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Pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [II]

ABSTRACT: pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [II]

PROVIDER: PRJNA858869 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR20215300_1.fastq.gz	Fastqsanger.gz
	SRR20215301_1.fastq.gz	Fastqsanger.gz
	SRR20215302_1.fastq.gz	Fastqsanger.gz
	SRR20215303_1.fastq.gz	Fastqsanger.gz

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pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts

Project description:pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts

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pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [I]

Project description:pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [I]

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pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [I]

Project description:Combinatorially, intron excision within a given nascent transcript could proceed down any of thousands of paths, each of which would expose different dynamic landscapes of cis-elements and contribute to alternative splicing. In this study, we found that post-transcriptional multi-intron splicing order in human cells is largely predetermined, with most genes spliced in one or a few predominant orders. Strikingly, these orders were conserved across cell types and stages of motor neuron differentiation. Introns flanking alternatively spliced exons were frequently excised last, after their neighboring introns. Perturbations to the spliceosomal U2 snRNA altered the preferred splicing order of many genes, and these alterations were associated with the retention of other introns in the same transcript. In one gene, early removal of specific introns was sufficient to induce delayed excision of three proximal introns, and this delay was caused by two distinct cis-regulatory mechanisms. Together, our results demonstrate that multi-intron splicing order in human cells is predetermined, is influenced by a component of the spliceosome and ensures splicing fidelity across long pre-mRNAs.

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pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts [II]

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pre-mRNA splicing order is defined and maintains splicing fidelity across multi-intronic transcripts

Project description:This SuperSeries is composed of the SubSeries listed below.

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QKI ensures splicing fidelity during cardiogenesis by engaging the U6 tri-snRNP to activate splicing at weak 5’splice sites [eCLIP Hues6]

Project description:During organogenesis, the establishment of tissue architecture requires precise RNA processing. Many developmentally essential exons bear weak 5′ splice sites (5′SS) yet are spliced with high precision, implying unknown yet active splicing fidelity mechanisms. Combining transcriptome and alternative splicing profiling and with temporal eCLIP mapping of RNA interactions across development, we identify the RNA-binding protein QKI as an essential direct regulator of splicing fidelity in key cardiac transcripts. Although QKI is dispensable for cardiac lineage specification, its loss disrupts sarcomere assembly despite intact expression of sarcomere mRNAs through exon skipping and intron retention in key sarcomeric mRNAs. QKI-dependent exons in essential cardiac genes have weak 5′SS and frequently show poor complementarity with U6 snRNA; we show that QKI directly interacts with U6 snRNA using an overlapping interface to its traditional intronic binding activity, securing U4/U6·U5 tri-snRNP recruitment to ensure exon inclusion. Thus, QKI exemplifies how context-aware RBPs enforce splicing fidelity at structurally vulnerable splice sites by coupling local intronic cues to spliceosome engagement, thereby securing accurate exon inclusion during organogenesis.

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QKI ensures splicing fidelity during cardiogenesis by engaging the U6 tri-snRNP to activate splicing at weak 5’splice sites [RNA-Seq]

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Pre-mRNA splicing order is predetermined and maintains splicing fidelity across multi-intronic transcripts.

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A network of DZF proteins controls alternative splicing regulation and fidelity [eCLIP-seq]

Project description:Proteins containing DZF (domain associated with zinc fingers) modules play important roles throughout gene expression, from transcription to translation. Derived from nucleotidyltransferases but lacking catalytic residues, DZF domains serve as heterodimerization surfaces between DZF protein pairs. Three DZF proteins are widely expressed in mammalian tissues, ILF2, ILF3, and ZFR, which form mutually exclusive ILF2-ILF3 and ILF2-ZFR heterodimers. Using eCLIP-Seq, we find that ZFR binds across broad intronic regions to regulate the alternative splicing of cassette and mutually exclusive exons. ZFR preferentially binds dsRNA in vitro and is enriched on introns containing conserved dsRNA elements in cells. Many splicing events are similarly altered upon depletion of any of the three DZF proteins; however, we also identify independent and opposing roles for ZFR and ILF3 in alternative splicing regulation. Along with widespread involvement in cassette exon splicing, the DZF proteins control the fidelity and regulation of over a dozen highly validated mutually exclusive splicing events. Our findings indicate that the DZF protein complexes form a complex regulatory network that leverages dsRNA binding by ILF3 and ZFR to modulate splicing regulation and fidelity.

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