glp-1 expression in AWC neurons is sufficient to correct glp-1-dependent dauer maintenance defects
| Transgene injected* . | Rescue of dauer maintenance defect±s.d.† . |
|---|---|
| myo-2p::GFP | 6.1±5.4% |
| gpa-2p::glp-1 | 70.0±9.6%‡ |
| odr-1p::glp-1 | 76.5±7.5%‡ |
| ser-2prom2::glp-1 | 14.3±3.8% |
| lim-6int3::glp-1 | 5.0±4.5% |
| unc-25p::glp-1 | 15.5±6.2% |
| ceh-6p::glp-1 | 6.6±12.6% |
| Transgene injected* . | Rescue of dauer maintenance defect±s.d.† . |
|---|---|
| myo-2p::GFP | 6.1±5.4% |
| gpa-2p::glp-1 | 70.0±9.6%‡ |
| odr-1p::glp-1 | 76.5±7.5%‡ |
| ser-2prom2::glp-1 | 14.3±3.8% |
| lim-6int3::glp-1 | 5.0±4.5% |
| unc-25p::glp-1 | 15.5±6.2% |
| ceh-6p::glp-1 | 6.6±12.6% |
Neuronal promoters were used to drive GLP-1 expression in various types of neurons to determine whether neuron-specific GLP-1 expression would suppress the dauer maintenance defects associated with glp-1 If mutations. p, promoter.
All constructs were injected with myo-2p::GFP as a co-transformation marker in the parental strain glp-1(e2141)daf-7(e1372).
See Materials and methods; s.d., standard deviation; n=100.
Statistical analyses were performed: P<0.005, compared with control myo-2::GFP-expressing transgenic lines.