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To evaluate the soil-surface rooting phenotype of the mutant, we used four different methods: the pot method, the cup method, the glass tube method, and the basket method.
To provide an explanation for the residual activity in the hcpA mutant we used a flagella mutant of EDL933.
As previously described the 212-C-ter mutant we used is comprised of the fourth RBD and the GAR domains.
Taken together, the tw mutant was a null mutant and the rt mutant we used was an almost null or a strong hypomorphic mutant for POMT activity.
Since phase information can be directly obtained from images of the mutant, we used this in the present work to obtain more accurate difference maps.
To validate the cep-1 mutant, we used IR to introduce DNA damage-induced apoptosis.
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For 91 mutants, we used the protein design algorithm FoldX.
To study the relation between phenotype and rhodopsin stability in disease mutants, we used a structure-based approach.
The Tah18 essential function is affected in the two mutants we used in this study tah18-5H8 and tah18-5I5, as they are unable to grow at 37°C.
To further investigate the relationship between EAT-6 function and phenotypes seen in eat-6 mutants, we used RNA interference (RNAi) to knock down eat-6 gene activity.
For construction of double mutants we used pHT315Ab-D136N harboring a point mutation D136N as template to introduce additional point mutations as E129K or T143D.
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