Distinct thresholds condition sense PTGS initiation and amplification

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ID: 316477
2026
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Abstract
Abstract It has long been known that Pro35S-driven sense transgenes have a high propensity to undergo post-transcriptional gene silencing (S-PTGS). However, what exactly conditions S-PTGS initiation and amplification to make it systemic remains unknown. Through genetic screens, we show that antagonistic chromatin-related mutations enhancing and reducing transgene expression, result in enhanced and reduced S-PTGS amplification capacities, respectively, without affecting the initiation rate. Analysis of a large set of independent transgenic plants confirm a direct relationship between transgene expression and its capacity to amplify S-PTGS. Combining an inducible or a tissue-specifically expressed GUS transgene with a Pro35S:GUS transgene locus prone to amplify S-PTGS but unable to spontaneously initiate it induces systemic S-PTGS, indicating that transient and/or local passing of a discrete threshold is sufficient to initiate S-PTGS. Together, these results call for the existence of distinct thresholds related to transiently produced aberrant RNA and permanently produced target mRNA levels, which condition S-PTGS initiation and amplification, respectively. We show that this model also applies to endogenous genes for which RNA Quality Control (RQC) acts as a first layer of protection against S-PTGS, and DCL2’s obscuration by DCL4 as a second layer, allowing RQC to dysfunction locally without translating into the drama of systemic S-PTGS.
Reference Key
openalex_W7164029070 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Martin Lacroix, Nicolas Butel, Andana Barrios, Agnès Yu, Nathalie Bouteiller, Ivan Le Masson, Hervé Vaucheret
Journal The Plant cell
Year 2026
DOI
10.1093/plcell/koag166
URL
https://doi.org/10.1093/plcell/koag166
Keywords Keywords not found

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