AP2/ERF 轉錄因子對生物性及非生物性逆境反應之研究

Abstract

APETALA 2/ ethylene-responsive element binding factors (AP2/ERFs) play a crucial role in both plant defense- and stress-signaling pathways through specifically binding to cis-acting DNA regulatory elements such as DRE element or GCC-box. In this study, two ERFs including Arabidopsis AF9 and tomato SlERF3 were functionally investigated. AF9 had early response to salt-, pathogen-, and oxidative stresses, and acted as a GCC-mediated activator. Overexpression of AF9 reduced chlorophyll content through light-dependent pathway, and enhanced salt tolerance of transgenic Arabidopsis. Meanwhile, transgenic plants expressing AF9 resulted in transcripts accumulation of pathogenesis-related proteins 14 (PR14) genes such as LTP1 (lipid transfer proteins 1), LTP2, LTP3, LTP6, LTP7, and three LTP-like genes, and enhanced tolerance of soft rot bacteria. In addition, tomato SlERF3 acted as GCC-mediated transcriptional repressor and suppressed tomato growth when overexpressed. The character of SlERF3 can be reversed from a transcriptional repressor to an activator after deleting the EAR repressor-domain deletion (SlERF3ΔRD). Constitutively expression of SlERF3ΔRD resulted in incomed expression of PR1, PR2, and PR5, and enhanced tolerance to salinity and to pathogen infection in transgenic plants. Meanwhile, the seed number, fruit number and fresh weight of transgenic SlERF3ΔRD were mostly maintained under normal condition. Furthermore, the SlERF3ΔRD transgenic tomato preserved better agronomical traits under salt stress or pathogen inoculation when compared with wild-type plants. This study illustrated that Arabidopsis AF9 gene participated in defense pathway possibly through enhanced expression of PR14, and tomato SlERF3 gene enhancing tolerance to both biotic and abiotic stresses in transgenic plants after the deletion of the EAR repressor domain. Our findings suggest that ERF proteins are important and useful in crop improvement or genetic engineering to increase stress tolerance in plants.