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TMV induces RNA decay pathways to modulate gene silencing and disease symptoms
Author(s) -
Conti Gabriela,
Zavallo Diego,
Venturuzzi Andrea L.,
Rodriguez Maria C.,
Crespi Martin,
Asurmendi Sebastian
Publication year - 2017
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.13323
Subject(s) - rna , rna silencing , gene silencing , biology , gene knockdown , rna interference , microbiology and biotechnology , exosome complex , antisense rna , rna induced silencing complex , gene expression , trans acting sirna , small interfering rna , tobacco mosaic virus , non coding rna , messenger rna , rna induced transcriptional silencing , rna binding protein , gene , genetics , virus
Summary RNA decay pathways comprise a combination of RNA degradation mechanisms that are implicated in gene expression, development and defense responses in eukaryotes. These mechanisms are known as the RNA Quality Control or RQC pathways. In plants, another important RNA degradation mechanism is the post‐transcriptional gene silencing ( PTGS ) mediated by small RNA s (si RNA s). Notably, the RQC pathway antagonizes PTGS by preventing the entry of dysfunctional mRNA s into the silencing pathway to avoid global degradation of mRNA by si RNA s. Viral transcripts must evade RNA degrading mechanisms, thus viruses encode PTGS suppressor proteins to counteract viral RNA silencing. Here, we demonstrate that tobacco plants infected with TMV and transgenic lines expressing TMV MP and CP (coat protein) proteins (which are not linked to the suppression of silencing) display increased transcriptional levels of RNA decay genes. These plants also showed accumulation of cytoplasmic RNA granules with altered structure, increased rates of RNA decay for transgenes and defective transgene PTGS amplification. Furthermore, knockdown of RRP 41 or RRP 43 RNA exosome components led to lower levels of TMV accumulation with milder symptoms after infection, several developmental defects and mi RNA deregulation. Thus, we propose that TMV proteins induce RNA decay pathways (in particular exosome components) to impair antiviral PTGS and this defensive mechanism would constitute an additional counter‐defense strategy that lead to disease symptoms.