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Transcriptomic analysis of 52 hpf mbd5 KO & KD embryos and 7 dpf mb5 KO & OE larves

ABSTRACT: Transcriptomic analysis of 52 hpf mbd5 KO & KD embryos and 7 dpf mb5 KO & OE larves

PROVIDER: PRJNA934332 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23441700.fastq.gz	Fastqsanger.gz
	SRR23441700_1.fastq.gz	Fastqsanger.gz
	SRR23441700_2.fastq.gz	Fastqsanger.gz
	SRR23441701.fastq.gz	Fastqsanger.gz
	SRR23441701_1.fastq.gz	Fastqsanger.gz

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Transcriptomic analysis of 52 hpf mbd5 KO & KD embryos and 7 dpf mb5 KO & OE larves

Project description:To dissect the molecular function of mbd5 in zebrafish embryonic development, we carried out transcriptomic analyses at those two developmental stages.

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Project description:MBD5 can physically interact with BAP1. Some genes may be regulated by both MBD5 and BAP1. We used microarrays to check whether the overlaps of differentially expressed genes when knockdown MBD5 or BAP1 were more than that would be expected by chance. Thus, we could suggest that BAP1 was required for the regulatory effect of MBD5

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Project description:Background: MBD5, encoding the methyl-CpG-binding domain 5 protein, has been proposed as a necessary and sufficient driver of the 2q23.1 microdeletion syndrome. De novo missense and protein-truncating variants from exome sequencing studies have directly implicated MBD5 in the etiology of autism spectrum disorder (ASD) and related neurodevelopmental disorders (NDDs). However, little is known concerning the specific function(s) of MBD5. Methods: In an effort to gain insight into the complex interactions associated with genetic alteration of MBD5 in individuals with ASD and related NDDs, we explored the transcriptional landscape of MBD5 haploinsufficiency across multiple mouse brain regions of the heterozygous hypomorphic Mbd5+/GT mouse model and compared these results to CRISPR-mediated mutations of MBD5 in human iPSC-derived neuronal models. Results: Gene expression analyses of three brain regions from Mbd5+/GT mice showed cortex as the region most affected by the knockdown, indicating context-dependent effects. Gene co-expression network analyses revealed gene clusters that are associated with MBD5 knockdown and enriched for GPCR signaling and terms related to ciliary function. We also identified genes that were downregulated in both models such as EPHA3, OLIG1, related to neuronal development and glial function. Limitations: These analyses were performed in a limited number of brain regions and neuronal models, and the effects of the gene knockdown are subtle. As such, these results will not reflect the full extent of MBD5 disruption across brain tissues during early brain developmentneurodevelopment in ASD. Conclusions: Our study points to transcriptional consequences of Mbd5 disruption in the brain and suggests a link between MBD5 and pathways such as ciliary function that are associated with established developmental disorders and syndromes.

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