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Light regulates nuclear detainment of intron-retained transcripts through COP1-spliceosome to modulate photomorphogenesis

ABSTRACT: Intron retention (IR) is the most common alternative splicing (AS) event in Arabidopsis. Increasing studies have demonstrated a major role of IR in gene expression regulation. The impacts of IR on plant growth and development, and response to environments remains under explored. Here, we found that IR functions directly in gene expression regulation on a genome-wide scale through detainment of the intron-retained transcripts (IRTs) in the nucleus. Through this mechanism, nuclear-retained IRTs can be kept away from translation. COP1-dependent light modulation of IRTs of light signaling genes, such as PIF4, RVE1, and ABA3, contribute to seedling morphological development in responding to changing light conditions. Further, light-induced IR changes are under the control of the spliceosome, and in part through COP1-dependent ubiquitination and degradation of DCS1, a plant-specific spliceosomal component. Our data suggests that light regulates the activity of the spliceosome and the consequent IRTs nucleus detainment to modulate photomorphogenesis through COP1.

INSTRUMENT(S): Orbitrap Fusion

ORGANISM(S): Arabidopsis Thaliana (mouse-ear Cress)

TISSUE(S): Whole Body

SUBMITTER: Hua Zhou

LAB HEAD: Xing Wang

PROVIDER: PXD043190 | Pride | 2024-05-20

REPOSITORIES: Pride

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Dataset's files

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			Action	DRS
	Flag-DCS4.msf	Msf
	Flag-DCS4.raw	Raw
	HA-DCS3.msf	Msf
	HA-DCS3.raw	Raw
	YFP-DCS1.msf	Msf

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DNA methylation regulates intron retention via altered MeCP2-mediated splicing factor recruitment

Project description:While intron retention (IR) is now recognized as a widespread and conserved mechanism of gene expression control, its regulation is poorly understood. Here, we identify significantly reduced DNA methylation levels near splice junctions flanking retained introns compared to non-retained introns in diverse primary cells and cell lines. Further, we identify increased IR following inhibition of DNA methylation indicating that reduced DNA methylation promotes IR. We demonstrate reduced occupancy of MeCP2 near the splice junctions of retained introns, mirroring the reduced DNA methylation at these sites. Accordingly, MeCP2 depletion in tissues/cells enhances IR. By analyzing the MeCP2 interactome, we demonstrate that decreased MeCP2 binding near splice junctions facilitates IR via reduced recruitment of the splicing factor, Tra2b, and increased RNA polymerase II stalling. Our study identifies a dynamic interplay between DNA methylation, MeCP2 and splicing factors including Tra2b in IR regulation and provides novel insights into the mechanisms governing splicing.

2017-02-28 | GSE85517 | GEO

Orchestrated intron retention regulates normal granulocyte differentiation [RNA-Seq]

Project description:Using mRNA-seq, we determined intron retaining genes that were differentially regulated in FACS purified cells at three progressive stages of mouse granulopoiesis; CD34+Kit+Gr-1low promyelocytes, CD34-Kit-Gr-1mid myelocytes and CD34-Kit-Gr-1high granulocytes. We found that IR affects 86 genes, including those specific to granulocyte (Lyz2 and MMP8) and nuclear architecture (Lmnb1 and Lbr). IR was associated with the decrease in protein levels measured by mass spectrometry (P=0.0015, binomial test). There was a significant overlap of IR between human and mouse (P=2.85E-22, hypergeometric test), showing that IR is conserved.Inhibition of NMD in granulocytes resulted in marked accumulation of 39/86 intron retaining mRNAs (P<0.05, RUV procedure with Holm-Bonferroni correction), indicating that IR triggers NMD to downregulate mRNA and protein expression. Sequencing of polyadenylated RNA from three types of myeloid cells (promyelocytes, myelocytes and granulocytes) using Illumina GAIIx

2013-06-27 | E-GEOD-48305 | biostudies-arrayexpress

Effect of CLK2 expression in the regulation of intron retention during heat shock [RNA-seq]

Project description:Intron retention (IR) constitutes a less explored form of alternative splicing, wherein introns are retained within mature mRNA transcripts. Our investigation demonstrates that the CDC-like kinase 2 (CLK2) undergoes liquid-liquid phase separation (LLPS) within nuclear speckles in response to heat shock (HS). The formation of CLK2 condensates depends on the intrinsically disordered region (IDR) located within the N-terminal amino acids 1-148. Phosphorylation at residue T343 sustains CLK2 kinase activity and facilitates autophosphorylation, thus inhibiting the LLPS activity of the IDR. These CLK2 condensates initiate the reorganization of nuclear speckles, transforming them into larger, rounded structures. Moreover, these condensates facilitate the recruitment of splicing factors into these compartments, potentially restricting their access to mRNA for intron splicing. Consequently, the formation of CLK2 condensates promotes the IR.

