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Defective expression of mitochondrial, histone and vesicle genes in a C. elegans SMA model

ABSTRACT: Defective expression of mitochondrial, histone and vesicle genes in a C. elegans SMA model

PROVIDER: PRJNA492792 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7892680_1.fastq.gz	Fastqsanger.gz
	SRR7892680_2.fastq.gz	Fastqsanger.gz
	SRR7892681_1.fastq.gz	Fastqsanger.gz
	SRR7892681_2.fastq.gz	Fastqsanger.gz
	SRR7892682_1.fastq.gz	Fastqsanger.gz

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Defective expression of mitochondrial, histone and vesicle genes in a C. elegans SMA model

Project description:Spinal muscular atrophy (SMA) is a severe congenital motor neuron degenerative disease caused by loss-of-function mutations in the conserved survival motor neuron gene SMN1. SMN is required for the assembly of small nuclear ribonucleoprotein complexes, the core components of the spliceosome and also affects other molecular processes. It is hypothesized that defective gene expression and pre-mRNA splicing underlie SMA. However the immediate target genes of SMN are unclear. We used the nematode Caenorhabditis elegans as a model to study the function of SMN. We analyzed the transcriptome of a C. elegans smn-1 deletion mutant and identified that multiple biological processes were affected. Specifically the expression of numerous mitochondrial genes and vacuolar H+ -ATPase was significantly reduced while the expression of multiple histone genes was significantly increased. We also found that the U2AF large subunit mutation n4588 could ameliorate the defective expression of genes in the mitochondrial and V-ATPase pathways caused by the smn-1 mutation, which is consistent with our previous finding that uaf-1(n4588) could improve the behavior and lifespan of smn-1 mutants. Our study identified key molecular processes affected by SMN and suggests that mitochondrial and V-ATPase dysfunctions might contribute to SMA.

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Project description:Spinal muscular atrophy (SMA) is a severe motor neuron degenerative disease caused by loss-of-function mutations in the survival motor neuron gene SMN1. It is widely posited that defective gene expression underlies SMA. However, the identities of these affected genes remain to be elucidated. By analyzing the transcriptome of a Caenorhabditis elegans SMA model at the pre-symptomatic stage, we found that the expression of numerous nuclear encoded mitochondrial genes and vacuolar H+-ATPase genes was significantly down-regulated, while that of histone genes was significantly up-regulated. We previously showed that the uaf-1 gene, encoding key splicing factor U2AF large subunit, could affect the behavior and lifespan of smn-1 mutants. Here, we found that smn-1 and uaf-1 interact to affect the recognition of 3' and 5' splice sites in a gene-specific manner. Altogether, our results suggest a functional interaction between smn-1 and uaf-1 in affecting RNA splicing and a potential effect of smn-1 on the expression of mitochondrial and histone genes.

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