Two- and three-factor crosses showed that the T4 rIII gene is located between genes 31 and 30 rather than between genes 31 and 63

Lielausis, Ilga

Revel, Helen R.

PubMed

Caltech Authors - Main

0022-538X/78/0025-0439$02.00/O
JOURNAL OF VIROLOGY, Jan. 1978, p. 439441
Copyright i) 1978 American Society for Microbiology
Vol. 25, No. 1
Printed in U.S.A.
Revised Location of the rIII Gene on the Genetic Map of
Bacteriophage T4
HELEN R. REVEL* AND ILGA LIELAUSIS
Division ofBiology, California Institute of Technology, Pasadena, California 91125
Received for publication 22 August 1977
Two- and three-factor crosses showed that the T4 rIII gene is located between
genes 31 and 30 rather than between genes 31 and 63.
The current genetic map of bacteriophage T4
shows the arrangement of genes in the gene 31
region as: 63-[pseT-unf-cd]-riI-31-30 (14). A
more recent paper presents evidence that the
unf and alc markers are in the same gene and
that akc also maps in the 63-31 interval (10).
However, discrepancies in the ordering of amber
mutations within gene 31 with respect to genes
rIl and 30 as outside markers suggest that this
order may be incorrect. Georgopoulos et al. (7)
reported the order rIHI-amN54 (gene 31)-
amNG71 (gene 31), whereas Simon et al. (9)
have found that apparent arrangement of these
gene 31 mutants to be amNG71 (gene 31)-
amN54 (gene 31)-gene 30. We have confirmed
these observations by independent crosses
shown in Table 1 (crosses 1-4). When amN54
carrying r67 (gene rII) as an unselected outside
marker was crossed with amNG71, the majority
of the am' recombinant progeny were r+. Con-
versely, when amNG71 carrying r67 was crossed
with amN54, the majority of the am' recombi-
nants had the r67 allele. When amN54 carrying
tsB20 (gene 30) as an outside marker was crossed
with amNG71, the majority of the am+ recom-
binants were ts+, whereas the reverse was true
when amNG71 carrying tsB20 was crossed with
amN54.
These results are paradoxical in view of the
previously published gene order rHI-31-30 (6, 8),
but can be resolved by assuming that the rIH
gene is located to the right of gene 31. Data
from crosses 1 through 4 (Table 1) suggest that
genes rnI and 30 are on the same side of gene
31. The results of cross 5 support this conclusion.
The finding that the majority of am+ r+ recom-
binants were ts when amNG71 carrying tsB20
was crossed with r67 indicates that the rnI gene
is located between genes 31 and 30. Table 2
gives the results of two three-factor crosses be-
tween markers in genes 31, rnI, and 30, where
all progeny genotypes were identified. The most
frequent classes represent the parents of the
crosses. Assuming that the least frequent class
identifies the progeny resulting from a double-
crossover event, these results indicate the gene
order to be 31-rIII-30. High negative interference
(2) was evident from the frequency of the dou-
ble-recombinant class, which was higher than
TABLE 1. Gene 31 region of the T4 genetic map
analyzed by three-factor crossesa
Cross % Outside markerRecombination mutant/total
I. NG716+r7 1.05 .14
NG71 + r672. + .85 .88
3 NG71 + + 1.14 .31/N54 tsB20
4 NG71 + tsB20 1.16 .66
+ N54 +
5 NG7 + tsB2O 2.15 .68
+ /r67 +
6. + NG71 + 1.05 .66
pseT-I + /54
7. + N54 r67 2.0 .63
pseT-1 + +
8. + N54 + 12.63 .83
pseT-1 + tsB20
' Crosses were in Escherichia coli strain B40su1+
at 300C under standard conditions (12, 13). Total
progeny were determined by plating on B40sul+ at300C. am+ recombinants were determined on S/6/5
sui at 300C (crosses 1-6), am+ r recombinants were
determined by plaque morphology on S/6/5 su- at
300C (cross 7), and am' ts+ recombinants were deter-
mined on S/6/5 suf at 420C (cross 8). Heavy lines in
the figure indicate the designated recombinant with
an arrow directed towards the unselected outside
marker. Percent recombination = (designated recom-
binant x 200)/total progeny. The status of the outside
marker in the recombinant class selected was deter-
mined by differentiating r from r+ plaques (crosses 1
and 2), by plating on S/6/5 at 420C (crosses 3-5), or
by stabbing the selected recombinants to lawns of
CTr5x sU- (nonpermissive for pseTl growth) at 300C
(crosses 6-8). Mutants used: pseTl (gene pseT),
amNG71 (gene 31), amN54 (gene 31), r67 (gene nII),
and tsB20 (gene 30). For simplicity, the am prefixes
have been omitted.
