Sentence examples for mutant nematodes when from inspiring English sources

We analyzed the survival of glp-4 and glp-1 mutant nematodes when infected with a wide array of pathogens, including the Gram negative bacteria P. aeruginosa and S. enterica, the Gram positive bacterium E. faecalis, and the fungal pathogen C. neoformans.

Furthermore, the lifespans of lin-7 mutants and wild-type nematodes when grown on non-pathogenic E. coli were indistinguishable, suggesting that the infection phenotype exhibited by lin-7 mutants is not simply a consequence of aberrant organismal development.

However, it was reported that daf-16 and dbl-1 mutants have an increased amount of live bacteria in their intestine compared to N2 nematodes when maintained on E. coli OP50 [ 49].

To test whether the increased resistance observed in glp-4 and glp-1 mutants was due to a lack of matricide, we compared the survival of N2 wild-type, glp-4 mutant, and glp-1 mutant nematodes to that of fer-1 and fer-15 mutant nematodes.

Under these conditions, we found that both glp-4 and glp-1 mutant nematodes live considerably longer than N2 wild-type animals (Figure 2C).

These data imply that the adaptive response to neurobehavioral toxicity induced by metal exposure could not be effectively activated in mtl-1 and mtl-2 mutant nematodes.

Synchronized populations of wild-type and mutant nematodes were prepared by standard methods and cultivated at 20°C on NGM agar containing E. Coli (OP50) [32].

The analysis of motility behavior has traditionally relied on qualitative observations to describe C. elegans' locomotion and discriminate between wild-type and mutant nematodes.

The adaptive response to the neurobehavioral toxicity induced by metal exposure can not be detected in mtl-1 and mtl-2 mutant nematodes.

The presence of DA exacerbated toxicity because neurodegeneration was attenuated in mutant nematodes depleted for tyrosine hydroxylase (TH), the rate-limiting enzyme in DA production.

Therefore, the mutant nematodes generated in this study could be a hypothetical model for the lean body symptom of human patients linked to PQBP1 mutations.