Table 2.

Influence of various virB gene deletions on the capacity of A. tumefaciens strain A348 to function as recipient in virB-mediated transfer of the RSF1010 derivative pJB31

Recipient strain†	Gene disrupted	Absolute number of output*
		Donor, 108	Recipient, 108	Tcs	Tcs/output recipient ± SD‡	% of A348 value
PC1001	virB1	4.0	1.8	375	(2.12 ± 0.24) 10−6	3.58
PC1002	virB2	3.9	2.7	425	(1.52 ± 0.39) 10−6	2.48
PC1003	virB3	5.3	1.3	5	(3.71 ± 2.84) 10−8	0.06
PC1004	virB4	6.0	1.4	24	(1.71 ± 0.73) 10−7	0.28
PC1005	virB5	5.0	1.2	4,083	(3.54 ± 0.49) 10−5	57.65
PC1006	virB6	5.0	1.6	1,080	(6.69 ± 169) 10−6	10.90
PC1007	virB7	5.1	1.6	0	0	0
PC1008	virB8	5.3	1.4	20	(1.41 ± 0.91) 10−7	0.23
PC1009	virB9	5.7	1.2	<2	(1.01 ± 0.95) 10−8	0.02
PC1010	virB10	5.7	1.1	<1	(4.1 ± 7.1) 10−9	0.01
PC1011	virB11	5.5	1.3	3,023	(2.39 ± 0.77) 10−5	38.02
A348		4.8	1.2	6,910	(6.14 ± 2.08) 10−5	100.00
At12506	virD4	3.1	0.2	697	(3.48 ± 1.93) 10−5	110.00
A348		2.9	0.3	950	(3.16 ± 1.50) 10−5	100.00

Tcs, transconjugants. 

^*Output donor, recipient, and transconjugants were recovered after 3 days growth on induction media containing 250 μM AS at 25°C. 

^†Recipients contained the gentamicin resistant vector pJB61 as counterselectable marker. 

^‡Data represent the means of triplicates (±SD) from a single experiment. A total of four independent experiments showing similar results were performed. Although absolute numbers varied between individual experiments, the relative frequencies between the mutant strains and the wild type showed the same tendencies in every experiment. Input recipient and donor (A. tumefaciens pJB31) were added in a ratio of 1:5 (≈5 × 10⁵ and 2.5 × 10⁶, respectively).