439
440 NOTES
TABLE 2. Location of rIII on the T4 genetic mapa
Cross Cross 2
Progeny genotypes frequency frequency
gene 31 r.mI 30 Number % Number %
+ r67 + 568 922 56 84
NG71 + H39X 656 47
NG71 + + 51 5695 } 89.9
+ r67 H39X 28 437
NG71 r67 + 6 1.28 }
+ + H39X 1 4
.53 1. 15
NG71 r67 H39X 2 6
Total plaques identified 1327 1220
1.80 6.48
cross 7.23
1.64 8.93
cross 2 9.59
a Crosses were performed in Escherichia coli strain
B40sui+ at 300C under standard conditions (12, 13).
Total progeny was assayed on B40sul'. Progeny gen-
otypes were analyzed by picking plaques from B40sul'
into 0.1 ml of H broth in wells in a plastic tray and
spotting with a brass replicator into the following
lawns of bacteria: (i) CR63sui+ Str; (ii) S/6/5 su-
Strr; (iii) S/6/5 su- Strr + 2 x 107 amH39X (gene 30);
(iv) S/6/5 su- Strr + 2 x 107 amNG71 (gene 31).
Plates 2 to 4 contained 500 ,jg of streptomycin per ml
of top agar to eliminate phage growth due to transfer
of B40su,+ StrW cells to these test plates. The test
plates were incubated at 30°C overnight and scored
for phage growth. The parents of each cross are rep-
resented by the most frequent progeny genotype. The
recombinant class with the fewest progeny presumably
represents progeny arising from a double-crossover
event, and it is designated by underlining. Mutants
used: amNG71 (gene 31) r67 (HII), amH39X (gene 30).
For simplicity, the am prefixes have been omitted.
expected from a consideration of the frequency
of single-crossover events. Although this effect
distorts the data in the three-factor crosses, as
also observed by Simon et al. (9), the consistency
of all two-factor crosses (su d in Fig. 1)
and three-factor crosses presented strongly sup-
ports the relocation of rIII to a position between
genes 31 and 30. Furthermore, when an allele
ofpseT, a gene located to the left of the contro-
versial gene 31 region, was the outside marker
in simnilar three-factor crosses (Table 1, crosses
6-8), its segregation indicated that the order of
genes in the 31 region is pseT-31 (amNG71-
amN54)-rn-30.
Independent evidence that the gene 31 alleles
are oriented in the order amNG71-amN54-gene
30 comes from recent investigations of Castillo
et al. (1) on the characterization of the gene 31
product (gp3l) by sodium dodecyl sulfate-urea-
acrylamide gradient gel electrophoresis. The
protein is made early and thus presumably is
transcribed counterclockwise from the light
strand. The fact that a relatively large gp3l
fragment is found in amN54 infections but not
in amNG71 infections indicates that the
amNG71 locus is near the promoter of gene 31,
furthest from gene 30. This arrangement is con-
sistent with the order amNG71-amN54-r67 only
if rII is also on the promoter-distal side of gene
31.
