of Mice: LT
Inbr (Sv) 121. Colour: Light brown a,Blt.
Origin: MacDowell 1950 from a mutation at the brown locus in strain C58.
Outcrossed to BALB/c. To Chase, to Re in 1957 at F28.
Ovarian teratomas occur spontaneously in about half of the females. Ultrastructurally
the stem cells do not differ from those of testicular or embryo-derived
teratomas (Damjanov et al., 1975
Some tumours begin to develop at about 30 days and the incidence rises
to 50% at 90 days. These resemble normal embryos until blastocyst stage
and then become disorganised. A small percentage of ovulated eggs also
develop parthenogenetically, but die at 5-7 days (Stevens and Varnum, 1974
). Oocytes arrest at metaphase of
meiosis I rather than progressing to metaphase II like other strains.
This is a necessary, but not sufficient condition for parthogenetic activation
(Eppig et al, 1996). Metaphase I arrest is frequently followed by parthogenetic
activation. Oocytes typically contain a single large centrosome with microtubules
being shorter than usual (Albertini and
). Metaphase I arrest is associated with a sustained elevation
of p34 (Cdc2
) kinase activity, sustained in part by restricted
degradation of cyclin B (Hampl and Eppig, 1995
Oocytes ovulated at metaphase I are not capable of undergoing normal fertilisation
. Only 13% of such oocytes penetrated by sperm formed
a diploid female pronucleus and a haploid male pronucleus by 4hr. after
insemination (Maleszweski and Yanagimachi, 1995). Spontaneously digynic
triploid embryos result from the fertilization of primary oocytes. These
embryos develop to the forelimb-bud stage but invariably posess neural
tube and cardiac abnormalities (Henery and
). Treatment with cisplatin reduced the incidence of
ovarian teratomas, and those that did develop were not transplantable
(Nishida et al, 1995
). A locus on chromosome
6 designated Ots1
(ovarian teratoma susceptibility) is the single
major locus that increases the frequency of teratomas in a semidominant
manner (Lee et al, 1997
D. F. and Eppig J. J. (1995) Unusual cytoskeletal and chromatin configurations
in mouse oocytes that are atypical in meiotic progression. Developmental
Genetics 16, 13-19.
I., Katic V., and Stevens L. C. (1975) Ultrastructure of ovarian teratomas
in LT mice. Z. Krebsforsch. 83, 261-267.
and Eppig J. J. (1995) Analysis of the mechanism(s) of metaphase I arrest
in maturing mouse oocytes. Development 121, 925-933.
C. C. and Kaufman M. H. (1993) Cellular and nuclear volume of primitive
red blood cells in digynic and diandric triploid and control diploid mouse
embryos. European Journal of Morphology 31, 237-249.
Lee G. H., Bugni
J. M., Obata M., Nishimori H., Ogawa K., and Drinkwater N. R. (1997) Genetic
dissection of susceptibility to murine ovarian teratomas that originate
from parthenogenetic oocytes. Cancer Res. 57, 590-593.
T., Sugiyama T., Kataoka A., Ushijima K., Ueyama T., and Yakushiji M.
(1995) Cytotoxic impacts on the tumorigenesis and transplantability of
ovarian teratoma in LT/Sv mouse. Oncology Reports 2, 1045-1048.
L. C. and Varnum D. S. (1974) Development of teratomas from parthenogenetically
activated ovarian mouse eggs. Devel. Biol. 37, 369-380.
INBRED STRAINS OF MICE
Updated 9 Apr. 1998
MRC Toxicology Unit, Hodgkin Building,
University of Leicester,