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The results indicate that gene-targeted and mutant animals have soft tissue mechanical phenotypes that differ in complex ways.
Additionally, these mutant animals have a very short lifespan.
acs-20 mutant animals have an impaired cuticle barrier that results in an increase in small molecule accessibility.
Compared to wild type, eat-2 ad1116) eat-2 ad1116ls have reduced pharyngeal pumutantranimalsd are long-lived.
Germ cells from him-6 mutant animals have increased sensitivity to ionizing radiation, but surprisingly have decreased germ cell apoptosis after genotoxic stress [25].
Therefore, it is quite possible that very mild neurological symptoms in heterozygous mutant animals have not been recognized in the past.
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These mutant animals had no obvious physical defects from their wild-type littermates.
Male mutant animals had reduced glucose-clearing abilities and abnormal multi-hormone-expressing cells present in their endocrine islets.
All mec-10 mutant animals had properly localized channel complexes, indicating that the loss of MRCs was not attributable to a dramatic mislocalization of transduction channels.
The mutant animals had no apparent phenotypic abnormalities.
But when Karsenty and his colleagues examined the bones of mice that lacked leptin or its receptor, they found that the mutant animals had up to three times the bone volume and strength of their normal counterparts.
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