How can the relocation of the rIII gene, sug-
gested by the present data, be reconciled with
previous assignments ofthe rIl gene to a position
just clockwise from gene 31 (6, 8)? A survey of
the literature suggests that the basis for the
previous placement was somewhat arbitrary. In
the original map ofamber mutants, the rIH gene
31 rM
f-- /
pseT
C,Q
(6) (3)
1.091_50_
(8)
8.34
30
/ '
(3)
7.82
(3)
3.47
(4) (I)
1.95 8.65
(3)
.4
9.53
(l)
12.20
(2)8.95
(3)12.02
(1)16.8
FIG. 1. Gene 31 region of the T4 genetic map an-
alyzed by two-factor crosses. Crosses wereperformed
in Escherichia coli strain B40sul+ at 300C under
standard conditions (12, 13). Total progeny was de-
terinined on B40su1+ at 300C. In crosses between am
mutants, the am+ recombinants were determined by
plating on S/6/5 su- at 30°C. In crosses between an
am mutant and a ts mutant, am+ ts+ recombinants
were selected on S/6/5 su- at 42°C. In crosses between
an am mutant and r67, am+ re recombinants were
selected on S/6/5 su- at 30°C. In crosses between a
ts mutant and r67, ts+ r+ recombinants were selected
on S/6/5 su- at 42°C. In crosses between pseTi and
an am mutant, am+pse7' recombinants were selected
on CTr5x su-, which is nonpermissive for pseT1, at
300C (3). In crosses between pseTi and a ts mutant,
ts+pseTf recombinants were determined both byplat-
ing on CTr5x at 420C and by selecting ts+ progeny
on S/6/5 su- at 42°C and analyzing their ability to
grow on CTr5x at 30°C. The orientation of amH39x
and tsB20 in gene 30 was established by a three-
factor cross relative to r67 as an outside marker
(data not shown). Figures in parentheses represent
the number of times the cross was done. Mutants
used: pseTi (gene pseT), amNG71 (gene 31), amN54
(gene 31), r67 (gene rIII), amH39x (gene 30), and
tsB20 (gene 30). For simplicity, the am prefixes have
been omitted.
J. VIROL.
NOTES 441
was placed in this position on the basis of "data
to be published" (6). The recombination values,
when published, showed that gene 31 is closer
to rIl than is gene 30, but there was no evidence
indicating the order of these genes (4, 5). In
fact, these authors as well as Stahl et al. (11),
who published a composite map including more
unpublished data, were noncommittal as to the
location of rIII in relation to genes 31 and 30.
They presented two concentric maps, one of rIII
and various standard morphology and host
range mutants and the other of amber mutants
in essential genes, including genes 30 and 31. In
Mosig's elegant experiments to physically map
the T4 genome by marker rescue from light T4
particles, the various rapid lysis genes rI, rnI, and
rIII were used as reference points to map dis-
tances to am mutations and thus provided no
information on the absolute position of r67 (8).
We conclude that there is no essential conflict
with previous data, only with their representa-
tion, and that the present work establishes the
position of the rIII gene relative to adjacent
genes.
This work was supported by Public Health Service grant
AI-09238, from the National Institute ofAllergy and Infectious
Diseases, to W. B. Wood.
ITERATURE CITED
1. Castillo, C. J., C. Hsiao, P. Coon, and L W. Black.
1977. Identification and properties of bacteriophage T4
capsid forming gene products. J. Mol. Biol. 110:585-601.
2. Chase, M, and A. EL Doermann. 1958. High negative
interference over short intervals of the genetic structure
of bacteriophage T4. Genetics 43:332-353.
3. Depew, R. E., and N. R. Cozzarelli. 1974. Genetics and
physiology of bacteriophage T4 3'-phosphatase: evi-
dence for involvement of the enzyme in T4 DNA me-
tabolism. J. Virol. 13:888-897.
