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Minor alterations in neuronal circuits in these mutant animals are explained by redundancy and/or adaptive changes of other genes relevant for brain development.
The glp-1 mutant animals are also able to survive long-term anoxia [37].
We found that, contrary to previous reports, rde-4 mutant animals are not completely RNAi defective.
cat-2 mutant animals are hypersensitive and respond better than wild-type animals to dilute concentrations of octanol [13], [18].
RDE-4 facilitates processing of dsRNA by DCR-1, and rde-4 mutant animals are defective for RNAi [2], [13], [14].
Since Dnmt2 mutant animals are viable and fertile and do not display obvious phenotypes we could not positively test whether the genomic Dnmt2-EGFP contstruct is functional.
Rad21+/− mutant animals are thus a unique resource for dissecting the molecular determinants of IR responses in the context of whole mammals.
Consistent with this, tax-2 and tax-4 mutant animals are defective in soluble and odorant chemotaxis as well as thermotaxis [14], [15].
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Synchronized L1 glp-4 mutant animals were fed on RNAi bacterial clones at 16°C until they reached adulthood.
Understanding anatomical aspects of mammalian organ development, in both normal and mutant animals, is important for basic biology and also for regenerative medicine and tissue engineering.
rho-1 ok2418) rho-1 ok2418ls were generated by the C. elegans Gene Knockout Consortiumutant
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