Schmidt Sarah, Märker Ramona, Ramšak Barbara, Beier-Rosberger Anna M, Teichert Ines, Kück Ulrich
Allgemeine und Molekulare Botanik, Ruhr-Universität Bochum, Bochum, Germany.
Front Microbiol. 2020 Jul 28;11:1722. doi: 10.3389/fmicb.2020.01722. eCollection 2020.
Sexual and asexual development in filamentous ascomycetes is controlled by components of conserved signaling pathways. Here, we investigated the development of mutant strains lacking genes for kinases MAK2, MEK2, and MIK2, as well as the scaffold protein HAM5 of the pheromone response (PR) pathway. All had a defect in fruiting body development and hyphal fusion. Another phenotype was a defect in melanin-dependent ascospore germination. However, this deficiency was observed only in kinase deletion mutants, but not in strains lacking HAM5. Notably, the same developmental phenotypes were previously described for nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 1 (NOX1) mutants, but the germination defect was only seen in NOX2 mutants. These data suggest a molecular link between the pheromone signaling pathway and both NOX complexes. Using data from yeast two-hybrid (Y2H) analysis, we found that the scaffolding protein HAM5 interacts with NOR1, the regulator of NOX1 and NOX2 complexes. This interaction was further confirmed using differently fluorescent-labeled proteins to demonstrate that NOR1 and HAM5 co-localize at cytoplasmic spots and tips of mature hyphae. This observation was supported by phenotypic characterization of single and double mutants. The oxidative stress response and the initiation of fruiting bodies were similar in Δham5Δnor1 and Δham5, but distinctly reduced in Δnor1, indicating that the double deletion leads to a partial suppression of the Δnor1 phenotype. We conclude that the PR and NOX1 complexes are connected by direct interaction between HAM5 and NOR1. In contrast, PR kinases are linked to the NOX2 complex without participation of HAM5.
丝状子囊菌的有性和无性发育受保守信号通路成分的控制。在此,我们研究了缺乏激酶MAK2、MEK2和MIK2以及信息素反应(PR)通路支架蛋白HAM5基因的突变菌株的发育情况。所有突变菌株在子实体发育和菌丝融合方面均存在缺陷。另一个表型是黑色素依赖性子囊孢子萌发缺陷。然而,这种缺陷仅在激酶缺失突变体中观察到,而在缺乏HAM5的菌株中未观察到。值得注意的是,之前已描述过烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶1(NOX1)突变体具有相同的发育表型,但萌发缺陷仅在NOX2突变体中出现。这些数据表明信息素信号通路与两种NOX复合物之间存在分子联系。利用酵母双杂交(Y2H)分析的数据,我们发现支架蛋白HAM5与NOX1和NOX2复合物的调节因子NOR1相互作用。使用不同荧光标记的蛋白质进一步证实了这种相互作用,以证明NOR1和HAM5在成熟菌丝的细胞质斑点和顶端共定位。单突变体和双突变体的表型特征支持了这一观察结果。Δham5Δnor1和Δham5的氧化应激反应和子实体起始相似,但在Δnor1中明显降低,表明双缺失导致Δnor1表型的部分抑制。我们得出结论,PR和NOX1复合物通过HAM5和NOR1之间的直接相互作用相连。相比之下,PR激酶与NOX2复合物相连,且不涉及HAM5。