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Immune receptor genes and pericentromeric transposons as targets of common epigenetic regulatory elements
Author(s) -
Cambiagno Damián A.,
Nota Florencia,
Zavallo Diego,
Rius Sebastián,
Casati Paula,
Asurmendi Sebastián,
Alvarez María E.
Publication year - 2018
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.14098
Subject(s) - biology , gene , epigenetics , transposable element , genetics , gene silencing , dna methylation , psychological repression , rna silencing , rna , gene expression , microbiology and biotechnology , mutant , rna interference
Summary Pattern recognition receptors ( PRR ) and nucleotide‐binding leucine‐rich repeat proteins ( NLR ) are major components of the plant immune system responsible for pathogen detection. To date, the transcriptional regulation of PRR / NLR genes is poorly understood. Some PRR / NLR genes are affected by epigenetic changes of neighboring transposable elements ( TE s) ( cis regulation). We analyzed whether these genes can also respond to changes in the epigenetic marks of distal pericentromeric TE s ( trans regulation). We found that Arabidopsis tissues infected with Pseudomonas syringae pv. tomato ( Pst ) initially induced the expression of pericentromeric TE s, and then repressed it by RNA ‐directed DNA methylation (Rd DM ). The latter response was accompanied by the accumulation of small RNA s ( sRNA s) mapping to the TE s. Curiously these sRNA s also mapped to distal PRR / NLR genes, which were controlled by Rd DM but remained induced in the infected tissues. Then, we used non‐infected mom1 (Morpheus’ molecule 1) mutants that expressed pericentromeric TE s to test if they lose repression of PRR / NLR genes. mom1 plants activated several PRR / NLR genes that were unlinked to MOM 1‐targeted TE s, and showed enhanced resistance to Pst . Remarkably, the increased defenses of mom1 were abolished when MOM 1/Rd DM ‐mediated pericentromeric TE s silencing was re‐established. Therefore, common sRNA s could control PRR / NLR genes and distal pericentromeric TE s and preferentially silence TE s when they are activated.