Comparative transcriptome analysis of juniper branches infected by Gymnosporangium spp. highlights their different infection strategies associated with cytokinins

Abstract

Background Gymnosporangium asiaticum and G. yamadae can share Juniperus chinensis as the telial host, but the symptoms are completely different. The infection of G. yamadae causes the enlargement of the phloem and cortex of young branches as a gall, but not for G. asiaticum, suggesting that different molecular interaction mechanisms exist the two Gymnosporangium species with junipers. Results Comparative transcriptome analysis was performed to investigate genes regulation of juniper in responses to the infections of G. asiaticum and G. yamadae at different stages. Functional enrichment analysis showed that genes related to transport, catabolism and transcription pathways were up-regulated, while genes related to energy metabolism and photosynthesis were down-regulated in juniper branch tissues after infection with G. asiaticum and G. yamadae. The transcript profiling of G. yamadae-induced gall tissues revealed that more genes involved in photosynthesis, sugar metabolism, plant hormones and defense-related pathways were up-regulated in the vigorous development stage of gall compared to the initial stage, and were eventually repressed overall. Furthermore, the concentration of cytokinins (CKs) in the galls tissue and the telia of G. yamadae was significantly higher than in healthy branch tissues of juniper. As well, tRNA-isopentenyltransferase (tRNA-IPT) was identified in G. yamadae with highly expression levels during the gall development stages. Conclusions In general, our study provided new insights into the host-specific mechanisms by which G. asiaticum and G. yamadae differentially utilize CKs and specific adaptations on juniper during their co-evolution.

Cytokinin-induced immunity enhances rice blast resistance

“…Additionally, CKs are acknowledged to affect microbial development and physiology 30,31 . However, even if their role in the virulence of the tumor-inducing pathogens is well understood it remains mostly elusive in the case of the non-tumor inducing ones [31][32][33][34][35][36] .…”