Genetic dissection of susceptibility to murine ovarian teratomas that originate from parthenogenetic oocytes.

نویسندگان

  • G H Lee
  • J M Bugni
  • M Obata
  • H Nishimori
  • K Ogawa
  • N R Drinkwater
چکیده

The LT/Sv mouse strain is characterized by its abnormally high incidence of spontaneous ovarian teratomas. These tumors have been shown to originate from parthenogenetic oocytes, which are spontaneously induced to divide. Both spontaneous parthenogenesis and ovarian teratomas are extremely rare for other mouse strains, including C57BL/6J. To identify the genes responsible for this unique phenotype of female LT/Sv mice, we performed linkage analysis of female (C57BL/6J x LT/Sv)F2 mice. A locus on chromosome 6 designated Ots1 (ovarian teratoma susceptibility) was identified as the single major locus that increases the frequency of teratomas in a semidominant manner.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Genetic regulation of traits essential for spontaneous ovarian teratocarcinogenesis in strain LT/Sv mice: aberrant meiotic cell cycle, oocyte activation, and parthenogenetic development.

Strain LT/Sv female mice show a high frequency of spontaneous ovarian teratomas arising from parthenogenetically activated follicular oocytes. LT/Sv oocytes also arrest at metaphase of meiosis I, rather than progressing through to metaphase II, as do almost all fully grown oocytes from most other strains. We investigated a new set of recombinant inbred strains derived from BALB/c and C58 (the p...

متن کامل

P-70: The Effect of Hydrostatic Pressure on Parthenogenetic Activation of Mouse Oocytes Derived from In vitro Grown Ovarian Follicles

Background: Parthenogenesis is the production of an embryo from a female gamete in the absence of any contribution from a male gamete, with or without the eventual development into an adult. In vivo, mammalian parthenogenesis is a rare event. Parthenogenesis can be efficiently induced in vitro with a variety of mechanical, chemical, and electrical stimuli in several species. Hydrostatic pressur...

متن کامل

Inactivation of Retinoblastoma Protein (Rb1) in the Oocyte: Evidence That Dysregulated Follicle Growth Drives Ovarian Teratoma Formation in Mice

The origin of most ovarian tumors is undefined. Here, we report development of a novel mouse model in which conditional inactivation of the tumor suppressor gene Rb1 in oocytes leads to the formation of ovarian teratomas (OTs). While parthenogenetically activated ooctyes are a known source of OT in some mutant mouse models, enhanced parthenogenetic propensity in vitro was not observed for Rb1-d...

متن کامل

P-76: Cytogenetic Investigation of Parthenogenetic Mouse Embryos Generated from In Vitro Activated Oocytes by Hydrostatic Pressure in The Presence of Calcium Ionophore and Ethanol

Background: The advances in cytogenetic techniques during the last few years have permitted not only the study of large populations of wild and domestic animals, but also the detection of chromosome anomalies in embryos. Chromosomal abnormalities are the most common cause of embryonic and fetal mortality in mammals. Most reports of chromosome anomalies in parthenogenetic embryos describe numeri...

متن کامل

The Ovarian Teratoma Mapping Method in the Mouse

Murine ovarian teratomas were used to determine recombination percentages for gene-gene and centromere-gene intervals. Data were obtained utilizing a recombinant inbred strain, LTXBJ, and a number of newly developed LT/SvEi congenic strains. --Centromere-gene recombination was measured at 11.3 & 1.2% for the centromere of chromosome 7 Gpi-1 interval and 15.8 2 2.4% for the centromere of chromos...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Cancer research

دوره 57 4  شماره 

صفحات  -

تاریخ انتشار 1997