4. Edgar, R. S., G. H. Denhardt, and R. H. Epstein.
1964. A comparative genetic study of conditional lethal
mutations of bacteriophage T4D. Genetics 49:635-648.
5. Edgar, R. S., and . Lielausis. 1964. Temperature-sen-
sitive mutants of bacteriophage T4D: their isolation
and genetic characterization. Genetics 49:649-662.
6. Epstein, R. H., A. Bolle, C. M. Steinberg, E. Kellen-
berger, E. Boy de la Tour, R. Chevalley, RI S.
Edgar, M. Susman, G. H. Denhardt, and A. Uelau-
sis. 1963. Physiological studies of conditional lethal
mutations in bacteriophage T4D. Cold Spring Harbor
Symp. Quant. Biol. 28:375-394.
7. Georgopoulos, C. P., RI W. Hendrix, A. D. Kaiser,
and W. B. Wood. 1972. Role of the host cell in bacte-
riophage morphogenesis: effects of a bacterial mutation
on T4 head assembly. Nature (London) New Biol.
239:38-41.
8. Mosig, G. 1968. A map of distances along the DNA
molecules of phage T4. Genetics 59:137-151.
9. Simon, L. D., D. Snover, and A. H. Doermann. 1974.
Bacterial mutation affecting T4 phage DNA synthesis
and tail production. Nature (London) 252:451-455.
10. Sirotkin, K., J. Wei, and L Snyder. 1977. T4 bacterio-
phage-coded RNA polymerase subunit blocks host tran-
scription and unfolds the host chromosome. Nature
(London) 265:28-32.
11. Stahl, F. W., RI S. Edgar, and J. Steinberg. 1964. The
linkage map of bacteriophage T4. Genetics 50:539-552.
12. Steinberg, C. M., and R. S. Edgar. 1962. A critical test
of a current theory of genetic recombination in bacte-
riophage. Genetics 47:187-208.
13. Wilson, J. IL, and S. Kelis. 1972. Bacteriophage T4
transfer RNA. I. Isolation and characterization of two
phage-coded nonsense suppressors. J. Mol. Biol.
69:39-56.
14. Wood, W. B., and H. R. Revel. 1976. The genome of
bacteriophage T4. Bacteriol. Rev. 40:847-868.
VoL 25, 1978


Revised Location of the rIII Gene on the Genetic Map of Bacteriophage T4

0022-538X/78/0025-0439$02.00/O
JOURNAL OF VIROLOGY, Jan. 1978, p. 439441
Copyright i) 1978 American Society for Microbiology
Vol. 25, No. 1
Printed in U.S.A.
Revised Location of the rIII Gene on the Genetic Map of
Bacteriophage T4
HELEN R. REVEL* AND ILGA LIELAUSIS
Division ofBiology, California Institute of Technology, Pasadena, California 91125
Received for publication 22 August 1977
Two- and three-factor crosses showed that the T4 rIII gene is located between
genes 31 and 30 rather than between genes 31 and 63.
The current genetic map of bacteriophage T4
shows the arrangement of genes in the gene 31
region as: 63-[pseT-unf-cd]-riI-31-30 (14). A
more recent paper presents evidence that the
unf and alc markers are in the same gene and
that akc also maps in the 63-31 interval (10).
However, discrepancies in the ordering of amber
mutations within gene 31 with respect to genes
rIl and 30 as outside markers suggest that this
order may be incorrect. Georgopoulos et al. (7)
reported the order rIHI-amN54 (gene 31)-
amNG71 (gene 31), whereas Simon et al. (9)
have found that apparent arrangement of these
gene 31 mutants to be amNG71 (gene 31)-
amN54 (gene 31)-gene 30. We have confirmed
these observations by independent crosses
shown in Table 1 (crosses 1-4). When amN54
carrying r67 (gene rII) as an unselected outside
marker was crossed with amNG71, the majority
of the am' recombinant progeny were r+. Con-
versely, when amNG71 carrying r67 was crossed
with amN54, the majority of the am' recombi-
nants had the r67 allele. When amN54 carrying
tsB20 (gene 30) as an outside marker was crossed
with amNG71, the majority of the am+ recom-
binants were ts+, whereas the reverse was true
when amNG71 carrying tsB20 was crossed with
amN54.
