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未折叠蛋白反应与支架非依赖性信息素丝裂原活化蛋白激酶信号传导调控生长、发育及植物发病机制。

Unfolded Protein Response and Scaffold Independent Pheromone MAP Kinase Signaling Control Growth, Development, and Plant Pathogenesis.

作者信息

Starke Jessica, Harting Rebekka, Maurus Isabel, Leonard Miriam, Bremenkamp Rica, Heimel Kai, Kronstad James W, Braus Gerhard H

机构信息

Department of Molecular Microbiology and Genetics, Institute of Microbiology and Genetics and Göttingen Center for Molecular Biosciences (GZMB), University of Göttingen, 37077 Göttingen, Germany.

Michael Smith Laboratories, Department of Microbiology and Immunology, University of British Columbia, Vancouver, BC V6T 1Z4, Canada.

出版信息

J Fungi (Basel). 2021 Apr 15;7(4):305. doi: 10.3390/jof7040305.

Abstract

Differentiation, growth, and virulence of the vascular plant pathogen depend on a network of interconnected cellular signaling cascades. The transcription factor Hac1 of the endoplasmic reticulum-associated unfolded protein response (UPR) is required for initial root colonization, fungal growth, and vascular propagation by conidiation. Hac1 is essential for the formation of microsclerotia as long-time survival resting structures in the field. Single endoplasmic reticulum-associated enzymes for linoleic acid production as precursors for oxylipin signal molecules support fungal growth but not pathogenicity. Microsclerotia development, growth, and virulence further require the pheromone response mitogen-activated protein kinase (MAPK) pathway, but without the Ham5 scaffold function. The MAPK phosphatase Rok1 limits resting structure development of , but promotes growth, conidiation, and virulence. The interplay between UPR and MAPK signaling cascades includes several potential targets for fungal growth control for supporting disease management of the vascular pathogen .

摘要

维管束植物病原体的分化、生长和毒力取决于相互连接的细胞信号级联网络。内质网相关未折叠蛋白反应(UPR)的转录因子Hac1是根部初始定殖、真菌生长以及通过分生孢子进行维管束传播所必需的。Hac1对于微菌核的形成至关重要,微菌核是该病原体在田间长期存活的休眠结构。用于生产作为氧脂信号分子前体的亚油酸的单一内质网相关酶支持真菌生长,但不支持致病性。微菌核的发育、生长和毒力还需要信息素反应丝裂原活化蛋白激酶(MAPK)途径,但不需要Ham5支架功能。MAPK磷酸酶Rok1限制了该病原体休眠结构的发育,但促进了生长、分生孢子形成和毒力。UPR和MAPK信号级联之间的相互作用包括几个潜在的真菌生长控制靶点,以支持对维管束病原体的病害管理。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/92de/8071499/f7d35744e9c2/jof-07-00305-g001.jpg

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