4.8 Article

SICKLE modulates lateral root development by promoting degradation of lariat intronic RNA

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PLANT PHYSIOLOGY
卷 190, 期 1, 页码 548-561

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OXFORD UNIV PRESS INC
DOI: 10.1093/plphys/kiac301

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资金

  1. National Natural Science Foundation of China [32000149, 32070208]
  2. Outstanding Youth Foundation of Henan Province [202300410041]
  3. Programs for Team and Talents of Innovative Research (in Science and Technology) in Henan Province [21IRTSTHN019, 20HASTIT041]
  4. Foundation of Henan Educational Committee [212102110151]
  5. 111 Project [D16014]

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The degradation of lariat intronic RNAs (lariRNAs) modulated by SICKLE (SIC) is essential for lateral root development in Arabidopsis. SIC interacts with DBR1 and facilitates its nuclear accumulation, leading to lariRNA decay and fine-tuning of miRNA biogenesis, thereby regulating lateral root development.
Plant lateral roots (LRs) play vital roles in anchorage and uptake of water and nutrients. Here, we reveal that degradation of lariat intronic RNAs (lariRNAs) modulated by SICKLE (SIC) is required for LR development in Arabidopsis (Arabidopsis thaliana). Loss of SIC results in hyper-accumulation of lariRNAs and restricts the outgrowth of LR primordia, thereby reducing the number of emerged LRs. Decreasing accumulation of lariRNAs by over-expressing RNA debranching enzyme 1 (DBR1), a rate-limiting enzyme of lariRNA decay, restored LR defects in SIC-deficient plants. Mechanistically, SIC interacts with DBR1 and facilitates its nuclear accumulation, which is achieved through two functionally redundant regions (SIC1-244 and SIC252-319) for nuclear localization. Of the remaining amino acids in this region, six (SIC245-251) comprise a DBR1-interacting region while two (SICM246 and SICW251) are essential for DBR1-SIC interaction. Reducing lariRNAs restored microRNA (miRNA) levels and LR development in lariRNA hyper-accumulating plants, suggesting that these well-known regulators of LR development mainly function downstream of lariRNAs. Taken together, we propose that SIC acts as an enhancer of DBR1 nuclear accumulation by driving nuclear localization through direct interaction, thereby promoting lariRNA decay to fine-tune miRNA biogenesis and modulating LR development.

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