Document Type
Article
Publication Date
7-2009
Originally Published In
Gracheva E, Dus M, Elgin SC. Drosophila RISC component VIG and its homolog Vig2 impact heterochromatin formation. PLoS One. 2009;4(7):e6182. doi:10.1371/journal.pone.0006182
Abstract
Heterochromatin formation plays an important role in gene regulation and the maintenance of genome integrity. Here we present results from a study of the D. melanogaster gene vig, encoding an RNAi complex component and its homolog vig2 (CG11844) that support their involvement in heterochromatin formation and/or maintenance. Protein null mutations vig(EP812) and vig2(PL470) act as modifiers of Position Effect Variegation (PEV). VIG and Vig2 are present in polytene chromosomes and partially overlap with HP1. Quantitative immunoblots show depletion of HP1 and HP2 (large isoform) in isolated nuclei from the vig(EP812) mutant. The vig2(PL470) mutant strain demonstrates a decreased level of H3K9me2. Pull-down experiments using antibodies specific to HP1 recovered both VIG and Vig2. The association between HP1 and both VIG and Vig2 proteins depends on an RNA component. The above data and the developmental profiles of the two genes suggest that Vig2 may be involved in heterochromatin targeting and establishment early in development, while VIG may have a role in stabilizing HP1/HP2 chromatin binding during later stages.
ORCID
https://orcid.org/0000-0002-5176-2510 [Elgin]
Creative Commons License
This work is licensed under a Creative Commons Attribution 3.0 License.
Recommended Citation
Gracheva, Elena; Dus, Monica; and Elgin, Sarah C.R., "Drosophila RISC component VIG and its homolog Vig2 impact heterochromatin formation" (2009). Biology Faculty Publications & Presentations. 192.
https://openscholarship.wustl.edu/bio_facpubs/192
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Comments
This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.