Lariat RNA debranching prevents harmful siRNA burst in plants.
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| Title: | Lariat RNA debranching prevents harmful siRNA burst in plants. |
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| Authors: | Tang, Qi (AUTHOR), Ding, Chenxi (AUTHOR), Zhang, Xiaotuo (AUTHOR), Wang, Taiyun (AUTHOR), Zhu, Mengjie (AUTHOR), Cui, Ruixue (AUTHOR), Yang, Wenya (AUTHOR), Ma, Jinbiao (AUTHOR), Ren, Guodong (AUTHOR), Zhang, Xiaoming (AUTHOR), Zheng, Binglian (AUTHOR) |
| Source: | Science. 6/25/2026, Vol. 392 Issue 6805, p1401-1407. 7p. |
| Subjects: | Small interfering RNA, Disease resistance of plants, RNA splicing, RNA synthesis, Non-coding RNA, Enzymes, Arabidopsis |
| Abstract: | Lariat RNAs are formed from introns during pre–messenger RNA splicing, after which they are degraded by the debranching enzyme DBR1. Impairment of DBR1 leads to developmental arrest, yet the mechanism remains unclear. In this study, we found that debranching of lariat RNA prevents production of 21- and 22-nucleotide lariat-derived small interfering RNAs (lasiRNAs), which causes a burst of exonic siRNAs, thereby safeguarding development and defense response. LasiRNA biogenesis relied on RNA-dependent RNA polymerases and Dicer-like proteins (DCLs). Upon pathogen infection and dysfunction of DBR1, many lariat RNAs were hijacked by DCL4 and DCL2 and processed into siRNAs that particularly target immunity genes, ultimately disrupting plant defense responses. Collectively, DBR1-mediated lariat RNA removal serves as a protective mechanism to prevent the activation of a small RNA–based defense system in plants. Editor's summary: Lariat RNAs are generated from excised introns during splicing of pre-messenger RNAs. They are rapidly degraded by the debranching enzyme DBR1. Using a partial loss-of-function dbr1 mutant in the model plant Arabidopsis, Tang et al. found that lariat RNAs can be processed into 21- and 22-nucleotide small interfering RNAs, which they named lasiRNAs. In the absence of DBR1, lariat RNAs are preferentially processed by the dicer-like protein DCL4 into 21-nucleotide lasiRNAs. However, when DCL4 function is compromised, such as during viral infection, lariat RNAs are processed by DCL2 into 22-nucleotide lasiRNAs, which in turn repress immunity genes through exonic small interfering RNA burst. —Unnati Sonawala and Madeleine Seale [ABSTRACT FROM AUTHOR] |
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| Database: | Psychology and Behavioral Sciences Collection |
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| Abstract: | Lariat RNAs are formed from introns during pre–messenger RNA splicing, after which they are degraded by the debranching enzyme DBR1. Impairment of DBR1 leads to developmental arrest, yet the mechanism remains unclear. In this study, we found that debranching of lariat RNA prevents production of 21- and 22-nucleotide lariat-derived small interfering RNAs (lasiRNAs), which causes a burst of exonic siRNAs, thereby safeguarding development and defense response. LasiRNA biogenesis relied on RNA-dependent RNA polymerases and Dicer-like proteins (DCLs). Upon pathogen infection and dysfunction of DBR1, many lariat RNAs were hijacked by DCL4 and DCL2 and processed into siRNAs that particularly target immunity genes, ultimately disrupting plant defense responses. Collectively, DBR1-mediated lariat RNA removal serves as a protective mechanism to prevent the activation of a small RNA–based defense system in plants. Editor's summary: Lariat RNAs are generated from excised introns during splicing of pre-messenger RNAs. They are rapidly degraded by the debranching enzyme DBR1. Using a partial loss-of-function dbr1 mutant in the model plant Arabidopsis, Tang et al. found that lariat RNAs can be processed into 21- and 22-nucleotide small interfering RNAs, which they named lasiRNAs. In the absence of DBR1, lariat RNAs are preferentially processed by the dicer-like protein DCL4 into 21-nucleotide lasiRNAs. However, when DCL4 function is compromised, such as during viral infection, lariat RNAs are processed by DCL2 into 22-nucleotide lasiRNAs, which in turn repress immunity genes through exonic small interfering RNA burst. —Unnati Sonawala and Madeleine Seale [ABSTRACT FROM AUTHOR] |
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| ISSN: | 00368075 |
| DOI: | 10.1126/science.aeb4938 |