These results are paradoxical in view of the
previously published gene order rHI-31-30 (6, 8),
but can be resolved by assuming that the rIH
gene is located to the right of gene 31. Data
from crosses 1 through 4 (Table 1) suggest that
genes rnI and 30 are on the same side of gene
31. The results of cross 5 support this conclusion.
The finding that the majority of am+ r+ recom-
binants were ts when amNG71 carrying tsB20
was crossed with r67 indicates that the rnI gene
is located between genes 31 and 30. Table 2
gives the results of two three-factor crosses be-
tween markers in genes 31, rnI, and 30, where
all progeny genotypes were identified. The most
frequent classes represent the parents of the
crosses. Assuming that the least frequent class
identifies the progeny resulting from a double-
crossover event, these results indicate the gene
order to be 31-rIII-30. High negative interference
(2) was evident from the frequency of the dou-
ble-recombinant class, which was higher than
TABLE 1. Gene 31 region of the T4 genetic map
analyzed by three-factor crossesa
Cross % Outside markerRecombination mutant/total
I. NG716+r7 1.05 .14
NG71 + r67
2. + .85 .88
3 NG71
+ + 1.14 .31
/N54 tsB20
4 NG71 + tsB20 1.16 .66
+ N54 +
5
NG7 + tsB2O 2.15 .68
+ /r67 +
6. + NG71 + 1.05 .66
pseT-I + /54
7. + N54 r67 2.0 .63
pseT-1 + +
8. + N54 + 12.63 .83
pseT-1 + tsB20
' Crosses were in Escherichia coli strain B40su1+
at 300C under standard conditions (12, 13). Total
progeny were determined by plating on B40sul+ at
300C. am+ recombinants were determined on S/6/5
sui at 300C (crosses 1-6), am+ r recombinants were
determined by plaque morphology on S/6/5 su- at
300C (cross 7), and am' ts+ recombinants were deter-
mined on S/6/5 suf at 420C (cross 8). Heavy lines in
the figure indicate the designated recombinant with
an arrow directed towards the unselected outside
marker. Percent recombination = (designated recom-
binant x 200)/total progeny. The status of the outside
marker in the recombinant class selected was deter-
mined by differentiating r from r+ plaques (crosses 1
and 2), by plating on S/6/5 at 420C (crosses 3-5), or
by stabbing the selected recombinants to lawns of
CTr5x sU- (nonpermissive for pseTl growth) at 300C
(crosses 6-8). Mutants used: pseTl (gene pseT),
amNG71 (gene 31), amN54 (gene 31), r67 (gene nII),
and tsB20 (gene 30). For simplicity, the am prefixes
have been omitted.
439
440 NOTES
TABLE 2. Location of rIII on the T4 genetic mapa
Cross Cross 2
Progeny genotypes frequency frequency
gene 31 r.mI 30 Number % Number %
+ r67 + 568
922
56
84
NG71 + H39X 656 47
NG71 + + 51 5695 } 89.9
+ r67 H39X 28 437
NG71 r67 + 6 1.28 }
+ + H39X 1 4
.53 1. 15
NG71 r67 H39X 2 6
Total plaques identified 1327 1220
1.80 6.48
cross 7.23
1.64 8.93
cross 2 9.59
a Crosses were performed in Escherichia coli strain
B40sui+ at 300C under standard conditions (12, 13).
