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The ter mutation first causes primordial germ cell deficiency in ter/ter mouse embryos at 8 days of gestation
Author(s) -
Sakurai Takayuki,
Iguchi Taisen,
Moriwaki Kazuo,
Noguchi Motoko
Publication year - 1995
Publication title -
development, growth and differentiation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.864
H-Index - 66
eISSN - 1440-169X
pISSN - 0012-1592
DOI - 10.1046/j.1440-169x.1995.t01-2-00007.x
Subject(s) - biology , embryo , genotype , gonadal ridge , genetics , locus (genetics) , congenic , germ cell , andrology , mutation , microbiology and biotechnology , embryogenesis , gene , medicine
The ter (teratoma) mutation causes primordial germ cell (PGC) deficiency in ter/ter embryos at 9.5–12.5 days of post‐coitum (dpc) in mouse strains 129/Sv‐ ter and LTXBJ‐ ter . To study the effects of the ter mutation on the PGC development more precisely, we examined the PGC number and distribution in 7.5–12.5 dpc embryo of ter congenic C57BL/6J‐ ter strain using their complete serial sections. The ter genotypes of embryos were identified by the polymerase chain reaction (PCR) polymorphisms of the microsatellite DNA of the Grl ‐1 locus mapped near the ter locus. Results showed that: (i) the PGC number in ter/ter embryos was similar to those of + / ter and + / + embryos at 7.5 dpc, and did not increase at 8.0–12.5 dpc, although those of normal littermates did usually; (ii) the PGC migration to genital ridges was never affected in all embryos; and (iii) the ter genotype difference in the PGC numbers was not recognized between + / ter and + / + embryos. We concluded that the ter mutation does not affect the PGC appearance around 7.5 dpc, but first causes PGC deficiency around 8.0 dpc at the beginning of their migration and proliferation, suggesting that the normal function of the ter gene may be essential for the proliferation or survival mechanisms of PGC.