CRY2 interacts with CIS1 to regulate thermosensory flowering via FLM alternative splicing

Zhao, Zhi-Wei; Dent, Craig; Liang, Huafeng; Lv, Junqing; Shang, Guan-Dong; Liu, Yawen; Feng, Fan; Wang, Fei; Pang, Jifeng; Li, Xu; Ma, Libang; Li, Bing; Sureshkumar, Sridevi; Wang, Jiawei; Balasubramanian, Sureshkumar; Liu, Hongtao

doi:10.1038/s41467-022-34886-2

Cited by 22 publications

(14 citation statements)

References 72 publications

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“…The transformed cells were grown on the selective media for 2–4 d. (b) Physical interaction between SRRM1L and SnRK1 confirmed by bimolecular florescence complementation (BiFC) in Nicotiana benthamiana leaves. The interacting proteins CRY2 and CIS1 were used as negative controls (Zhao et al ., 2022). Bars: 25 μm.…”

Section: Resultsmentioning

confidence: 99%

Regulation of plant resistance to salt stress by the SnRK1‐dependent splicing factor SRRM1L

Sun,

Liu

et al. 2024

New Phytologist

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Summary Most splicing factors are extensively phosphorylated but their physiological functions in plant salt resistance are still elusive. We found that phosphorylation by SnRK1 kinase is essential for SRRM1L nuclear speckle formation and its splicing factor activity in plant cells. In Arabidopsis, loss‐of‐function of SRRM1L leads to the occurrence of alternative pre‐mRNA splicing events and compromises plant resistance to salt stress. In Arabidopsis srrm1l mutant line, we identified an intron‐retention Nuclear factor Y subunit A 10 (NFYA10) mRNA variant by RNA‐Seq and found phosphorylation‐dependent RNA‐binding of SRRM1L is indispensable for its alternative splicing activity. In the wild‐type Arabidopsis, salt stress can activate SnRK1 to phosphorylate SRRM1L, triggering enrichment of functional NFYA10.1 variant to enhance plant salt resistance. By contrast, the Arabidopsis srrm1l mutant accumulates nonfunctional NFYA10.3 variant, sensitizing plants to salt stress. In summary, this work deciphered the molecular mechanisms and physiological functions of SnRK1‐SRRM1L‐NFYA10 module, shedding light on a regulatory pathway to fine‐tune plant adaptation to abiotic stress at the post‐transcriptional and post‐translational levels.

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Section: Resultsmentioning

confidence: 99%

Regulation of plant resistance to salt stress by the SnRK1‐dependent splicing factor SRRM1L

Sun,

Liu

et al. 2024

New Phytologist

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“…This type of regulation at the post-transcriptional splicing level may be applicable for the regulation of AS of AtU2AF65a pre-mRNAs, although the switch from isoform 1 to isoform 3 of AtU2AF65a AS transcripts was not an intron retention type, but an alternative 3 splice site type (Figure 6e or Figure 7a, Table S4). Recently, it was proposed that AtU2AF65a, but not AtU2AF65b, interacts with an RNA-binding protein (CIS) to regulate AS of FLM pre-mRNA in ambient temperaturemodulated flowering of Arabidopsis [45]. Further study on this aspect is required to obtain better insight into the significance of this interaction.…”

Section: Discussionmentioning

confidence: 99%

Two Arabidopsis Splicing Factors, U2AF65a and U2AF65b, Differentially Control Flowering Time by Modulating the Expression or Alternative Splicing of a Subset of FLC Upstream Regulators

Lee

Park

Lee

et al. 2023

Plants

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We investigated the transcriptomic changes in the shoot apices during floral transition in Arabidopsis mutants of two closely related splicing factors: AtU2AF65a (atu2af65a) and AtU2AF65b (atu2af65b). The atu2af65a mutants exhibited delayed flowering, while the atu2af65b mutants showed accelerated flowering. The underlying gene regulatory mechanism of these phenotypes was unclear. We performed RNA-seq analysis using shoot apices instead of whole seedlings and found that the atu2af65a mutants had more differentially expressed genes than the atu2af65b mutants when they were compared to wild type. The only flowering time gene that was significantly up- or down-regulated by more than two-fold in the mutants were FLOWERING LOCUS C (FLC), a major floral repressor. We also examined the expression and alternative splicing (AS) patterns of several FLC upstream regulators, such as COOLAIR, EDM2, FRIGIDA, and PP2A-b’ɤ, and found that those of COOLAIR, EDM2, and PP2A-b’ɤ were altered in the mutants. Furthermore, we demonstrated that AtU2AF65a and AtU2AF65b genes partially influenced FLC expression by analyzing these mutants in the flc-3 mutant background. Our findings indicate that AtU2AF65a and AtU2AF65b splicing factors modulate FLC expression by affecting the expression or AS patterns of a subset of FLC upstream regulators in the shoot apex, leading to different flowering phenotypes.

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“…BiFC assays have been done according to Walter et al as described previously 39,40 . The CDS of AL3 was cloned into the pUC-SPYNE (nYFP-X) vector.…”

Section: Methodsmentioning

confidence: 99%

“…Yeast two-hybrid screening was done as described previously 39 . The CDS of FUG1 was cloned into the pBridge vector (Clonetech) and FUG-pBridge was used as the bait for Yeast two-hybrid screening.…”

Section: Yeast Two-hybrid Screening Librarymentioning

confidence: 99%

SUMO protease FUG1, histone reader AL3 and the PRC1 Complex are integral to repeat-expansion induced epigenetic silencing inArabidopsis thaliana

Sureshkumar

Bandaranayake

et al. 2023

Preprint

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Epigenetic gene silencing induced by expanded repeats can cause diverse phenotypes ranging from severe growth defects in plants to genetic diseases such as Friedreichs ataxia in humans (1). The molecular mechanisms underlying repeat expansion-induced epigenetic silencing remain largely unknown (2,3). Using a plant model, we have previously shown that expanded repeats can induce smallRNAs which in turn can lead to epigenetic silencing through the RNA-dependent DNA methylation pathway (4,5). Here, using a genetic suppressor screen, we confirm a key role for the RdDM pathway and identify novel components required for epigenetic silencing caused by expanded repeats. We show that FOURTH ULP LIKE GENE CLASS 1 (FUG1)- a SUMO protease, ALFIN-LIKE 3 - a histone reader and LIKE HETEROCHROMATIN 1 (LHP1) - a component of the PRC1 complex are required for repeat expansion-induced epigenetic silencing. Loss of any of these components suppress repeat expansion-associated phenotypes. SUMO protease FUG1 physically interacts with AL3 and perturbing its potential SUMOylation site disrupts its nuclear localisation. AL3 physically interacts with LHP1 of the PRC1 complex and the FUG1-AL3-LHP1 module is essential to confer repeat expansion-associated epigenetic silencing. Our findings highlight the importance post-translational modifiers and histone readers in epigenetic silencing caused by repeat expansions.

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CRY2 interacts with CIS1 to regulate thermosensory flowering via FLM alternative splicing

Cited by 22 publications

References 72 publications

Regulation of plant resistance to salt stress by the SnRK1‐dependent splicing factor SRRM1L

Regulation of plant resistance to salt stress by the SnRK1‐dependent splicing factor SRRM1L

Two Arabidopsis Splicing Factors, U2AF65a and U2AF65b, Differentially Control Flowering Time by Modulating the Expression or Alternative Splicing of a Subset of FLC Upstream Regulators

SUMO protease FUG1, histone reader AL3 and the PRC1 Complex are integral to repeat-expansion induced epigenetic silencing inArabidopsis thaliana

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