C# 实战:.NET 2008 Domain-Driven Design教程

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".NET Domain-Driven Design with C# (Apr 2008)" 是一本由 Tim McCarthy 撰写的实用指南,它结合了领域驱动设计(Domain-Driven Design, DDD)理论与 Microsoft .NET 2008 开发环境,为读者提供了丰富的实战经验。该书主要围绕一个名为 "Smart CA Application" 的项目展开,结构清晰地分为多个章节,每个章节深入探讨了软件架构、业务逻辑实现以及与服务器同步等关键概念。 在《介绍项目:Smart CA 应用》(Chapter 1)中,作者首先引导读者理解项目的背景和目标,为后续的设计和开发奠定了基础。接着的章节逐步深入,如《设计分层架构》(Chapter 2)涵盖了如何构建模块化、可扩展的架构,确保各个层次间的职责明确。 在《管理项目》(Chapter 3)中,作者详细介绍了项目管理流程的集成,包括如何处理项目生命周期中的不同阶段和任务。《公司和联系人》(Chapter 4)、《提交单》(Chapter 5)、《请求信息》(Chapter 6)和《提案请求》(Chapter 7)分别展示了如何处理与项目相关的商业实体和交互,这些都是领域模型的核心组成部分。 《变更订单》(Chapter 8)和《施工变更指令》(Chapter 9)着重讨论了如何应对项目执行过程中可能出现的变更管理和控制。而《与服务器同步》(Chapter 10)则涉及了如何利用 .NET 技术与远程服务器进行数据交换,保持数据一致性。 最后一章,《客户端会员系统》(Chapter 11)可能涵盖了用户界面设计和安全性的考虑,展示了一个完整的业务场景是如何在 DDD 指导下构建和实现的。全书以索引(Chapter 11)收尾,便于读者查找特定主题。 这本书是 .NET 开发者学习如何将DDD原则应用于实际项目中的宝贵资源,提供了从问题定义、设计到解决方案的具体实施步骤,对于提升软件工程实践中的业务理解和设计能力具有很高的价值。同时,作为版权作品,确保遵循了出版许可和复制规定。

Rab GTPases serve as master regulators of membrane trafficking. They can be activated by guanine nucleotide exchange factors (GEF) and be inactivated by GTPase-activating proteins (GAPs). The roles of some GAPs have been explored in Saccharomyces cerevisiae, but are largely unknown in filamentous fungi. Here, we investigated the role of GAP Gyp3 gene, an ortholog of S. cerevisiae Gyp3, in an entomopathogenic fungus, Metarhizium acridum. We found that MaGyp3 is mainly localized to the endoplasmic reticulum (ER) of vegetative hyphae, nuclei of mature conidia, and both ER and nuclei in invasive hyphae. Lack of MaGyp3 caused a decreased tolerance to hyperosmotic stress, heat-shock and UV-B radiation. Moreover, the ΔMaGyp3 mutant showed a significantly decreased pathogenicity owing to delayed germination, reduced appressorium-mediated penetration and impaired invasive growth. Loss of MaGyp3 also caused impaired fungal growth, advanced conidiation and defects in utilization of carbon and nitrogen sources, while overexpression of MaGyp3 exhibited delayed conidiation on nutrient-rich medium and conidiation pattern shift from microcycle conidiation to normal conidiation on nutrient-limited medium. Mavib-1, a tanscription factor invloved in conidiation by affecting nutrient utilizaiton, can directly bind to the promoter of MaGyp3. ΔMaGyp3 and ΔMavib-1 mutants shared similar phenotypes, and overexpression mutants of MaGyp3 and Mavib-1 (Mavib-1-OE) exhibited similar phenotypes in growth, conidiation and pathogenicity. Reintroduction of the Magyp3 driven by strong promoter gpd in ΔMavib-1 mutant recovered the defects in growth and conidiation for dysfunction of Mavib1. Taken together, our findings uncovered the role of GAP3 in a filamentous pathogenic fungus and and illustrated the upstream regulatory mechanism by direct interaction with Mavib-1.请用nature杂志的风格润色成学术论文的形式。

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