2024-07-15 | GSE271918 | GEO

Macrophage development and activation involve coordinated intron retention in key inflammatory regulators

Project description:Monocytes and macrophages are essential components of the innate immune system. Herein, we report that intron retention (IR) plays an important role in the development and function of these cells. Using mRNA sequencing, bioinformatics analyses and RT-qPCR validation, we identified differential IR and altered expression of key genes involved in macrophage development and function, both in vitro and in vivo. We demonstrate that decreased IR in nuclear-detained mRNA is coupled to increased expression of genes encoding regulators of macrophage transcription, phagocytosis and inflammatory signalling, including ID2, IRF7, ENG and LAT. We further show that this dynamic IR program persists during the polarisation of resting macrophages into activated macrophages. In the presence of proinflammatory stimuli, intron-retaining CXCL2 and NFKBIZ transcripts in macrophages are rapidly spliced, leading to timely expression of these key inflammatory regulators by macrophages. Our study provides novel insights into the molecular mechanisms controlling vital regulators of the innate immune response.

2020-05-27 | PXD017391 | Pride

Orchestrated intron retention regulates normal granulocyte differentiation [Affymetrix arrays]

Project description:Using mRNA-seq, we determined intron retaining genes that were differentially regulated in FACS purified cells at three progressive stages of mouse granulopoiesis; CD34+Kit+Gr-1low promyelocytes, CD34-Kit-Gr-1mid myelocytes and CD34-Kit-Gr-1high granulocytes. We found that IR affects 86 genes, including those specific to granulocyte (Lyz2 and MMP8) and nuclear architecture (Lmnb1 and Lbr). IR was associated with the decrease in protein levels measured by mass spectrometry (P=0.0015, binomial test). Inhibition of NMD in granulocytes resulted in marked accumulation of 39/86 intron retaining mRNAs (P<0.05, RUV procedure with Holm-Bonferroni correction), indicating that IR triggers NMD to downregulate mRNA and protein expression. We used Affymetrix's Mouse Gene 1.0 ST array to determine accumulation of RNA-transcripts following inhibition of nonsense-mediated decay in primary mouse granulocytes using caffeine.

2013-06-27 | E-GEOD-48306 | biostudies-arrayexpress

Minor intron retention drives clonal hematopoietic disorders and diverse cancer predisposition

Project description:Most eukaryotes harbor two distinct pre-mRNA splicing machineries: the major spliceosome, which removes >99% of introns, and the minor spliceosome, which removes rare, evolutionarily conserved introns. Although hypothesized to serve important regulatory functions, physiologic roles for the minor spliceosome are not well understood. For example, the minor spliceosome component ZRSR2 is subject to recurrent, leukemia-associated mutations, yet functional connections between minor introns, hematopoiesis, and cancers are unclear. Here, we identify that impaired minor intron excision via ZRSR2 loss enhances hematopoietic stem cell self-renewal. CRISPR screens mimicking nonsense-mediated decay of minor intron-containing mRNAs converged on LZTR1, a regulator of Ras-related GTPases. LZTR1 minor intron retention was also discovered in the RASopathy Noonan syndrome, due to intronic mutations disrupting splicing, and diverse solid tumors. These data uncover minor intron recognition as a regulator of hematopoiesis, noncoding mutations within minor introns as cancer drivers, and links between ZRSR2 mutations, LZTR1 regulation, and leukemias.

2021-02-09 | GSE149455 | GEO

Minor intron retention drives clonal hematopoietic disorders and diverse cancer predisposition.

Project description:Most metazoans contain two distinct pre-mRNA splicing machineries: the major spliceosome, which removes >99% of introns, and the minor spliceosome, which recognizes <1% of introns. Despite their rarity, minor introns are exquisitely conserved amongst species, suggesting important regulatory functions. However, physiologic roles for the minor spliceosome and the relevance of recurrent, leukemia-associated mutations affecting minor spliceosome components are not well understood. Here, we identify that mutational loss of the minor spliceosomal factor ZRSR2 enhances hematopoietic stem cell self-renewal via impaired minor intron splicing that converges on LZTR1, a regulator of Ras-related GTPases. LZTR1 minor intron retention is additionally observed in Noonan syndrome and diverse cancers. These data uncover minor intron recognition as a regulator of hematopoiesis and mechanistic links between ZRSR2 mutations, LZTR1, and leukemia.

2020-11-26 | GSE162136 | GEO

Orchestrated intron retention regulates normal granulocyte differentiation [RNA-Seq]

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Bud13 Promotes a Type I Interferon Response by Countering Intron Retention in Irf7

Project description:Intron retention (IR) has emerged as an important mechanism of gene expression control. Despite this, the factors that control IR events remain poorly understood. We observed consistent IR in one intron of the Irf7 gene and identified Bud13 as an RNA-binding protein that acts at this intron to increase the amount of successful splicing. Deficiency in Bud13 led to increased IR, decreased mature Irf7 transcript and protein levels, and consequently to a dampened type I interferon response. This impairment of Irf7 production in Bud13 deficient cells compromised their ability to withstand VSV infection. Global analysis of Bud13 knockdown and BUD13 cross-linking to RNA revealed a subset of introns that share many characteristics with the one found in Irf7 and are spliced in a Bud13-dependent manner. Deficiency of Bud13 led to decreased mature transcript from genes containing such introns. Thus, by acting as an antagonist to IR, Bud13 facilitates the expression of genes at which IR occurs.

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Orchestrated intron retention regulates normal granulocyte differentiation [Affymetrix arrays]

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2013-06-27 | GSE48306 | GEO

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