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Precise RNA knockdown of smn1,or tardbp and tarbpl by CRISPR-QKD and transcription activation of lin28a and sox9b by CRISPR-Qa in zebrafish

ABSTRACT: Precise RNA knockdown of smn1,or tardbp and tarbpl by CRISPR-QKD and transcription activation of lin28a and sox9b by CRISPR-Qa in zebrafish

PROVIDER: PRJNA1116733 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29187762_1.fastq.gz	Fastqsanger.gz
	SRR29187762_2.fastq.gz	Fastqsanger.gz
	SRR29187763_1.fastq.gz	Fastqsanger.gz
	SRR29187763_2.fastq.gz	Fastqsanger.gz
	SRR29187764_1.fastq.gz	Fastqsanger.gz

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Precise RNA knockdown of smn1,or tardbp and tarbpl by CRISPR-QKD and transcription activation of lin28a and sox9b by CRISPR-Qa in zebrafish

Project description:CRISPR-Cas systems have revolutionized gene regulation technologies in various organisms, including zebrafish. However, most zebrafish studies rely on transient injections of CRISPR components, with limited use of transgenic models, primarily for Cas9-mediated knockouts. This is largely due to challenges in achieving sustained and effective expression of Cas effectors. To address these challenges, we introduce the CRISPR-Q system, which integrates the QFvpr/QUAS binary expression system with CRISPR-Cas effectors. This approach overcomes limitations associated with transient mRNA or protein delivery and circumvents the toxicity and silencing issues typical of other binary systems, such as Gal4/UAS. The CRISPR-Q system enables robust expression of CasRx or dCas9vpr, facilitating efficient transcript knockdown (CRISPR-QKD) and gene activation (CRISPR-Qa). Using this system, we successfully achieved significant knockdown of smn1 and the simultaneous knockdown of the paralogs tardbp and tardbpl, modeling phenotypes of spinal muscular atrophy (SMA) and amyotrophic lateral sclerosis (ALS), respectively. Furthermore, CRISPR-Qa effectively activated the endogenous genes lin28a and sox9b, demonstrating the system's broad applicability. The CRISPR-Q system represents a significant advancement in zebrafish genetic manipulation, providing a robust and versatile platform for studying gene function and modeling human diseases, with potential extensions to other model organisms

2024-06-25 | GSE268371 | GEO

Zebrafish embryos: Control MO vs. Lin28A MO vs. Lin28B MO injected

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Project description:TARDBP is TARDBP (TDP-43) is a DNA/RNA binding protein and was mutated in human amyotrophic lateral sclerosis (ALS). However, its function in human cancer has not been fully identified, yet.Thus, We carried out microarray to investigate the down-stream target genes of TARDBP after silencing TARDBP in liver cancer cell SK-Hep1. To identify the role of TARDBP in hepatocellular carcinoma cell line, we performed microarray after knocking down TARDBP in hepatocellular carcinoma cell line (3 siLuc, 3 siTARDBP)

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Project description:miRNA profiling of zebrafish embryos comparing control MO with Lin28A MO or Lin28B MO injected embryos at 5hpf

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Project description:We report the upregulated genes by the expression of LIN28A or loss of function mutant of LIN28A for 293FTcells..

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Expression profiling in LIN28A, SET7/9, and TUT4 depleted H9 cells, or in the silent mutations (siR) of LIN28A and LIN28A-K135R overexpressed H9 cells

Project description:A developmentally regulated RNA binding protein, LIN28A and its homolog LIN28B may share a similar mechanism to regulate the processing of let-7 microRNAs (miRNAs) in embryonic stem cells (ESCs) or certain cancer cells, although their predominant localization is different in cells. However, little is known about the regulatory mechanism of LIN28A for miRNA processing in the nucleus. Here, we show that SET7/9, a known histone methyltransferase, associates with LIN28A in vivo and in vitro. SET7/9-mediated methylation significantly leads to the nuclear retention and protein stability of LIN28A, and remarkably regulated RNA binding ability of LIN28A to pri-let-7. Using RNAi knockdown approach, we find that the methylated nuclear form of LIN28A may function in the nucleoli by sequestering the primary let-7 miRNA to block their processing through a Tut4 (Zcchc11)-independent mechanism to regulate human ESC pluripotency. We propose a new insight toward the understanding of the molecular mechanism for post-translational methylation of nuclear LIN28A along modulating pluripotency by regulating pri-let-7 miRNAs in human ESCs.

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Lin28A binds active promoters and recruits Tet1 to regulate gene expression

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