@article{sing_klaenhammer_1993, title={A strategy for rotation of different bacteriophage defenses in a lactococcal single-strain starter culture system}, volume={59}, number={2}, journal={Applied and Environmental Microbiology}, author={Sing, W. D. and Klaenhammer, T. R.}, year={1993}, pages={365} }
 @article{sing_klaenhammer_1991, title={Characterization of restriction-modification plasmids from Lactococcus lactis spp. cremoris and their effects when combined with pTR2030}, volume={74}, DOI={10.3168/jds.S0022-0302(91)78265-9}, abstractNote={Abstract Three different restriction-modification plasmids (pTRK12, pTRK30, pTRK317) were isolated from an industrial starter strain, Lactococcus lactis ssp. cremoris TDM1. A lactose-fermenting transconjugant, Lactococcus lactis ssp. lactis NCK40, was isolated from matings between L. lactis ssp. cremoris TDM1 and a plasmid-free recipient. The NCK40 transconjugant contained a 100-kb self-transmissible plasmid (pTRK11) encoding for restriction-modification and a 13.5-kb plasmid (pTRK10) encoding proteolytic activity. Following isolation of lactosenegative derivatives from NCK40, a 30.5-kb plasmid, pTRK12, was identified that encoded proteolytic and restriction-modification of the identical specificity as pTRK11. Restriction analyses and hybridization experiments indicated that pTRK12 contained sequences from pTRK11 and all of pTRK10. Cotransformation of tatal plasmid DNA from L. lactis ssp. cremoris TDM1 with vector pVS2 identified two other restriction-modification plasmids, pTRK30 (28.0kb) and pTRK317 (15.5kb). Efficiencies of plaquing for phage c2 on restriction-modification transconjugants and transformants was 10 –2 to 10 –4 . The specificity of restriction-modification activities conferred by each of the three plasmids was different. When the abortive infection plasmid pTR2030 was combined with pTRK30, both phage inhibition phenotypes were expressed. However, when pTR2030 was combined with pTRK12, the abortive infection phenotype was not fully expressed. Significant cell death occurred when abortive infection cells containing only pTR2030 were infected with phage. Combining the restriction-modification system of p-0 with pTR2030 significantly improved cell survival following phage infection. Operation of restriction-modification systems in conjunction with the abortive defense mechanism maximized cell survival. The data suggest that cell death is minimized when the lytic cycle is halted by restriction before abortive infection responses induce phage abortion and kill the cell.}, number={4}, journal={Journal of Dairy Science}, author={Sing, W. D. and Klaenhammer, T. R.}, year={1991}, pages={1133} }
 @article{sing_klaenhammer_1990, title={Characteristics of phage abortion conferred in lactococci by the conjugal plasmid pTR2030}, volume={136}, DOI={10.1099/00221287-136-9-1807}, abstractNote={Summary: The effect of pTR2030 on phage DNA injection, transfection, release of progeny phage, and cell death was evaluated for a number of lactococcal phages. Infection by prolate phage c2 and small isometric phage p2 of derivatives of Lactococcus lactis LM2301 with or without pTR2030, and infection by small isometric phage o31 of derivatives of L. lactis NCK202 with or without pTR2030 was studied. Phage DNA injection was not affected by pTR2030 when examined using blender-resistant-complex assays with 32P-labelled DNA or by observation of phage labelled with the fluorescent dye 4′,6-diamidino-2-phenylindole (DAPI). Successful transfection of hosts bearing pTR2030 indicated that the plasmid did not retard passage of naked phage DNA across the membrane. Infective-centre assays were used to determine whether progeny were released from phage-infected pTR2030 hosts that do not support plaque formation by small isometric phages. In all cases, pTR2030 reduced the number of infected hosts which generated viable phage. When progeny were released, the phage burst size was reduced. The data confirmed that pTR2030 interferes with development of prolate and small isometric phages in a similar manner via a classical abortive infection mechanism.}, number={9}, journal={Journal of General Microbiology}, author={Sing, W. D. and Klaenhammer, T. R.}, year={1990}, pages={1807} }
 @misc{sing_klaenhammer_1990, title={PLASMID-INDUCED ABORTIVE INFECTION IN LACTOCOCCI - A REVIEW}, volume={73}, ISSN={["0022-0302"]}, DOI={10.3168/jds.S0022-0302(90)78904-7}, abstractNote={Abstract The longevity of mesophilic lactococci in dairy fermentations depends to a large extent on whether or not the strains carry effective phage-resistance mechanisms. Among the different systems that exist in lactococci, abortive infection is highly significant because it is the cell's strongest defense against the phages that most often disrupt cheese making. Phage-resistant strains that carry plasmids encoding abortive defenses have already been constructed using genetic strategies. These strains have been used successfully in commercial cheese making since 1986. Still, our knowledge of the molecular mechanisms underlying abortive infection and the means through which it retards phage development is limited. This review addresses abortive infection in lactococci relative to similar phenomena in other bacteria. Further understanding of the abortive infection process should accelerate genetic efforts to strengthen this phage defense as well as facilitate efforts to combine it with other mechanisms in the construction of specialized strains that are insensitive to attack by phage.}, number={9}, journal={JOURNAL OF DAIRY SCIENCE}, author={SING, WD and KLAENHAMMER, TR}, year={1990}, month={Sep}, pages={2239–2251} }