These mutants were named A1, A2, A3, B1, B3, H4.
We addressed this question by sequencing both HA and NA genes of 40 previously described anti-HA mAb escape mutants (mutants are named based on their selecting mAb).
The putative mutants were named as P hytophthora s ojae susceptible 1 (pss1) through pss30.
Hereafter, mutants are named as follows: the native amino acid residue, the residue number, and the new residue.
The double mutants were named according to the remaining tryptophans present (Trp42/ Trp130/Trp42// Trp68/Trp1302/ Trp42/Trp1308/Trp130, Trp42/Trp130, and Trp68/ Trp68/).
These mutants were named mildew-induced lesions (mil) mutants and below we describe the characterization of the mil1 mutant and cloning of MIL1 gene.
The CipA mutants are named CipA-ΔXDocII, CipA-Δ6CohI, CipA-ΔCBM-1, and CipA-ΔCBM-2 according to the farthest upstream module that was deleted (Additional file 4).
The ΔrcsA and ΔrcsB E. coli K92 mutants were named E. coli K92 ΔrcsA and E. coli K92 ΔrcsB, respectively.
The bm mutants were named based on the red – brown coloration of the lamina midrib, which intriguingly accompanied low levels of lignification in stem tissue [ 20, 21].
Such high levels of INO1 expression lead to over- production of inositol (the Opi− phenotype for which the opi1 mutants are named) and the excess inositol excreted from Opi− mutants can be detected in a plate assay (Greenberg et al. 1982a, b).
