International Mammalian Genome Society

The 14th International Mouse Genome Conference (2000)

H6. A Large Scale ENU Mutagenesis Project in RIKEN Genomic Sciences Center (GSC)

Shigeharu Wakana, Hiroshi Masuya, Osamu Minowa, Maki Inoue, Tomohiro Suzuki, Hiroyuki Iwama, Hideaki Toki, Hiromi Motegi, Toru Shibuya, Yoichi Gondo, Tetsuo Noda, Toshihiko Shiroishi
Mouse Functional Genomics Research Group RIKEN Genomics Sciences Center (GSC), Maeda-cho, Totsuka-ku, Yokohama, 244-0804, Japan

Manifested progress of genome sequencing of human and mouse and comparison of the two species would promote identification of genes and open reading frames (ORFs) in their genomes. Extensive delineation of gene functions would be the next challenge in Genome Science. Use of mutant mice that have dysfunction of genes would provide a clue to elucidate the gene functions in a systematic way. ENU is the most potent germline mutagen in the mouse. Feasibility of ENU mutagenesis in mice has been well established by foregoing projects in UK and Germany.

In the mutagenesis project of RIKEN-Genomic Sciences Center (GSC), we set out mutant screen focussing on several unique phenotypes: 1) The late-onset phenotypes, such as tumorigenesis and senescence. The current large-scale mouse mutagenesis projects are conducted to screen mainly for early-onset phenotypes up to 3 months old. We extend the observation period to more than one full year. 2) The phenotypes specific to wild mice erived inbred strains. We use MSM as a target strain for mutagenesis, which is derived from Japanese wild mice, Mus musculus molossinus, in addition to conventional laboratory inbred strains developed from European subspecies, M. m. domesticus. MSM still retains wild mice specific phenotypes, e.g. tumor resistance and hyper locomotion activity, which have been lost during domestication of the many laboratory inbred mouse strains. These unique phenotypes of MSM strain are targets in our mutagenesis program. 3)Synthetic mutant phenotypes or maltigenic traits. It is generally accepted that many human diseases are caused by additive or epistatic effect of oligo-genic or maltigenic dysfunction. In order to develop animal models to understand the genetic basis of such complex traits, we plan to screen the new phenotypes by mutagenesis for known mutant mice. From this screen, the novel genes that are interactive to the known mutant gene will be identified.

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