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SET-9 and SET-26, the C. elegans homologs of human MLL5, are critical for germline development and longevity

ABSTRACT: SET-9 and SET-26 are highly homologous paralogs that share redundant function in germline development, but SET-26 alone plays a key role in longevity and heat stress response. SET-26 is broadly expressed, but SET-9 is only detectable in the germline, which likely account for their different biological roles. SET-9 and SET-26 bind to H3K4me3 in vitro and in vivo, and their loss results in broadening of H3K4me3 domains. SET-9 and SET-26 also regulate the RNA expression of a subset of their target genes, irrespective of their H3K4me3 status. We propose that SET-9 and SET-26 function to organize local chromatin environment and to regulate the expression of specific target genes, and these activities together contribute to their critical roles in germline development, stress response, and longevity. SET-9 and SET-26 are highly homologous to human MLL5, a factor implicated in leukemia and glioblastoma, and our findings help to provide new insights into MLL5.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE100623 | GEO | 2018/05/31

REPOSITORIES: GEO

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SET-9 and SET-26 are H3K4me3 readers and play critical roles in germline development and longevity

Project description:SET-9 and SET-26 are highly homologous paralogs that share redundant function in germline development, but SET-26 alone plays a key role in longevity and heat stress response. SET-26 is broadly expressed, but SET-9 is only detectable in the germline, which likely account for their different biological roles. SET-9 and SET-26 bind to H3K4me3 in vitro and in vivo, and their loss results in broadening of H3K4me3 domains. SET-9 and SET-26 also regulate the RNA expression of a subset of their target genes, irrespective of their H3K4me3 status. We propose that SET-9 and SET-26 function to organize local chromatin environment and to regulate the expression of specific target genes, and these activities together contribute to their critical roles in germline development, stress response, and longevity. SET-9 and SET-26 are highly homologous to human MLL5, a factor implicated in leukemia and glioblastoma, and our findings help to provide new insights into MLL5.

2018-05-31 | GSE108848 | GEO

Molecular basis for chromatin binding and regulation of MLL5

Project description:The human mixed lineage leukemia 5 (MLL5) protein mediates hematopoietic cell homeostasis, cell cycle and survival, however, the molecular basis underlying MLL5 activities remains unknown. Here, we show that MLL5 is recruited to gene-rich euchromatic regions via the interaction of its PHD finger with the histone mark H3K4me3. The 1.48 Å resolution crystal structure of the MLL5 PHD finger in complex with the H3K4me3 peptide reveals a non-canonical binding mechanism, whereby K4me3 is recognized through a single aromatic residue and an aspartate. The binding induces a His-Asp swapping rearrangement mediated by a C-terminal α-helix. Phosphorylation of H3T3 and H3T6 abrogates the association with H3K4me3 in vitro and in vivo, releasing MLL5 from chromatin in mitosis. This regulatory switch is conserved in the Drosophila ortholog of MLL5, MLL5, and suggests the developmental control for targeting of H3K4me3. Together, our findings provide insight into the molecular basis for the recruitment, exclusion and regulation of MLL5 at chromatin.

2013-07-01 | GSE47100 | GEO

Molecular basis for chromatin binding and regulation of MLL5

Project description:The human mixed lineage leukemia 5 (MLL5) protein mediates hematopoietic cell homeostasis, cell cycle and survival, however, the molecular basis underlying MLL5 activities remains unknown. Here, we show that MLL5 is recruited to gene-rich euchromatic regions via the interaction of its PHD finger with the histone mark H3K4me3. The 1.48 Ã resolution crystal structure of the MLL5 PHD finger in complex with the H3K4me3 peptide reveals a non-canonical binding mechanism, whereby K4me3 is recognized through a single aromatic residue and an aspartate. The binding induces a His-Asp swapping rearrangement mediated by a C-terminal Î±-helix. Phosphorylation of H3T3 and H3T6 abrogates the association with H3K4me3 in vitro and in vivo, releasing MLL5 from chromatin in mitosis. This regulatory switch is conserved in the Drosophila ortholog of MLL5, MLL5, and suggests the developmental control for targeting of H3K4me3. Together, our findings provide insight into the molecular basis for the recruitment, exclusion and regulation of MLL5 at chromatin. For determaning MLL5 chromatin profile, DamID-MLL5 chromatin profiling was determined in C2C12 cells . Three biological replicates were performed. Normalized data was averaged and HMM approach was applied to establish the bound regions (Straub, T., Grimaud, C., Gilfillan, G. D., Mitterweger, A., and Becker, P. B. (2008). PLoS Genet 4, e1000302)

2013-07-01 | E-GEOD-47100 | biostudies-arrayexpress

SET-9 and SET-26 are H3K4me3 readers and play critical roles in germline development and longevity

Project description:SET-9 and SET-26 are H3K4me3 readers and play critical roles in germline development and longevity

| PRJNA428937 | ENA

Caenorhabditis elegans

Project description:SET-9 and SET-26, the C. elegans homologs of human MLL5, are critical for germline development and longevity

| PRJNA392315 | ENA

Project description:SET-9 and SET-26, the C. elegans homologs of human MLL5, are critical for germline development and longevity

| PRJNA392182 | ENA

Murine Histone Methyltransferase Mll5, is involved in Male Gametogenesis

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2010-09-30 | GSE19648 | GEO

Murine Histone Methyltransferase Mll5, is involved in Male Gametogenesis

2010-09-30 | E-GEOD-19648 | biostudies-arrayexpress

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Project description:SET-26, HCF-1, and HDA-1 are highly conserved chromatin factors with key roles in development and aging. Here we present mechanistic insights into how these factors regulate gene expression and modulate longevity in C. elegans. We show that SET-26 and HCF-1 cooperate to regulate a common set of genes, and both antagonize the histone deacetylase HDA-1 to limit longevity. We propose a model in which SET-26 recruits HCF-1 to chromatin in somatic cells, where they stabilize each other at the promoters of a subset of genes, particularly mitochondrial function genes, and regulate their expression. HDA-1 opposes SET-26 and HCF-1 on the regulation of a subset of their common target genes and in longevity. Our findings suggest that SET-26, HCF-1, and HDA-1 comprise a mechanism to fine-tune gene expression and longevity and likely have important implications for the mechanistic understanding of how these factors function in diverse organisms, particularly in aging biology.

2024-01-29 | GSE224075 | GEO

The chromatin factors SET-26 and HCF-1 oppose the histone deacetylase HDA-1 in longevity and gene regulation in C. elegans [CUT&RUN]

2024-01-29 | GSE224076 | GEO

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