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SMN MO, Gemin2 MO knockdown vs Control MO injected

ABSTRACT: Transcriptiome profiling of SMN MO injected, Gemin2 MO injected zebrafish embryos vs Control MO injected Two condition experiment : MO injected vs control. Biological replicates for SMN MO injected : 6, Biological replicates for Gemin2 MO injected: 7; Control MO injected from 6 independent batches pooled to serve as common control sample in all arrays.

ORGANISM(S): Danio rerio

SUBMITTER: Kelvin See

PROVIDER: E-GEOD-47001 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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SMN deficiency alters Nrxn2 expression and splicing in zebrafish and mouse models of spinal muscular atrophy.

See Kelvin K Yadav Preeti P Giegerich Marieke M Cheong Pearl S PS Graf Martin M Vyas Himanshu H Lee Serene G P SG Mathavan Sinnakaruppan S Fischer Utz U Sendtner Michael M Winkler Christoph C

Human molecular genetics 20131111 7

Spinal muscular atrophy (SMA) is a progressive neurodegenerative disease affecting lower motor neurons. SMA is caused by mutations in the Survival Motor Neuron 1 (SMN1) gene, which result in reduced levels of functional SMN protein. Biochemical studies have linked the ubiquitously expressed SMN protein to the assembly of pre-mRNA processing U snRNPs, raising the possibility that aberrant splicing is a major defect in SMA. Accordingly, several transcripts affected upon SMN deficiency have been re ...[more]

PMID: 24218366

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SMN MO, Gemin2 MO knockdown vs Control MO injected

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Project description:Although recent advances in gene therapy provide hope for spinal muscular atrophy (SMA) patients, the pathology remains the leading genetic cause of infant mortality. SMA is a monogenic pathology that originates from the loss of the SMN1 gene in most cases or mutations in rare cases. Interestingly, SMN1 mutations occur broadly either within the TUDOR methyl-arginine (Rme) reader domain of SMN or its carboxy terminal oligomerization domain. We hypothesized that in SMN1 mutant cases, SMA may emerge from aberrant protein-protein interactions between SMN and key neuronal factors. Using a proximity-dependent biotinylation proteomic (BioID) approach, we have identified and validated a number of SMN-interacting proteins, including Fragile X mental retardation family members (FMRFM), such as FMRP itself as well as FXR1 and FXR2, some depending on a wild-type version of the TUDOR domain.

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