Nitrogen 学习过程实录(1)

一、第一阶段,熟悉Quickstart基本情况

Quickstart是Nitrogen的样本应用,通过分析它,了解如何制作处理动态网页,如何完成Web操作,如何装配“网站”等等。

1、把目录D:/nitrogen/Quickstart复制到D:,改名Quickstart2后,复制回D:/nitrogen/Quickstart2

以后的实验,在目录D:/nitrogen/Quickstart2中进行。

2、在DOS shell中执行命令:

D:/nitrogen/Quickstart2 > quickstart.bat

屏上显示:

Eshell V5.6.5  (abort with ^G)

(nitrogen@127.0.0.1)1>

---

(nitrogen@127.0.0.1)1> Nitrogen is now running on inets.

(nitrogen@127.0.0.1)1> Serving files from: ./wwwroot.

(nitrogen@127.0.0.1)1> Open your browser to: http://localhost:8000

(nitrogen@127.0.0.1)1> ---

可见,Nitrogen依托的服务器,是Erlang自带的Inets;

网页文件,保存在子目录/wwwroot;

服务器运行在端口8000: 

验证运行,可在浏览器中打开:http://localhost:8000

3、分析批命令文件quickstart.bat

@echo off

echo Copy Nitrogen WWW files into ./content/wwwroot/nitrogen

rmdir /s /q ./wwwroot/nitrogen

mkdir ./wwwroot/nitrogen

copy ../www/* ./wwwroot/nitrogen

echo Starting Nitrogen on Inets...

erl -make

erl -name nitrogen@127.0.0.1 -pa apps ebin include -pa ../ebin ../include -eval "application:start(quickstart_inets)"

前6句的操作任务是:

@echo off 不显示命令执行的过程和结果

echo Copy Nitrogen WWW files into ./content/wwwroot/nitrogen

显示一行:Copy Nitrogen WWW files into ./content/wwwroot/nitrogen

rmdir /s /q ./wwwroot/nitrogen

删除目录wwwroot/nitrogen及其子目录,并且不需要用户确认

mkdir ./wwwroot/nitrogen

创建目录wwwroot/nitrogen

copy ../www/* ./wwwroot/nitrogen

从目录D:/nitrogen/www中,复制全部文件到D:/nitrogen/Quickstart2/nitrogen

echo Starting Nitrogen on Inets...

显示一行:Starting Nitrogen on Inets...

 

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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。
02-10
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