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. 2001 Mar 15;15(6):672–686. doi: 10.1101/gad.867301

Table 5.

Modulation of dauer arrest induced by ins-1 and human insulin by daf-2 and daf-7 pathway mutants

Dauer defective mutation
Transgene
Phenotype at 26°C (%)a
L3 and L4 larvae and adult
Dauer
Otherb
Nc
Wild type control 95.4 0 4.6 521
daf-16(mgDf47) control 95.0 0 5.0 380
daf-3(mgDf90) control 90.6 0 9.4 416
daf-16(mgDf47); daf-3(mgDf90) control 79.8 16.5 3.6 689
Wild type ins-1d 84.1 12.5 3.4 615
daf-16(mgDf47) ins-1 82.0 7.7 10.3 534
daf-3(mgDf90) ins-1 89.3 6.5 4.2 742
daf-16(mgDf47); daf-3(mgDf90) ins-1 84.6 9.1 6.3 760
Wild type human insulind 54.3 35.4 10.3 477
daf-16(mgDf47) human insulin 83.6 10.0 6.4 659
daf-3(mgDf90) human insulin 85.8 2.7 11.5 550
daf-16(mgDf47); daf-3(mgDf90) human insulin 80.3 2.9 16.8 720
a

To maximize the synchronicity of the progeny, parents were allowed to lay eggs for 2 h at 25°C. 

b

This category includes animals that could not be classified as either dauers or L3 and older at the time of scoring, due to less synchronous growth of the progeny than in the other sets of experiments. 

c

Total number of transgenic animals scored after 50 h at 26°C. Numbers represent the summary of at least two separate trials from a single transgenic line of each genotype. 

d

In this set of experiments, we found that both transgenes caused a somewhat higher level of dauer formation in the wild-type background than the experiments shown in Table 2, perhaps due to fluctuations in incubator temperature between the two sets.