4.2 Article

Silencing of phosphoinositide dependent protein kinase orthologs reduces hypersensitive cell death in Nicotiana benthamiana

Journal

PLANT BIOTECHNOLOGY
Volume 37, Issue 3, Pages 363-367

Publisher

JAPANESE SOC PLANT CELL & MOLECULAR BIOLOGY
DOI: 10.5511/plantbiotechnology.20.0511b

Keywords

effector-triggered immunity; hypersensitive cell death; Nicotiana benthamiana; phosphoinositide dependent protein kinase; Ralstonia solanacearum; virus-induced gene silencing

Funding

  1. Cabinet Office grant in aid, the Advanced Next-Generation Greenhouse Horticulture by IoP (Internet of Plants), Japan
  2. Ministry of Education, Culture, Sports, Science and Technology (MEXT) as part of Joint Research Program
  3. Ministry of Education, Science, Sports, and Culture, Japan [24580066]
  4. Asahi Glass Foundation
  5. Agricultural Chemical Research Foundation
  6. Sapporo Bioscience Foundation
  7. Grants-in-Aid for Scientific Research [24580066] Funding Source: KAKEN

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Phosphatidic acid plays an important role in plant immune responses against phytopathogenic bacteria in Nicotiana benthamiana. here we focused on phosphoinositide dependent protein kinases (PDKs) as a candidate required for phosphatidic acid signaling. Based on Arabidopsis PDK sequences, we identified four putative PDK orthologs in N. benthamiana genome. To address the role of PDKs in plant defense responses, we created all four NbPDKs-silenced plants by virus-induced gene silencing. the NbPDKs-silenced plants showed a moderately reduced growth phenotype. Induction of hypersensitive cell death was compromised in the NbPDKs-silenced plants challenged with Ralstonia solanacearum. The hypersensitive cell death induced by bacterial effectors was also reduced in the NbPDKs-silenced plants. the NbPDKs-silenced plants showed decreased production of salicylic acid, jasmonic acid and jasmonoyl-L-isoleucine, as well as hydrogen peroxide after inoculation with R. solanacearum. These results suggest that NbPDKs might have an important role in the regulation of the hypersensitive cell death via plant hormone signaling and oxidative burst.

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