Function and molecular mechanism analysis of CaLasSDE460 effector involved in the pathogenesis of Candidatus Liberibacter asiaticus in citrus

Citrus Huanglongbing (HLB), caused by Candidatus Liberibacter asiaticus (CaLas), is the most serious disease worldwide. CaLasSDE460 was previously characterized as a potential virulence factor of CaLas. However, the function and mechanism of CaLasSDE460 involved in CaLas against citrus is still elusive. Here, we showed that transgenic expression of CaLasSDE460 in Wanjincheng oranges (C. sinensis Osbeck) contributed to the early growth of CaLas and the development of symptoms. When the temperature increased from 25 degrees C to 32 degrees C, CaLas growth and symptom development in transgenic plants were slower than those in WT controls. RNA-seq analysis of transgenic plants showed that CaLasSDE460 affected multiple biological processes. At 25 degrees C, transcription activities of the Protein processing in endoplasmic reticulum and Cyanoamino acid metabolism pathways increased while transcription activities of many pathways decreased at 32 degrees C. 124 and 53 genes, separately annotated to plant-pathogen interaction and MAPK signaling pathways, showed decreased expression at 32 degrees C, compared with these (38 for plant-pathogen interaction and 17 for MAPK signaling) at 25 degrees C. Several important genes (MAPKKK14, HSP70b, NCED3 and WRKY33), remarkably affected by CaLasSDE460, were identified. Totally, our data suggested that CaLasSDE460 participated in the pathogenesis of CaLas through interfering transcription activities of citrus defense response and this interfering was temperature-dependent.

Automated summary

The study found that CaLasSDE460 is a potential virulence factor of citrus Huanglongbing (HLB), and it participates in the pathogenesis of the disease by interfering with the transcription activities of citrus defense response. The transgenic expression of CaLasSDE460 in oranges resulted in slower CaLas growth and symptom development at higher temperatures.