Tissue-specific silencing of integrated transgenes achieved through endogenous RNA interference in Caenorhabditis elegans
Transgene silencing is a common phenomenon observed in , particularly in the germline, but the precise mechanisms underlying this process remain elusive. Through an analysis of the transcription factors profile of , we discovered that the expression of several transgenic reporter lines exhibited tis...
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Published in | RNA biology Vol. 21; no. 1; pp. 1 - 10 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Taylor & Francis
2024
Taylor & Francis Group |
Subjects | |
Online Access | Get full text |
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Summary: | Transgene silencing is a common phenomenon observed in
, particularly in the germline, but the precise mechanisms underlying this process remain elusive. Through an analysis of the transcription factors profile of
, we discovered that the expression of several transgenic reporter lines exhibited tissue-specific silencing, specifically in the intestine of
. Notably, this silencing could be reversed in mutants defective in endogenous RNA interference (RNAi). Further investigation using knock-in strains revealed that these intestine-silent genes were indeed expressed
, indicating that the organism itself regulates the intestine-specific silencing. This tissue-specific silencing appears to be mediated through the endo-RNAi pathway, with the main factors of this pathway,
and
, are significantly enriched in the intestine. Additionally, histone modification factors, such as
, are involved in this silencing mechanism. Given the crucial role of the intestine in reproduction alongside the germline, the transgene silencing observed in the intestine reflects the self-protective mechanisms employed by the organisms. In summary, our study proposed that compared to other tissues, the transgenic silencing of intestine is specifically regulated by the endo-RNAi pathway. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
ISSN: | 1547-6286 1555-8584 |
DOI: | 10.1080/15476286.2024.2332856 |