Use of the Plant Defense Protein Osmotin To Identify Fusarium oxysporum Genes That Control Cell Wall Properties
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ArticleKAUST Department
Biological and Environmental Science and Engineering (BESE) DivisionCenter for Desert Agriculture
Plant Stress Genomics Research Lab
Date
2010-02-26Online Publication Date
2010-02-26Print Publication Date
2010-04-01Permanent link to this record
http://hdl.handle.net/10754/553078
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Fusarium oxysporum is the causative agent of fungal wilt disease in a variety of crops. The capacity of a fungal pathogen such as F. oxysporum f. sp. nicotianae to establish infection on its tobacco (Nicotiana tabacum) host depends in part on its capacity to evade the toxicity of tobacco defense proteins, such as osmotin. Fusarium genes that control resistance to osmotin would therefore reflect coevolutionary pressures and include genes that control mutual recognition, avoidance, and detoxification. We identified FOR (Fusarium Osmotin Resistance) genes on the basis of their ability to confer osmotin resistance to an osmotin-sensitive strain of Saccharomyces cerevisiae. FOR1 encodes a putative cell wall glycoprotein. FOR2 encodes the structural gene for glutamine:fructose-6-phosphate amidotransferase, the first and rate-limiting step in the biosynthesis of hexosamine and cell wall chitin. FOR3 encodes a homolog of SSD1, which controls cell wall composition, longevity, and virulence in S. cerevisiae. A for3 null mutation increased osmotin sensitivity of conidia and hyphae of F. oxysporum f. sp. nicotianae and also reduced cell wall β-1,3-glucan content. Together our findings show that conserved fungal genes that determine cell wall properties play a crucial role in regulating fungal susceptibility to the plant defense protein osmotin.Citation
Use of the Plant Defense Protein Osmotin To Identify Fusarium oxysporum Genes That Control Cell Wall Properties 2010, 9 (4):558 Eukaryotic CellPublisher
American Society for MicrobiologyJournal
Eukaryotic CellPubMed ID
20190074PubMed Central ID
PMC2863404Additional Links
http://ec.asm.org/cgi/doi/10.1128/EC.00316-09ae974a485f413a2113503eed53cd6c53
10.1128/EC.00316-09