- page settings
- showhide sidebar
- showhide empty fields
- layout
- (too narrow)
- open all
- close all
Expression cluster » WBPaper00060014:set-2(tm1630)_downregulated
- Page Content
- Overview
- Associations
- Clustered data
- Genes
- References
- Regulation
- Tools
- Tree Display
- My WormBase
- My Favorites
- My Library
- Recent Activity
- Comments (0)
history logging is off
Tree Display
My Favorites
My Library
Overview
WBPaper00060014:set-2(tm1630)_downregulated
Algorithm:
DESeq2 (v2.1.8.3) was used to determine DE genes and to generate principal component and scatter plots. DE genes with FDR < 0.05 were analysed using g:Profiler with Bonferroni correction.References
- Filter by article type
1
Post-translational histone modifications regulate chromatin compaction and gene expression to control many aspects of development. Mutations in genes encoding regulators of H3K4 methylation are causally associated with neurodevelopmental disorders characterized by intellectual disability and deficits in motor functions. However, it remains unclear how H3K4 methylation influences nervous system development and contributes to the aetiology of disease. Here, we show that the catalytic activity of <i>set-2</i>, the <i>C. elegans</i> homolog of the H3K4 methyltransferase KMT2F/G (SETD1A/B) genes, controls embryonic transcription of neuronal genes and is required for establishing proper axon guidance and for neuronal functions related to locomotion and learning. Moreover, we uncover a striking correlation between components of the H3K4 regulatory machinery mutated in neurodevelopmental disorders and the process of axon guidance in <i>C. elegans</i> Thus, our study supports an epigenetic-based model for the aetiology of neurodevelopmental disorders, based on aberrant axon guidance process originating from deregulated H3K4 methylation.
Rows per page: |