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粗糙脉孢菌ASM-1可弥补构巢曲霉stuA突变体的分生孢子形成缺陷。

Neurospora crassa ASM-1 complements the conidiation defect in a stuA mutant of Aspergillus nidulans.

作者信息

Chung Dawoon, Upadhyay Srijana, Bomer Brigitte, Wilkinson Heather H, Ebbole Daniel J, Shaw Brian D

机构信息

Program for the Biology of Filamentous Fungi, Department of Plant Pathology and Microbiology, Texas A&M University, College Station, Texas 77843.

Program for the Biology of Filamentous Fungi, Department of Plant Pathology and Microbiology, Texas A&M University, College Station, Texas 77843

出版信息

Mycologia. 2015 Mar-Apr;107(2):298-306. doi: 10.3852/14-079. Epub 2014 Dec 30.

Abstract

Aspergillus nidulans StuA and Neurospora crassa ASM-1 are orthologous APSES (ASM-1, PHD1, SOK2, Efg1, StuA) transcription factors conserved across a diverse group of fungi. StuA and ASM-1 have roles in asexual (conidiation) and sexual (ascospore formation) development in both organisms. To address the hypothesis that the last common ancestor of these diverse fungi regulated conidiation with similar genes, asm-1 was introduced into the stuA1 mutant of A. nidulans. Expression of asm-1 complemented defective conidiophore morphology and restored conidia production to wild type levels in stuA1. Expression of asm-1 in the stuA1 strain did not rescue the defect in sexual development. When the conidiation regulator AbaA was tagged at its C-terminus with GFP in A. nidulans, it localized to nuclei in phialides. When expressed in the stuA1 mutant, AbaA::GFP localized to nuclei in conidiophores but no longer was confined to phialides, suggesting that expression of AbaA in specific cell types of the conidiophore was conditioned by StuA. Our data suggest that the function in conidiation of StuA and ASM-1 is conserved and support the view that, despite the great morphological and ontogenic diversity of their condiphores, the last common ancestor of A. nidulans and N. crassa produced an ortholog of StuA that was involved in conidiophore development.

摘要

构巢曲霉的StuA和粗糙脉孢菌的ASM-1是直系同源的APSES(ASM-1、PHD1、SOK2、Efg1、StuA)转录因子,在多种真菌中保守存在。StuA和ASM-1在这两种生物体的无性(分生孢子形成)和有性(子囊孢子形成)发育中均发挥作用。为了验证这些不同真菌的最后一个共同祖先通过相似基因调控分生孢子形成这一假说,将asm-1导入构巢曲霉的stuA1突变体中。asm-1的表达弥补了分生孢子梗形态缺陷,并使stuA1中的分生孢子产量恢复到野生型水平。在stuA1菌株中asm-1的表达未能挽救有性发育缺陷。当在构巢曲霉中分生孢子形成调节因子AbaA的C末端用绿色荧光蛋白标记时,它定位于产孢细胞的细胞核中。当在stuA1突变体中表达时,AbaA::GFP定位于分生孢子梗的细胞核中,但不再局限于产孢细胞,这表明AbaA在分生孢子梗特定细胞类型中的表达受StuA调控。我们的数据表明,StuA和ASM-1在分生孢子形成中的功能是保守的,并支持以下观点:尽管构巢曲霉和粗糙脉孢菌的分生孢子梗在形态和个体发育上存在很大差异,但它们的最后一个共同祖先产生了一个参与分生孢子梗发育的StuA直系同源物。

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