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A genetic analysis of the Arabidopsi...

Nishimura, Marc Tad.

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A genetic analysis of the Arabidopsis-powdery mildew interaction: Cloning and characterization of mildew-induced lesion mutants.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	A genetic analysis of the Arabidopsis-powdery mildew interaction: Cloning and characterization of mildew-induced lesion mutants./
作者:	Nishimura, Marc Tad.
面頁冊數:	139 p.
附註:	Source: Dissertation Abstracts International, Volume: 66-08, Section: B, page: 4022.
Contained By:	Dissertation Abstracts International66-08B.
標題:	Agriculture, Plant Pathology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3187332
ISBN:	9780542296604

A genetic analysis of the Arabidopsis-powdery mildew interaction: Cloning and characterization of mildew-induced lesion mutants.
Nishimura, Marc Tad.

A genetic analysis of the Arabidopsis-powdery mildew interaction: Cloning and characterization of mildew-induced lesion mutants. - 139 p.

Source: Dissertation Abstracts International, Volume: 66-08, Section: B, page: 4022.

Thesis (Ph.D.)--Stanford University, 2005.

Plants commonly use cell death of infected tissues to limit the spread of pathogens into neighboring tissues. To better understand how pathogen-induced cell death is regulated, we have taken a genetic approach, characterizing mutants that have increased cell death in response to powdery mildew. The mildew-induced lesions class of mutants develops necrotic lesions in response to pathogens. This thesis describes the initial characterization of the mil collection and the cloning and characterization of the pmr4 (mil8) and mil4 mutants.

ISBN: 9780542296604Subjects--Topical Terms:

1028950
Agriculture, Plant Pathology.

A genetic analysis of the Arabidopsis-powdery mildew interaction: Cloning and characterization of mildew-induced lesion mutants.
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245 1 2 $a A genetic analysis of the Arabidopsis-powdery mildew interaction: Cloning and characterization of mildew-induced lesion mutants.
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500 $a Source: Dissertation Abstracts International, Volume: 66-08, Section: B, page: 4022.
500 $a Adviser: Shauna Somerville.
502 $a Thesis (Ph.D.)--Stanford University, 2005.
520 $a Plants commonly use cell death of infected tissues to limit the spread of pathogens into neighboring tissues. To better understand how pathogen-induced cell death is regulated, we have taken a genetic approach, characterizing mutants that have increased cell death in response to powdery mildew. The mildew-induced lesions class of mutants develops necrotic lesions in response to pathogens. This thesis describes the initial characterization of the mil collection and the cloning and characterization of the pmr4 (mil8) and mil4 mutants.
520 $a pmr4 was cloned and found to encode a callose synthase. This is unexpected since callose production is considered to be a defense response. We find that pmr4 mutants lack both pathogen-induced and wound-induced callose deposition. The pmr4 mutant is constitutively upregulated for salicylic acid-responsive defense gene expression. Double mutant analysis indicates that blocking the salicylic acid (SA) pathway is sufficient to restore compatibility to pmr4. These results suggest that callose or the callose synthase protein is negatively regulating SA-based defenses.
520 $a mil4 was cloned and found to encode a novel, plant-specific membrane protein. MIL4 contains four predicted transmembrane domains, but contains no obvious sequence similarity to known functional domains. MIL4 is only weakly expressed in uninfected tissues, but it is strongly induced by both pathogens and by the SA analog benzothiadiazole. MIL4 expression is initially limited to the mesophyll cells underlying pathogen-penetrated epidermal cells, a pattern that corresponds to the site of cell death in the mil4 mutant. Similar to pmr4 , the mil4 phenotype is SA-dependent and the mutant upregulates both SA responsive defense genes as well as SA accumulation.
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