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http://dx.doi.org/10.4014/jmb.0905.05044

The Gene fpk1, Encoding a cAMP-dependent Protein Kinase Catalytic Subunit Homolog, is Required for Hyphal Growth, Spore Germination, and Plant Infection in Fusarium verticillioides  

Pei-Bao, Zhao (College of Plant Protection, Shandong Agricultural University)
Ren, Ai-Zhi (Department of Plant Protection, Liaocheng University)
Xu, Hou-Juan (College of Plant Protection, Shandong Agricultural University)
Li, Duo-Chuan (College of Plant Protection, Shandong Agricultural University)
Publication Information
Journal of Microbiology and Biotechnology / v.20, no.1, 2010 , pp. 208-216 More about this Journal
Abstract
Fusarium verticillioides is an important pathogen of maize, being responsible for ear rots, stalk rots, and seedling blight worldwide. During the past decade, F. verticillioides has caused several severe epidemics of maize seedling blight in many areas of China, which lead to significant losses. In order to understand the molecular mechanisms regulating fungal development and pathogenicity in this pathogen, we isolated and characterized the gene fpk1 (GenBank Accession No. EF405959) encoding a homolog of the cAMP-dependent protein kinase catalytic subunit, which included a 1,854-bp DNA sequence from ATG to TAA, with a 1,680-bp coding region, and three introns (lengths: 66 bp, 54 bp, and 54 bp), and the predicated protein precursor had 559 aa. The mutant ${\Delta}fpk1$, which was disrupted of the fpkl gene, showed reduced vegetative growth, fewer and shorter aerial mycelia, strongly impaired conidiation, and reduced spore germination rate. After germinating, the fresh hypha was stubby and lacking of branch. When inoculated in susceptible maize varieties, the infection of the mutant ${\Delta}fpk1$ was delayed and the infection efficiency was reduced compared with that of the wild-type strain. AU this indicated that gene fpk1 participated in hyphal growth, conidiophore production, spore germination, and virulence in F. verticillioides.
Keywords
Fusarium verticillioides; serine-threonine protein kinase; gene disruption; pathogenicity;
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