Beier D R, Morton C C, Leder A, Wallace R, Leder P
Department of Genetics, Harvard Medical School, Howard Hughes Medical Institute, Boston, Massachusetts 02115.
Genomics. 1989 May;4(4):498-504. doi: 10.1016/0888-7543(89)90272-3.
We have used cytogenetic and recombinational analysis to determine the position of a transgene integrated into the mouse genome. The transgene maps to band F on the physical map of mouse chromosome 15 by in situ analysis and is tightly linked genetically to a cluster of loci that include the mutations caracul (Ca) and microcytic anemia (mk). Genetic analysis of the offspring of noninbred animals carrying the transgene and marker loci demonstrates a significant deficiency of homozygous progeny at weaning. When inbred mice heterozygous for the transgene are mated, about one-quarter of their offspring are homozygous; none of these animals survives more than 1 day after birth. It appears likely that a recessive insertional mutation has occurred as a result of transgene integration into a locus required for postnatal viability. We call this mutation transgenic perinatal lethality (Tg.ple).
我们利用细胞遗传学和重组分析来确定整合到小鼠基因组中的转基因的位置。通过原位分析,该转基因定位于小鼠15号染色体物理图谱上的F带,并且在遗传学上与一组基因座紧密连锁,这些基因座包括卡拉库尔(Ca)和小细胞贫血(mk)突变。对携带转基因和标记基因座的非近交动物后代的遗传分析表明,断奶时纯合子后代显著不足。当转基因杂合的近交小鼠交配时,它们约四分之一的后代是纯合子;这些动物在出生后存活不超过1天。似乎由于转基因整合到出生后生存所需的基因座中,发生了隐性插入突变。我们将此突变称为转基因围产期致死率(Tg.ple)。