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Cas9 interactions with host RNAs and transposable elements impair neurodevelopment (CUT&Tag)

ABSTRACT: Cas9 interactions with host RNAs and transposable elements impair neurodevelopment (CUT&Tag)

PROVIDER: PRJNA678978 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13074100_1.fastq.gz	Fastqsanger.gz
	SRR13074100_2.fastq.gz	Fastqsanger.gz
	SRR13074101_1.fastq.gz	Fastqsanger.gz
	SRR13074101_2.fastq.gz	Fastqsanger.gz
	SRR13074102_1.fastq.gz	Fastqsanger.gz

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Cas9 interactions with host RNAs and transposable elements impair neurodevelopment

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Cas9 interactions with host RNAs and transposable elements impair neurodevelopment (CUT&Tag)

Project description:The CRISPR (clustered regulatory interspaced short palindromic repeats)/ Cas9 (CRISPR-associated protein 9) system-based precise genome editing has revolutionized biomedical studies. As the CRISPR/Cas9 system has been also recently considered to permanently cure genetic diseases via human germline genome editing, a careful risk assessment of this genome engineering tool is required in human early development. Here we perform comprehensive analysis to evaluate the potential impact of Cas9 in human early embryogenesis. We find that even in the absence of synthetic guide RNA, Cas9 can be still guided by endogenous RNAs, and cut the genome of human embryonic cells at low frequency, and the resulting DNA damage induces the intrinsic immune response. Moreover, Cas9 interferes with the spliceosome, and with the suppressor machinery (e.g. L1TD1, APOBEC3G and PIWIL4) of LINE-1 (L1) retrotransposition. Even the transient presence of Cas9 in human embryonic cells induces robust de novo L1 retrotransposition that exacerbates DNA damage, and results in compromised neurodevelopment. Besides the ethical issues, these inevitable and detrimental Cas9-associated impacts on human embryonic development raise such serious safety concerns as to question the clinical use of human germline genome editing.

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Cas9 interactions with host RNAs and transposable elements impair neurodevelopment

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Epigenetic control of transposable elements in the mouse male germ line by Tex15

Project description:The piRNA biogenesis was evaluated in the mouse testes lacking TEX15. Total small RNAs, MILI-, and MIWI2-associated small RNAs from control (Tex15+/-) and Tex15(-/-) knock-out testes were sequenced. Data analysis revealed that the abundance of miRNAs and piRNAs was comparable between control and Tex15 knock-out testes, suggesting that loss of TEX15 function does not impair piRNA biogenesis. However, the relative abundance of MILI- and MIWI2-bound sense piRNAs derived from transposable elements was increased.

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