The t-Complex and Ovarian Teratocarcinogenesis

  • J. H. Nadeau
  • D. Varnum
Conference paper
Part of the Current Topics in Microbiology and Immunology book series (CT MICROBIOLOGY, volume 127)


Two of the many unanswered questions about the t-complex are the nature of the lethal effects controlled by recessive genes within the t-complex and whether recombination is suppressed between the t-complex and the centromere. Ovarian teratomas, which occur frequently in LT/Sv females (Stevens and Varnum 1974) and females of related strains, can be used to study both problems. Because ovarian teratomas originate from oocytes that have completed the first but not the second meiotic division (Eppig et al 1977), the vast majority of teratomas in heterozygous females are homozygous, unless recombination occurred between the centromere and a marker locus in which case the teratoma would be heterozygous. A number of congenic strains are being produced in which a t-complex is being transferred to the LT/Sv inbred strain or to the closely related LT.MA-Glo-1 b congenic strain. During construction of the LT.MA- + Glo-1 b .TT6- t 6 Glo-1 c congenic strain, which is hereafter designated LT-t 6 /+ and which is now at the 14th generation of back- crossing, it became apparent that heterozygosity for the t 6 -haplotype affected the frequency of ovarian teratomas. The purpose of this note is to document this effect and to present results of experiments whose purpose was to identify factors contributing to the reduced frequency.


Inbred Strain 14th Generation Meiotic Division Recessive Gene Congenic Strain 
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Copyright information

© Springer-Verlag Berlin · Heidelberg 1986

Authors and Affiliations

  • J. H. Nadeau
  • D. Varnum

There are no affiliations available

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