International Mammalian Genome Society

17th International Mouse Genome Conference

9-12 November 2003, Braunschweig, Germany

Plenary Presentations * Oral Presentations *
Poster Presentations: Behavioural Genetics and Genomics * Development and Stem Cells * Functional Genome Analysis * Mouse Models of Human Disease * Mouse System Biology Bioinformatics * Multigenic and Multifactorial Trait Analysis * Nutrition and Metabolic Disease * Phenotyping Methods Imaging * The Genetics and Genomics of Infectious Disease *
Verne Chapman Memorial Lecture * Table of Contents * Sponsor/Exhibitor List * Awards * Photographs

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POSTER 107 - PANCREAS ANOMALY AND INTESTINAL TUMORS IN THE MOUSE SMALL EYE MUTANTS, PAX6 ^SEY3H AND PAX6^SEY4H

Nitta Y
Hiroshima University

Co-Authors: 2)Yoshida K, 3) Nakagata N
Institutions: 2) National Institute for Radiological Science, 3) Kumamoto University

Deletions of the chromosome 2 middle regions are associated with the radiation-induced mouse acute myeloid leukemias, while murine small eye mutants delete the chromosome 2 middle regions genetically. Expecting the predisposition to acute myeloid leukemia, the tumorigenicity of the two small eye mutants, Pax6Sey3H and Pax6Sey4H was examined. The commonly deleted region of the two small eye mutants was the segment of 3.2Mb between 106.0Mb and 109.2Mb from the centromere, where the Wilm's tumor 1 (Wt1), Reticulocarbin (Rcn), Paired box gene 6 (Pax6), Elongation protein homolog 4 (Elp4) and other fourteen novel genes located. The two mutants produced glucagon in the islets, however, they impaired to elevate the blood glucose level up when loaded with insulin. Morphological anomaly of the Wirsung duct, chronic pancreatitis or fatty degeneration of the pancreas was observed with age. Both mutants developed intestinal tumors spontaneously (52.0% and 32.0% for the Pax6Sey3H and the Pax6Sey4H, respectively), which were not observed in the normal sibs. γ-rays and N-methyl-N-nitrosourea shortened the latency but did not increase the frequency of the hematopoetic tumors in the mutants. The hemizygous deletions of the 3.2Mb-segment of the chromosome 2 did not contribute for the development of hematopoietic tumors mainly.