The choice of the phenylalanine mutants was based on the structural studies described below.
Because of the ease of using lesion length as a quantitative trait, our initial screen for gain-of-resistance mutants was based on reaction to bacterial blight.
Previously, the method used to screen Al-sensitive mutants was based on the measurement of root length of each plant before and after Al treatment.
Note that the numbering used for these mutants is based on the mitochondrial UNG1, which includes a 9 residue N-terminal mitochondrial localization signal, which is subsequently cleaved off [50].
The strategy for selecting these mutants was based upon the presence of opposite charges on their side-chain at neutral pH, their position at the AChE586-599 termini and their fibrilization properties (see above).
The construction of acyltransferase deletion mutants was based on the gene deletion strategy described by Wach [29].
Briefly, all mutants are based on a triple-auxotrophic (trp1Δ, leu2Δ, his3Δ) derivative of the C. glabrata ATCC 2001 reference strain.
The design of the mutants was based on a structure-activity relationship study of penetratin that led us to perform a R16A and a K13A/R16A exchange [ 46].
The design of the mutants was based on the DrAqp3b deduced amino acid sequence since the corresponding cRNA was expressed apparently more efficiently in X. laevis oocytes than that of DrAqp3a.
