Combining wild type and mutant profiles of these transcripts demonstrates the activation of a complex genetic program that delineates symbiotic nitrogen fixation.
A reduced model combining wild type (785AA) and heterozygotes (785AG) produced a similar result (ΔOFV, −6.4; decrease in CL/F of 22.9% for homozygous mutants).
The bacteria inoculum was 5 × 108 CFU of combined wild-type and mutant strains (2.5 × 108 of each strain, at a ratio of 1 1).
Interestingly, the receptor with the GG46/GG79 combined genotype also displayed a greater degree of downregulation as compared to that found with the AA46/CC79 combined wild-type.
Furthermore, the homozygous variants had significantly higher AHH inducibility than the combined wild-type and heterozygous variants.
We combined wild-type and mutant Myo1 labeled with a fluorescent protein tag directly on the Myo1 heavy chain with Rng3 labeled with a contrasting fluorescent protein.
We also performed a QTL analysis with the combined wild-type and recq4a populations without removing any individuals and detected the same chromosome 5 QTL for both phenotypes.
Furthermore, the combined wild-type SEPT2 and MLL-SEPT2 expression was significantly lower (5.4 to 9.4 fold) in the MLL-SEPT2 cases than in all other leukemia genetic subgroups (Table 1).
Statistically significant differences were observed for the combined wild-type SEPT2 and MLL-SEPT2 expression in the MLL-SEPT2 cases when compared with the normal controls, showing a 12.8-fold lower median expression in the MLL-SEPT2 subset (p = 0.007).
One-way analysis of variance (ANOVA) using Tukey's multiple comparison test showed no significant difference for any measurement between wild-type (n = 2) and heterozygous Sox10 lacZ/+ embryos (n = 2), so we combined wild-type and heterozygote data (n = 4) for comparison with homozygotes (n = 3).
With gNCA, we analyzed the combined wild-type and fkh1 fkh2 mutant data set and showed that gNCA can be used to identify TFAs which are consistent with cell physiology, transcription factors with potential cell cycle dependent roles, as well as interactions between transcription factors.
