The powerful tools developed in Drosophila and C. elegans can be used to identify and characterize genes involved in cellular proliferation, and potentially in human cancer. The objective of Core B (Genetics) is to make these tools readily available to investigators in this P01, providing support for laboratories with established expertise, as well as those that may not routinely use one of these model systems. The core will support the generation and maintenance of mutant and transgenic strains in both C. elegans and Drosophila. Functional properties of novel genes will be studied using reverse genetic techniques, such as RNAi in both species and the identification of deletion alleles in C. elegans. Microarray expression analysis will be provided for Drosophila. The core will provide confocal microscope facilities to study expression and subcellular localization of gene products for Drosophila, C. elegans, as well as mammalian systems. The Genetics Core brings resources and technical expertise in two model systems into a single administrative facility so as to benefit from their evident synergy and maximize the allocation of resources to benefit P01 investigators. The core is under the direction of Dr. Artavanis-Tsakonas, an authority on Drosophila genetics and developmental biology, with Dr. Hart, an expert in signaling in C. Elegans, serving as Co-Director.

Agency
National Institute of Health (NIH)
Institute
National Cancer Institute (NCI)
Type
Research Program Projects (P01)
Project #
1P01CA095281-01A1
Application #
6681235
Study Section
Subcommittee E - Prevention &Control (NCI)
Project Start
2002-09-12
Project End
2007-08-31
Budget Start
Budget End
Support Year
1
Fiscal Year
2002
Total Cost
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
City
Boston
State
MA
Country
United States
Zip Code
02199
Korzelius, Jerome; The, Inge; Ruijtenberg, Suzan et al. (2011) C. elegans MCM-4 is a general DNA replication and checkpoint component with an epidermis-specific requirement for growth and viability. Dev Biol 350:358-69
Stetak, Attila; Hörndli, Frederic; Maricq, Andres V et al. (2009) Neuron-specific regulation of associative learning and memory by MAGI-1 in C. elegans. PLoS One 4:e6019
Boxem, Mike; Maliga, Zoltan; Klitgord, Niels et al. (2008) A protein domain-based interactome network for C. elegans early embryogenesis. Cell 134:534-45
Bell, Daphne W; Brannigan, Brian W; Matsuo, Keitaro et al. (2008) Increased prevalence of EGFR-mutant lung cancer in women and in East Asian populations: analysis of estrogen-related polymorphisms. Clin Cancer Res 14:4079-84
Godin-Heymann, Nadia; Ulkus, Lindsey; Brannigan, Brian W et al. (2008) The T790M ""gatekeeper"" mutation in EGFR mediates resistance to low concentrations of an irreversible EGFR inhibitor. Mol Cancer Ther 7:874-9
Godin-Heymann, Nadia; Bryant, Ianthe; Rivera, Miguel N et al. (2007) Oncogenic activity of epidermal growth factor receptor kinase mutant alleles is enhanced by the T790M drug resistance mutation. Cancer Res 67:7319-26
Pellock, Brett J; Buff, Eugene; White, Kristin et al. (2007) The Drosophila tumor suppressors Expanded and Merlin differentially regulate cell cycle exit, apoptosis, and Wingless signaling. Dev Biol 304:102-15
Di Stefano, Luisa; Ji, Jun-Yuan; Moon, Nam-Sung et al. (2007) Mutation of Drosophila Lsd1 disrupts H3-K4 methylation, resulting in tissue-specific defects during development. Curr Biol 17:808-12
Ceron, Julian; Rual, Jean-Francois; Chandra, Abha et al. (2007) Large-scale RNAi screens identify novel genes that interact with the C. elegans retinoblastoma pathway as well as splicing-related components with synMuv B activity. BMC Dev Biol 7:30
Morris, Erick J; Michaud, William A; Ji, Jun-Yuan et al. (2006) Functional identification of Api5 as a suppressor of E2F-dependent apoptosis in vivo. PLoS Genet 2:e196

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