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Use of enhancer trapping to identify pathogen‐induced regulatory events spatially restricted to plant–microbe interaction sites
Author(s) -
Schroeder Mercedes,
Tsuchiya Tokuji,
He Shuilin,
Eulgem Thomas
Publication year - 2016
Publication title -
molecular plant pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.945
H-Index - 103
eISSN - 1364-3703
pISSN - 1464-6722
DOI - 10.1111/mpp.12287
Subject(s) - biology , pathogen , enhancer , gene , virulence , population , genetics , gene expression , demography , sociology
Summary Plant genes differentially expressed during plant–pathogen interactions can be important for host immunity or can contribute to pathogen virulence. Large‐scale transcript profiling studies, such as microarray‐ or mRNA ‐seq‐based analyses, have revealed hundreds of genes that are differentially expressed during plant–pathogen interactions. However, transcriptional responses limited to a small number of cells at infection sites can be difficult to detect using these approaches, as they are under‐represented in the whole‐tissue datasets typically generated by such methods. This study examines the interactions between A rabidopsis thaliana ( A rabidopsis) and the pathogenic oomycete H yaloperonospora arabidopsidis ( H pa ) by enhancer trapping to uncover novel plant genes involved in local infection responses. We screened a β‐glucuronidase ( GUS ) reporter‐based enhancer‐trap population for expression patterns related to H pa infection. Several independent lines exhibited GUS expression in leaf mesophyll cells surrounding H pa structures, indicating a regulatory response to pathogen infection. One of these lines contained a single enhancer‐trap insertion in an exon of A t1g08800 ( MyoB1 , M yosin   B inding   P rotein 1 ) and was subsequently found to exhibit reduced susceptibility to Hpa . Two additional A rabidopsis lines with T‐DNA insertions in exons of MyoB1 also exhibited approximately 30% fewer spores than wild‐type plants. This study demonstrates that our enhancer‐trapping strategy can result in the identification of functionally relevant pathogen‐responsive genes. Our results further suggest that MyoB1 either positively contributes to Hpa virulence or negatively affects host immunity against this pathogen.

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