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Accueil du site > Animations Scientifiques > Séminaires 2007 > Function of C. elegans HP1 proteins in post-embryonic development
Function of C. elegans HP1 proteins in post-embryonic development
Orateur :
Francesca Palladino, Equipe Régulation Epigénétique chez C. elegans, Laboratoire de Biologie Moléculaire de la Cellule, ENS-Lyon
Salle :
C023 (RDC LR6 côté CECAM)
Sujet :
We are using the nematode C. elegans to study the epigenetic regulation of gene expression in a developmental context. Our studies are focused on the highly conserved HP1 protein, an essential player in the dynamic organization of nuclear architecture and transcriptional silencing. C. elegans contains two HP1 homomogues, which we named HPL-1 and HPL-2. HPL-2 acts in a transcriptional repressor pathway which includes homologues of Drosophila and human Rb complexes. We are now using microarray analysis and chromatin IPs to identify the targets of HPL-2. While deletion of hpl-2 results in sterility and growth defects, hpl-1 is dispensable for both germline and somatic development.
However, HPL-1 and HPL-2 are redundantly required for post-embryonic development, as hpl-1 ;hpl-2 double mutants do not develop past the larval stage. Our data provides the first direct evidence for both redundant and unique functions of HP1 family proteins in metazoan development.
In an RNAi based screen, we have isolated SET-2, the homolog of the human SET1 and mixed lineage leukemia (Mll) genes, as a suppressor of hpl-2 mutant phenotypes. Mammalian SET1/MLL proteins are found in a histone H3K4 specific methyltransferase complex and we have found that the nematode counterparts of other complex subunits also suppress hpl-2 mutant phenotypes. Furthermore, the H3K4 HMT activity of these proteins appears to be conserved in C. elegans. These results suggest that a C. elegans SET1/MLL complex may antagonize HPL-2 repressor function in development.
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