Document Type
Article
Language
eng
Format of Original
9 p.
Publication Date
2012
Publisher
Springer
Source Publication
Plant Cell, Tissue and Organ Culture
Source ISSN
0167-6857
Abstract
The aim of this study is to understand the function of EARLI1 in plants subjected to different biotic stresses using EARLI1 overexpressing (OX) and T-DNA knockout (KO) transgenic Arabidopsis lines. Higher levels of expression of EARLI1 in OX lines were confirmed by RT-PCR and Northern blot analysis. The full-length EARLI1 mRNA could not be detected by RT-PCR in KO lines, while only a shorter transcript could be found by RNA gel blotting. In wild-type Col-0 plants (Wt), EARLI1 could be induced by Botrytis cinerea and H2O2, indicating this gene might be involved in plant defense system against pathogens. Trypan blue staining of the infected leaves showed that overexpression of EARLI1 could inhibit the growth of B. cinerea and disruption of EARLI1 in KO lines led to vigorous propagation of the necrotrophic fungus. In addition, KO plants were attacked earlier and more frequently than the wild-type Col-0 plants by fungus gnat (Bradysia difformis). In vivo expression in Saccharomyces cerevisiae demonstrated that the secreted form of EARLI1 could suppress the cell viability by increasing the permeability of the plasma membrane. As a protein localized to cell wall, EARLI1 might play as a component of a receptor and function in resistant response of plants to biotic stresses by sensing environment changes and delivering the signals to intracellular regulation network.
Recommended Citation
Du, Zhen; Xu, Dan; Li, Lan; Shi, Yao; Schläppi, Michael; and Xu, Zi-Qin, "Inhibitory Effects of Arabidopsis EARLI1 Against Botrytis cinerea and Bradysia difformis" (2012). Biological Sciences Faculty Research and Publications. 122.
https://epublications.marquette.edu/bio_fac/122
Comments
Accepted version. Plant Cell, Tissue and Organ Culture, Vol. 110, No. 3 (2012): 435-443. DOI. © 2012 Springer. Used with permission.
Shareable Link. Provided by the Springer Nature SharedIt content-sharing initiative.