To construct a series of double-deletion strains (for example, Δ ypfI/Δ dusC), Δ ypfI∷Cm was transferred to a series of single-deletion strains (Kmr) by P1-transduction.
We chose nine deletion strains, Δ thiI, Δ dusA, Δ dusB, Δ dusC, Δ trmH, Δ truA, Δ trmB, Δ trmA and Δ truB, each of whose deletion was transferred to Δ ypfI by P1 transduction, to construct a series of double-deletion strains.
To construct a series of the arn1 mutant strains, arn1+ ORF and approximately 600 bp of its 5′ and 3′ flanking regions were cloned into pCR2.1.
In this study, metabolic engineering approaches were employed to construct a series of Synechocystis sp. PCC6803 mutant strains.
This allowed us to construct a series of TF activation networks for the 3 strains.
In addition, we have constructed a series of host strains containing all possible combinations of ade1, arg4, his4, and ura3 auxotrophies to be used with these new vectors.
To determine if the enhanced attachment of the clinical PVL-positive isolates to ECM proteins was mediated by gene products encoded by the phage that carries PVL (phiSLT), by PVL itself, or by other genes present in the S. aureus chromosome, we constructed a series of isogenic strains lysogenizing the phage phiSLT into several PVL negative clinical isolates.
To evaluate their potential roles as genetic switches, we constructed a series of isogenic strains, including LT2 mutLT2, LT2 mutLL3, LT2 mutLL4 and LT2 mutSL (Table 1), in which at least one base in the repeats within mutL or mutS was changed to disrupt the sequence identity among the repeats.
To test the effect of disruption type on response to mutational stress, we constructed a series of thirty secondary mutation-containing strains from each disruption strain.
