpPMA 1基因的VpCRZ 1调节响应于Ca 2+水平。总之，这些结果表明，VpCRZ 1是一个Ca 2+依赖性的转录因子，并需要调节菌丝形态，子实体的形成，和毒力的这一重要的梨和苹果病原体。(C)2016爱思唯尔有限公司版权所有
Valsa pyri is a fatal pathogenic fungus that causes pear and apple canker disease. To date, its cellular development and pathogenicity have been poorly understood. In this study, a V. pyri Ca2+/calcineurin-dependent transcription factor CRZ1 (VpCRZ1) is identified and functionally characterized. The Delta VpCRZ1 mutant exhibits impaired pathogenicity and is no longer able to form fruiting body. Interestingly, this mutant also exhibits enhanced pigment deposition and increased resistance to cell wall perturbing agents including SDS, Congo red and calcofluor white (CFW). The expression levels of Congo red resistance genes (VpRCR1 and VpRCR2) and chitin synthetase genes (VpCHS2 and VpCHS6) are upregulated in the Delta VpCRZ1 mutant compared to the wild type. Furthermore, We show that a VpCRZ1: eGFP fusion protein localizes to the nucleus in a Ca2+-dependent manner similar to its homologs in other fungi, and that the VpFKS1, VpPMC1, VpPMC2, VpPMR1, and VpPMA1 genes are regulated by VpCRZ1 in response to Ca2+ levels. Together, these results suggest that VpCRZ1 is a Ca2+-dependent transcription factor and required for regulating mycelial morphology, fruiting body formation, and virulence of this important pear and apple pathogen. (C) 2016 Elsevier Ltd. All rights reserved.