Table 1. Heterozygosity for Nipbl causes postnatal lethality.
Paternal genotype | Surviving≥3 postnatal weeks | Viable at E17.5–E18.5 | Resorption at E17.5 | ||||||
+/+ | +/− | ratio | +/+ | +/− | ratio | +/+ | +/− | ||
Chimera | 91 | 22 | 4.1∶1* | nd | nd | nd | nd | nd | |
N0 Nipbl+/− | 190 | 40 | 4.8∶1* | 37 | 30 | 1.2∶1† | 0 | 2 | |
N1 Nipbl+/− | 247 | 54 | 4.6∶1* | nd | nd | nd | nd | nd |
Data are presented on the frequencies of genotypes resulting from crosses between heterozygous mutant males and CD-1 females. The males referred to in the first row were the chimeras produced by injection of Nipbl+/− ES cells into C57BL/6 blastocysts, so in this case only progeny descended from ES cells (as distinguished by chinchilla coat color) were scored. Surviving Nipbl+/− mice from these crosses are referred to as the N0 generation; their offspring with CD-1 females are referred to as the N1 generation; their offspring with CD-1 females as the N2 generation; and so on. Note that although the ratio of mutant to wildtype animals at E17.5–E18.5 is not significantly different from 1∶1, the presence of identifiably-mutant, but not wildtype, resorbed embryos at this stage suggests that there may be a small amount of late embryonic loss.
*: P<0.001 by chi-squared analysis when compared with Mendelian expectations.
†: P = 0.67 compared with Mendelian expectations, and P<0.005 when compared with the postnatal distribution.