The role of fungal NADPH oxidase complexes in differentiation and virulence

NADPH氧化酶（Nox）产生的活性氧（ROS）在动植物的病原体防御反应和多种分化过程中起着重要作用。越来越多的证据表明，在真菌中，这些膜复合物也参与所有主要的发育过程：它们对极性生长，性别分化和毒性有影响。仍然有相当缺乏的知识复杂的组成，招聘和本地化，并在分子机制的基础上，他们对这么多重要的细胞过程的影响。基于广泛的分析，在第一个项目期间的氮氧化物复合物和活性氧信号转导成分一般在两种真菌具有完全不同的生活方式和明显显着不同的氮氧化物功能-的活体麦角菌和灰霉病菌-，我们将专注于在这第二个阶段的详细功能特性的氮氧化物复合物的模型系统灰霉病菌。 我们将研究Nox复合物的特定组成/募集，定位，与特定的发育阶段/代谢活动相关，重点关注ER中可能的功能。我们将研究Nox对细胞骨架的影响，在分化过程（例如渗透结构）的背景下，并分析影响哺乳动物系统中Nox活性的调节电路，例如脂质信号。此外，我们将尝试确定替代的活性氧来源，现有的活性氧过量产生突变体的基础上。

Reactive oxygen species (ROS) generated by NADPH oxidases (Nox) play an important role in pathogen defense reactions and a broad variety of differentiation processes in animals and plants. There is growing evidence that also in fungi these membrane complexes are involved in all major developmental processes: they have impact on polar growth, sexual differentiation and virulence. Still there is considerable lack of knowledge on complex composition, recruitment and localization, and on the molecular mechanisms underlying their impact on so many important cellular processes. Based on the broad analysis in the first project period of the Nox complexes and ROS signaling components in general in two fungi with completely different lifestyle and obviously significantly different Nox functions - the biotrophic ergot fungus Claviceps purpurea and the necrotrophic grey mold fungus Botrytis cinerea-, we will focus in this second period on a detailed functional characterization of the Nox complexes in the model system B.cinerea. We will investigate the specific composition/recruitment of the Nox complexes, the localization, linked to specific developmental stages/metabolic activities, focusing on a possible function in the ER. We will study the impact of Nox on the cytoskeleton, in the context of differentiation processes (e.g.penetration structures) and analyse regulatory circuits which affect Nox activity in mammalian systems, e.g. lipid signaling. In addition, we will try to identify alternative ROS sources, based on existing ROS overproducing mutants.