Abstract

In plants, growth–defense tradeoffs are essential for optimizing plant performance and adaptation under stress conditions, such as pathogen attack. Root-knot nematodes (RKNs) cause severe economic losses in many crops worldwide, although little is known about the mechanisms that control plant growth and defense responses during nematode attack. Upon investigation of Arabidopsis thaliana infected with RKN (Meloidogyne incognita), we observed that the atypical transcription factor DP-E2F-like 1 (DEL1) repressed salicylic acid (SA) accumulation in RKN-induced galls. The DEL1-deficient Arabidopsis mutant (del1-1) exhibited excessive SA accumulation in galls and is more resistant to RKN infection. In addition, excessive lignification was observed in galls of del1-1. On the other hand, the root growth of del1-1 is reduced after RKN infection. Taken together, these findings suggest that DEL1 plays an important role in the balance between plant growth and defense responses to RKN infection by controlling SA accumulation and lignification.

Details

Title
The atypical E2F transcription factor DEL1 modulates growth–defense tradeoffs of host plants during root-knot nematode infection
Author
Nakagami Satoru 1 ; Saeki Kentaro 1 ; Toda Kei 1 ; Ishida Takashi 2 ; Sawa Shinichiro 1 

 Kumamoto University, Graduate School of Science and Technology, Kumamoto, Japan (GRID:grid.274841.c) (ISNI:0000 0001 0660 6749) 
 Kumamoto University, Graduate School of Science and Technology, Kumamoto, Japan (GRID:grid.274841.c) (ISNI:0000 0001 0660 6749); Kumamoto University, International Research Organization for Advanced Science and Technology (IROAST), Kumamoto, Japan (GRID:grid.274841.c) (ISNI:0000 0001 0660 6749) 
Publication year
2020
Publication date
2020
Publisher
Nature Publishing Group
e-ISSN
20452322
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
2408511746
Copyright
© The Author(s) 2020. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.