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HPL-2 in GW638 (met-2 set-25) MxEmb

ABSTRACT: ChIP-chip of HPL-2 in met-2 set-25 C. elegans mixed-stage embryo

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE58761 | GEO | 2014/10/11

SECONDARY ACCESSION(S): PRJNA253400

REPOSITORIES: GEO

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HPL-2 in GW638 (met-2 set-25) MxEmb

Project description:ChIP-chip of HPL-2 in met-2 set-25 C. elegans mixed-stage embryo EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: GW638; Developmental Stage: Mixed-stage Embryo; Genotype: met-2(n4256) set-25(n5021); Sex: population predominantly Hermaphrodites perhaps with some Males; NUMBER OF REPLICATES: 2; EXPERIMENTAL FACTORS: temperature 20

2014-10-11 | E-GEOD-58761 | biostudies-arrayexpress

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HPL-2 in PFR40 (hpl-2) early embryo

Project description:ChIP-chip of HPL-2 in hpl-2 C. elegans early embryo EXPERIMENT TYPE: CHIP-chip. BIOLOGICAL SOURCE: Strain: PFR40; Developmental Stage: Early Embryo; Genotype: hpl-2(tm1489); Sex: population predominantly Hermaphrodites perhaps with some Males; NUMBER OF REPLICATES: 1; EXPERIMENTAL FACTORS: temperature 20

2014-10-11 | E-GEOD-58763 | biostudies-arrayexpress

HPL-2 in N2 (wild-type) early embryo

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Project description:We asked if the perinuclear position of chromosome arms in C. elegans depends on the histone methyltransferases MET-2 and SET-25. To this end, we performed LMN-1-DamID in wild-type (N2) and mutant (set-25 met-2) strains. LMN-1-DamID signal on chromosome arms was significantly reduced in the mutant. Three biological replicas were performed for each genotype. For one replica dyes were swapped. For each replica methylated DNA amplified from a strain expressing LMN-1-Dam was competitively hybridized against DNA amplified from a strain expressing GFP-Dam.

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Project description:Differentiated cells rely on segregation of the genome into heterochromatin and euchromatin, but the mechanisms that establish these domains in vivo are incompletely understood. The current models suggest that heterochromatin is marked by histone H3 lysine 9 methylation (H3K9me), which recruits heterochromatin protein 1 (HP1), to compact chromatin and repress transcription. In C. elegans, the SETDB1 homolog MET-2 is essential for H3K9me-mediated gene silencing; however, MET-2 also localizes to heterochromatic foci independently of H3K9me and exhibits non-catalytic functions that support both germline and somatic development. Here we extend these findings by examining the classical H3K9me reader HP1. We show that HPL-2/HP1 deficient in methyl-lysine binding or in the absence of H3K9me can still repress transcription, promote organogenesis and localize to heterochromatin foci. Whereas activity remains in the absence of the HPL-2:H3K9me interaction, complete loss of met-2 and hpl-2 shows synergistic phenotypes for organogenesis and gene de-repression, underscoring the existence of additional, H3K9me-independent functions. HPL-2 and MET-2 require distinct binding partners for their localization and activity: MET-2 associates with the disordered protein LIN-65/ATF7IP, while HPL-2 depends on the multi-zinc finger protein LIN-13, which interacts with the HPL-2 chromoshadow domain. Our findings suggest that HPL-2 and MET-2 operate in parallel pathways, localizing to heterochromatic foci and promoting gene silencing and organogenesis, with H3K9me acting as a reinforcing, but non-essential, element in these processes.

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