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<p><i>Pantoea ananatis</i> is an emerging plant pathogen that causes center rot disease of onion. To identify genes related to virulence, we inoculated transposon mutants of <i>P. ananatis</i> NR 53 into onion bulbs and screened them for mutants with reduced virulence. One mutant with reduced virulence was obtained in which the transposon was inserted into the <i>gla</i> gene, which encodes UDP-galacturonic acid 4-epimerase. A <i>gla</i> mutant strain in which the <i>gla</i> gene was complemented with a plasmid caused the same symptoms as the wild-type strain. To exclude the polar effect of the transposon insertion mutation, we constructed a <i>gla</i> deletion mutant of <i>P. ananatis</i> CTB1135, which is also pathogenic to onions as NR 53. Deletion of the <i>gla</i> gene also reduced the virulence of <i>P</i>. <i>ananatis</i> CTB1135. To investigate why deletion of the <i>gla</i> gene reduces virulence, we analyzed the phenotype of the <i>gla</i> deletion mutant. In the <i>gla</i> deletion mutant, lipopolysaccharide (LPS) biosynthesis was inhibited, resulting in reduced drug resistance. Furthermore, flagella formation was inhibited, and motility was reduced. These findings suggest that the <i>gla</i> gene contributes to the virulence of <i>P</i>. <i>ananatis</i> through its involvement in overall virulence mechanisms, including LPS biosynthesis, drug resistance, and motility.</p>

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UDP-galacturonic acid 4-epimerase is required for LPS biosynthesis, drug resistance, motility, and virulence in Pantoea ananatis, a causal agent of center rot disease of onion

  • 期刊论文

  • 发表日期：

    2025年1月6日

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  • Yuta Isobe,
  • Kenji Ueda,
  • Luna Kanatsu,
  • Keita Fukui,
  • Yoshihiko Hara,
  • Yuichi Takikawa,
  • Kenro Oshima

摘要

Pantoea ananatis is an emerging plant pathogen that causes center rot disease of onion. To identify genes related to virulence, we inoculated transposon mutants of P. ananatis NR 53 into onion bulbs and screened them for mutants with reduced virulence. One mutant with reduced virulence was obtained in which the transposon was inserted into the gla gene, which encodes UDP-galacturonic acid 4-epimerase. A gla mutant strain in which the gla gene was complemented with a plasmid caused the same symptoms as the wild-type strain. To exclude the polar effect of the transposon insertion mutation, we constructed a gla deletion mutant of P. ananatis CTB1135, which is also pathogenic to onions as NR 53. Deletion of the gla gene also reduced the virulence of P. ananatis CTB1135. To investigate why deletion of the gla gene reduces virulence, we analyzed the phenotype of the gla deletion mutant. In the gla deletion mutant, lipopolysaccharide (LPS) biosynthesis was inhibited, resulting in reduced drug resistance. Furthermore, flagella formation was inhibited, and motility was reduced. These findings suggest that the gla gene contributes to the virulence of P. ananatis through its involvement in overall virulence mechanisms, including LPS biosynthesis, drug resistance, and motility.