ArticleThe Plant cell2026
Distinct thresholds condition sense posttranscriptional gene silencing initiation and amplification.
Article in The Plant cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Transient abRNA and steady-state mRNA levels set the thresholds for sense PTGS initiation and amplification.The Plant cell · 2026Article
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7 authors.
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Abstract
It has long been known that Pro35S-driven sense transgenes have a high propensity to undergo posttranscriptional 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 confirms 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.
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