Total progeny was assayed on B40sul'. Progeny gen-
otypes were analyzed by picking plaques from B40sul'
into 0.1 ml of H broth in wells in a plastic tray and
spotting with a brass replicator into the following
lawns of bacteria: (i) CR63sui+ Str; (ii) S/6/5 su-
Strr; (iii) S/6/5 su- Strr + 2 x 107 amH39X (gene 30);
(iv) S/6/5 su- Strr + 2 x 107 amNG71 (gene 31).
Plates 2 to 4 contained 500 ,jg of streptomycin per ml
of top agar to eliminate phage growth due to transfer
of B40su,+ StrW cells to these test plates. The test
plates were incubated at 30°C overnight and scored
for phage growth. The parents of each cross are rep-
resented by the most frequent progeny genotype. The
recombinant class with the fewest progeny presumably
represents progeny arising from a double-crossover
event, and it is designated by underlining. Mutants
used: amNG71 (gene 31) r67 (HII), amH39X (gene 30).
For simplicity, the am prefixes have been omitted.
expected from a consideration of the frequency
of single-crossover events. Although this effect
distorts the data in the three-factor crosses, as
also observed by Simon et al. (9), the consistency
of all two-factor crosses (su d in Fig. 1)
and three-factor crosses presented strongly sup-
ports the relocation of rIII to a position between
genes 31 and 30. Furthermore, when an allele
ofpseT, a gene located to the left of the contro-
versial gene 31 region, was the outside marker
in simnilar three-factor crosses (Table 1, crosses
6-8), its segregation indicated that the order of
genes in the 31 region is pseT-31 (amNG71-
amN54)-rn-30.
Independent evidence that the gene 31 alleles
are oriented in the order amNG71-amN54-gene
30 comes from recent investigations of Castillo
et al. (1) on the characterization of the gene 31
product (gp3l) by sodium dodecyl sulfate-urea-
acrylamide gradient gel electrophoresis. The
protein is made early and thus presumably is
transcribed counterclockwise from the light
strand. The fact that a relatively large gp3l
fragment is found in amN54 infections but not
in amNG71 infections indicates that the
amNG71 locus is near the promoter of gene 31,
furthest from gene 30. This arrangement is con-
sistent with the order amNG71-amN54-r67 only
if rII is also on the promoter-distal side of gene
31.
How can the relocation of the rIII gene, sug-
gested by the present data, be reconciled with
previous assignments ofthe rIl gene to a position
just clockwise from gene 31 (6, 8)? A survey of
the literature suggests that the basis for the
previous placement was somewhat arbitrary. In
the original map ofamber mutants, the rIH gene
31 rM
f-- /
pseT
C,Q
(6) (3)
1.091_50_
(8)
8.34
30
/ '
(3)
7.82
(3)
3.47
(4) (I)
1.95 8.65
(3)
.4
9.53
(l)
12.20
(2)
8.95
(3)
12.02
(1)16.8
FIG. 1. Gene 31 region of the T4 genetic map an-
alyzed by two-factor crosses. Crosses wereperformed
in Escherichia coli strain B40sul+ at 300C under
standard conditions (12, 13). Total progeny was de-
terinined on B40su1+ at 300C. In crosses between am
mutants, the am+ recombinants were determined by
plating on S/6/5 su- at 30°C. In crosses between an
am mutant and a ts mutant, am+ ts+ recombinants
were selected on S/6/5 su- at 42°C. In crosses between
an am mutant and r67, am+ re recombinants were
selected on S/6/5 su- at 30°C. In crosses between a
ts mutant and r67, ts+ r+ recombinants were selected
on S/6/5 su- at 42°C. In crosses between pseTi and
an am mutant, am+pse7' recombinants were selected
on CTr5x su-, which is nonpermissive for pseT1, at
300C (3). In crosses between pseTi and a ts mutant,
ts+pseTf recombinants were determined both byplat-
ing on CTr5x at 420C and by selecting ts+ progeny
on S/6/5 su- at 42°C and analyzing their ability to
grow on CTr5x at 30°C. The orientation of amH39x
and tsB20 in gene 30 was established by a three-
factor cross relative to r67 as an outside marker
(data not shown). Figures in parentheses represent
the number of times the cross was done. Mutants
used: pseTi (gene pseT), amNG71 (gene 31), amN54
(gene 31), r67 (gene rIII), amH39x (gene 30), and
tsB20 (gene 30). For simplicity, the am prefixes have
been omitted.
