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保守转录因子的磷酸化编码决定真菌的毒力。

Phospho-code of a conserved transcriptional factor underpins fungal virulence.

机构信息

Co-Innovation Center for Sustainable Forestry in Southern China, Nanjing Forestry University, Nanjing, Jiangsu, 210037, China.

School of Agricultural Sciences, Zhengzhou University, Zhengzhou, Henan, 450001, China.

出版信息

BMC Biol. 2024 Aug 26;22(1):179. doi: 10.1186/s12915-024-01978-y.

Abstract

BACKGROUND

Cell wall integrity (CWI) is crucial for fungal growth, pathogenesis, and adaptation to extracellular environments. Calcofluor white (CFW) is a cell wall perturbant that inhibits fungal growth, yet little is known about how phytopathogenic fungi respond to the CFW-induced stress.

RESULTS

In this study, we unveiled a significant discovery that CFW triggered the translocation of the transcription factor CgCrzA from the cytoplasm to the nucleus in Colletotrichum gloeosporioides. This translocation was regulated by an interacting protein, CgMkk1, a mitogen-activated protein kinase involved in the CWI pathway. Further analysis revealed that CgMkk1 facilitated nuclear translocation by phosphorylating CgCrzA at the Ser280 residue. Using chromatin immunoprecipitation sequencing, we identified two downstream targets of CgCrzA, namely CgCHS5 and CgCHS6, which are critical for growth, cell wall integrity, and pathogenicity as chitin synthase genes.

CONCLUSIONS

These findings provide a novel insight into the regulatory mechanism of CgMkk1-CgCrzA-CgChs5/6, which enables response of the cell wall inhibitor CFW and facilitates infectious growth for C. gloeosporioides.

摘要

背景

细胞壁完整性(CWI)对真菌的生长、发病机制和适应细胞外环境至关重要。钙荧光白(CFW)是一种细胞壁扰动剂,能抑制真菌生长,但人们对植物病原真菌如何应对 CFW 诱导的应激知之甚少。

结果

在这项研究中,我们揭示了一个重要发现,即 CFW 诱使转录因子 CgCrzA 从 Colletotrichum gloeosporioides 的细胞质易位到细胞核。这种易位受细胞外信号调节激酶(MAPK)途径中参与 CWI 途径的互作蛋白 CgMkk1 调控。进一步分析表明,CgMkk1 通过磷酸化 CgCrzA 的 Ser280 残基促进核易位。通过染色质免疫沉淀测序,我们鉴定了 CgCrzA 的两个下游靶标 CgCHS5 和 CgCHS6,它们作为几丁质合酶基因对于生长、细胞壁完整性和致病性至关重要。

结论

这些发现为 CgMkk1-CgCrzA-CgChs5/6 的调控机制提供了新的见解,使细胞细胞壁抑制剂 CFW 能够做出反应,并促进 C. gloeosporioides 的感染性生长。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c0d2/11346053/176a47d654b1/12915_2024_1978_Fig1_HTML.jpg

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