The double KO mice are neurologically impaired and show spontaneous epileptic seizures, with lethality around the end of the second postnatal week (Corbetta et al. 2009).
Furthermore, knockout of Tardbp in mice causes early lethality around the blastocyst implantation stage of embryogenesis (12, 13), complicating analysis of its role in vertebrate neural development and function.
A null mutation of Fig4 in the pale tremor mouse results in the formation of vacuoles in the cell bodies of neurons of the central nervous system (CNS) and peripheral nervous system, with extensive degeneration of sensory neurons of the dorsal root ganglia (DRG) and juvenile lethality around the time of weaning (Chow et al, 2007).
CTCF expression was able to partially rescue both, lethality (around 75% of mutant larvae pupariate, data not shown) and, importantly, developmental delay (pupariation was clearly advanced by CTCF expression in the CTCF y+6 mutant background, supplementary material Fig. S1).
With all of this potentially large scale lethality floating around, the muzzle velocity of the MCX and other similar assault-type rifles is particularly important.
While we also observed embryonic lethality around E7, the ratio of pups born for the +/+, +/− and −/− genotype was 25∶55∶0 for our model eliminating exon 2, whereas the model disrupting exon 3 [34] reported a ratio of 414∶515∶0.
Loss of Shh caused fetal growth retardation and embryonic lethality at around E13.5 as described previously.
PDCD2 knockout in the mouse results in embryonic lethality around 3.5 d pc suggesting a critical role in embryonic development at the times of zygotic gene activation and implantation (Mu et al., 2010).
The effect of inbreeding on disease phenotype variability was first assessed by determining the percentage of perinatal lethality around week-3 in four congenic collagen X Tg lines (1.6 293Δ B6, 1.6 293Δ DBA, 4.7 21Δ B6 and 4.7 21Δ DBA) and two KO lines (KO B6 and KO DBA) as compared to outbred Tg and KO lines (a C57BL/6, SJL, 129Sv and DBA/2J mix).
For elucidating the physiological functions of Reck, conventional Reck-knockout mice have been of limited use, since they show embryonic lethality around E10.5 and provide little information on the functions of Reck in late-stage development and in the adult.
Mice that with components of the innate immune system knocked out, such as IFNAR-, PKR-, or STAT1-null animals, show lethality around 4 5 days after infection because of the virus's ability to replicate efficiently throughout the mouse [68]– [68].