J. VIROL.
NOTES 441
was placed in this position on the basis of "data
to be published" (6). The recombination values,
when published, showed that gene 31 is closer
to rIl than is gene 30, but there was no evidence
indicating the order of these genes (4, 5). In
fact, these authors as well as Stahl et al. (11),
who published a composite map including more
unpublished data, were noncommittal as to the
location of rIII in relation to genes 31 and 30.
They presented two concentric maps, one of rIII
and various standard morphology and host
range mutants and the other of amber mutants
in essential genes, including genes 30 and 31. In
Mosig's elegant experiments to physically map
the T4 genome by marker rescue from light T4
particles, the various rapid lysis genes rI, rnI, and
rIII were used as reference points to map dis-
tances to am mutations and thus provided no
information on the absolute position of r67 (8).
We conclude that there is no essential conflict
with previous data, only with their representa-
tion, and that the present work establishes the
position of the rIII gene relative to adjacent
genes.
This work was supported by Public Health Service grant
AI-09238, from the National Institute ofAllergy and Infectious
Diseases, to W. B. Wood.
ITERATURE CITED
1. Castillo, C. J., C. Hsiao, P. Coon, and L W. Black.
1977. Identification and properties of bacteriophage T4
capsid forming gene products. J. Mol. Biol. 110:585-601.
2. Chase, M, and A. EL Doermann. 1958. High negative
interference over short intervals of the genetic structure
of bacteriophage T4. Genetics 43:332-353.
3. Depew, R. E., and N. R. Cozzarelli. 1974. Genetics and
physiology of bacteriophage T4 3'-phosphatase: evi-
dence for involvement of the enzyme in T4 DNA me-
tabolism. J. Virol. 13:888-897.
4. Edgar, R. S., G. H. Denhardt, and R. H. Epstein.
1964. A comparative genetic study of conditional lethal
mutations of bacteriophage T4D. Genetics 49:635-648.
5. Edgar, R. S., and . Lielausis. 1964. Temperature-sen-
sitive mutants of bacteriophage T4D: their isolation
and genetic characterization. Genetics 49:649-662.
6. Epstein, R. H., A. Bolle, C. M. Steinberg, E. Kellen-
berger, E. Boy de la Tour, R. Chevalley, RI S.
Edgar, M. Susman, G. H. Denhardt, and A. Uelau-
sis. 1963. Physiological studies of conditional lethal
mutations in bacteriophage T4D. Cold Spring Harbor
Symp. Quant. Biol. 28:375-394.
7. Georgopoulos, C. P., RI W. Hendrix, A. D. Kaiser,
and W. B. Wood. 1972. Role of the host cell in bacte-
riophage morphogenesis: effects of a bacterial mutation
on T4 head assembly. Nature (London) New Biol.
239:38-41.
8. Mosig, G. 1968. A map of distances along the DNA
molecules of phage T4. Genetics 59:137-151.
9. Simon, L. D., D. Snover, and A. H. Doermann. 1974.
Bacterial mutation affecting T4 phage DNA synthesis
and tail production. Nature (London) 252:451-455.
10. Sirotkin, K., J. Wei, and L Snyder. 1977. T4 bacterio-
phage-coded RNA polymerase subunit blocks host tran-
scription and unfolds the host chromosome. Nature
(London) 265:28-32.
11. Stahl, F. W., RI S. Edgar, and J. Steinberg. 1964. The
linkage map of bacteriophage T4. Genetics 50:539-552.
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http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=353945

Revised Location of the rIII Gene on the Genetic Map of Bacteriophage T4

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