International Mammalian Genome Society

The 14th International Mouse Genome Conference (2000)


I36. Developmental Genetics and Candidate Search on Experimental Testicular Teratocarcinogenesis

M. Noguchi1, K. Niwa1, T. Kasai1, M. Tsunesada1, S. Suda1, H. Takai1, M. Kusakabe2
1Department of Biology and Geosciences, Faculty of Science, Shizuoka University, Shizuoka, Shizuoka 422-8529, 2Experimental Animal Research Division, Biogenic Resources Center, RIKEN, Tsukuba Institute, Tsukuba, Ibaraki 305-0074, Japan

Ninety four percent of the ter/ter males and only 0.4 % of the +/+ ones from the mouse strain 129/Sv-+/ter have the spontaneous testicular teratomas composed of various kinds of tissues that are thought to be derived from primordial germ cells (PGCs) in their fetal testes. More than 90 % of the grafts of the 129/Sv-+/+ (designated 129) fetal testes at 12.5 dpc developed the experimental testicular teratomas (designated ETT) similar to the spontaneous ones (Noguchi et al., Develop. Growth Differ. 36, 1996). The grafts from the strains LTXBJ and LTXBJ-CSA (designated LT-CSA), however, developed no ETT. To examine whether this strain difference in the incidences of the ETT could be ascribed to that in PGCs or that in the testicular somatic cells, we analyzed the reconstituted testes of 4 type combinations of the PGCs and somatic cells of the 12.5-dpc testes between the strains 129 and LT-CSA. LT-CSA strain is a CSA congenic strain whose cells ubiquitously express the CSA antigen encoded by the CSA gene that has been transferred from C3H/HeJ strain to the LTXBJ genetic background by us. The cells with the CSA-positive cytoplasm distinguished the cells originated from LT-CSA strain from the CSA negative cells derived from the 129 strain. The results showed that both 129 and LT-CSA PGCs combined with the 129 testicular somatic cells were differentiated to ETT. It is suggested that the 12.5-dpc testicular somatic cells bearing the genes from 129/Sv-+/+ mice could induce or permit also the 12.5-dpc PGCs having background genes other than 129 strain to develop ETT. The chromosomal mapping of the candidate genes involved in the ETT formation of the mouse PGCs will be reported.


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