The Meloidogyne javanica effector Mj2G02 interferes with jasmonic acid signalling to suppress cell death and promote parasitism in Arabidopsis.
Handa SongBorong LinQiuling HuangTianlin SunWenjun WangJinling LiaoKan ZhuoPublished in: Molecular plant pathology (2021)
Plant-parasitic nematodes can cause devastating damage to crops. These nematodes secrete effectors that suppress the host immune responses to enhance their survival. In this study, Mj2G02, an effector from Meloidogyne javanica, is described. In situ hybridization and transcriptional analysis showed that Mj2G02 was highly expressed in the early infection stages and exclusively expressed in the nematode subventral oesophageal gland cells. In planta RNA interference targeting Mj2G02 impaired M. javanica parasitism, and Mj2G02-transgenic Arabidopsis lines displayed more susceptibility to M. javanica. Using an Agrobacterium-mediated transient expression system and plant immune response assays, we demonstrated that Mj2G02 localized in the plant cell nuclei and could suppress Gpa2/RBP-1-induced cell death. Moreover, by RNA-Seq and quantitative reverse transcription PCR analyses, we showed that Mj2G02 was capable of interfering with the host jasmonic acid (JA) signalling pathway. Multiple jasmonate ZIM-domain (JAZ) genes were significantly upregulated, whereas the JAR1 gene and four JA-responsive genes, MYC3, UPI, THI2.1, and WRKY75, were significantly downregulated. In addition, HPLC analysis showed that the endogenous jasmonoyl-isoleucine (JA-Ile) level in Mj2G02-transgenic Arabidopsis lines was significantly decreased compared to that in wildtype plants. Our results indicate that the M. javanica effector Mj2G02 suppresses the plant immune response, therefore facilitating nematode parasitism. This process is probably mediated by a JA-Ile reduction and JAZ enhancement to repress JA-responsive genes.
Keyphrases
- immune response
- transcription factor
- cell death
- genome wide identification
- rna seq
- dendritic cells
- genome wide
- single cell
- cell wall
- cell cycle arrest
- cancer therapy
- gene expression
- toll like receptor
- type iii
- high throughput
- drug delivery
- mass spectrometry
- plant growth
- inflammatory response
- poor prognosis
- induced apoptosis
- cell therapy
- blood brain barrier
- mesenchymal stem cells
- endothelial cells
- oxidative stress
- diabetic rats
- heat shock
- high performance liquid chromatography