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However, the fact that MZezh2hu5670/hu5670 mutants develop a normal body plan raises the possibility that ezh1 could contribute to early embryogenesis in absence of ezh2 function.
crl1 and arl1 mutants develop a normal radicle but form no crown root primordium, indicating that CRL1/ARL1 is a master gene for crown root primordium formation.
Embryos were sorted based on their phenotype; mutants develop a swollen pericardium and lack fin buds.
(F ) Mafb null mutants develop a small and cystic inner ear compared to control littermates.
Therefore, Fgf23 −/− /VDRΔ/Δ and Kl −/− /VDRΔ/Δ compound mutants develop a more complex phenotype than Gitelman's syndrome.
The preliminary characterization of Ptrh2 mutant mice revealed homozygous Ptrh2 mutants develop a "runting" (dystrophy) syndrome postnatally and die within the first 2 weeks of life.
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The resulting mutants developed a severe aneurysmal arterial trunk that resulted in embryonic lethality during late gestation.
The resulting Ilk mutants developed a severe aneurysmal arterial trunk that resulted in embryonic lethality during late gestation.
Similarly, mice that express a cytoplasmically truncated type II receptor, which acts as a dominant-negative mutant, develop a degenerative joint disease resembling human OA [ 8].
Transgenic mice expressing CMT type 1C-linked human SIMPLE mutant develop a late-onset motor and sensory neuropathy associated with abnormal myelin infolding, paranodal defects, and altered nodal organization (Lee et al., 2013).
Supporting this concern, the AQP1 N76S mutant developed a proton conductance, but mediated a WT water-flux (39).
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