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粗糙脉孢菌细胞壁重塑通过cot-1途径的调控由gul-1介导。

Regulation of Neurospora crassa cell wall remodeling via the cot-1 pathway is mediated by gul-1.

作者信息

Herold Inbal, Yarden Oded

机构信息

Department of Plant Pathology and Microbiology, The Robert H. Smith Faculty of Agriculture, Food and Environment, The Hebrew University of Jerusalem, 7610000, Rehovot, Israel.

出版信息

Curr Genet. 2017 Feb;63(1):145-159. doi: 10.1007/s00294-016-0625-z. Epub 2016 Jun 30.

Abstract

Impairment of the Neurospora crassa Nuclear DBF2-related kinase-encoding gene cot-1 results in pleiotropic effects, including abnormally thick hyphal cell walls and septa. An increase in the transcript abundance of genes encoding chitin and glucan synthases and the chitinase gh18-5, but not the cell wall integrity pathway transcription factor rlm-1, accompany the phenotypic changes observed. Deletion of chs-5 or chs-7 in a cot-1 background results in a reduction of hyperbranching frequency characteristic of the cot-1 parent. gul-1 (a homologue of the yeast SSD1 gene) encodes a translational regulator and has been shown to partially suppress cot-1. We demonstrate that the high expression levels of the cell wall remodeling genes analyzed is curbed, and reaches near wild type levels, when gul-1 is inactivated. This is accompanied by morphological changes that include reduced cell wall thickness and restoration of normal chitin levels. We conclude that gul-1 is a mediator of cell wall remodeling within the cot-1 pathway.

摘要

粗糙脉孢菌核DBF2相关激酶编码基因cot-1的损伤会导致多效性效应,包括菌丝细胞壁和隔膜异常增厚。编码几丁质和葡聚糖合成酶以及几丁质酶gh18-5的基因转录丰度增加,但细胞壁完整性途径转录因子rlm-1没有增加,这与观察到的表型变化相伴。在cot-1背景中缺失chs-5或chs-7会导致cot-1亲本特有的超分支频率降低。gul-1(酵母SSD1基因的同源物)编码一种翻译调节因子,并且已被证明可部分抑制cot-1。我们证明,当gul-1失活时,所分析的细胞壁重塑基因的高表达水平受到抑制,并达到接近野生型水平。这伴随着形态学变化,包括细胞壁厚度降低和几丁质水平恢复正常。我们得出结论,gul-1是cot-1途径内细胞壁重塑的介导因子。

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