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. 2013 Feb 6;5(2):619–653. doi: 10.3390/v5020619

Figure 2.

Figure 2

Plaque type / formation by λcI72 on 594[pcIpR-P-timm] and 594 host cells. The ability of λcI72 to form plaques on 594[pcIpR-P-timm] host cells at 35-42 ˚C is attributed to loss, or considerable reduction, in plasmid copy number per cell. The immλ interference phenotype (compare EOP, Table 5, 25 and 30 ˚C vs. 35 ˚C) is dependent upon CI[Ts] repressor expressed from the plasmid. The cellular loss of immλ interference correlates with plasmid loss and the observed increase in plaque size between 35 and 42 ˚C; whereas, the plaque size was essentially constant between 30 to 42 ˚C when λcI72 was plated on 594 cells without the plasmid. The photos of the individual plaques shown in the top row were taken through the lens of a stereo microscope, from agar overlay plates (middle row) incubated at the indicated temperatures.