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Expanded versions of the 16S and 23S Ribosomal RNA Mutation Databases (16SMDBexp and 23SMDBexp)
Description
Availability
Acknowledgements
References
Expanded versions of the 16S and 23S Ribosomal RNA Mutation Databases (16SMDBexp and 23SMDBexp)
ABSTRACT
DESCRIPTION
The expanded version of the 16S Ribosomal RNA Mutation Database (16SMDBexp), currently at Franklin and Marshall College, consists of an annotated list of 295 alterations distributed over 157 positions in 16S ribosomal RNA from Escherichia coli and in 16S-like rRNA from other organisms. Table 1 illustrates the format for presentation of the data and includes 62 new alterations added to the 16SMDBexp database since the previous announcement (32). Mutated positions are arranged in order beginning with the 5[prime] end of 16S rRNA and ending with the 3[prime] end. Phenotypes associated with each alteration are briefly described and designated as to whether the phenotypes were detected in vivo or in vitro. Appropriate references are provided for each alteration. A review of the data and genetic methods employed in the detection of 16S rRNA mutant phenotypes has been published elsewhere (29).
The 23S Ribosomal RNA Mutation Database (23SMDB), currently at Franklin and Marshall College, consists of an annotated list of 271 alterations distributed over 143 positions in 23S ribosomal RNA from E.coli and in 23S-like rRNA from other organisms. Table 2 includes 36 new alterations added to the 23SMDBexp database since the previous announcement (32). A review of the data and genetic methods employed in the detection of 23S rRNA mutant phenotypes will be published elsewhere (33).
There are currently six text files of ribosomal RNA mutations available: (i) 16SMDBexp and (ii) 23SMDBexp, both described above, (iii) 16SMDB and (iv) 23SMDB, files containing only the data from E.coli, and (v) 16S-likeMDB and (vi) 23S-likeMDB, files containing only the data from organisms other than E.coli (28,30-32). Ultimately the goal of this work is to provide a database that can be queried for specific kinds of information. Our plan is to organize the data, so that one can access, for example: (i) all the data from one specific organism, (ii) all the data for one specific nucleotide position, or (iii) all the data for one specific phenotype.
Individuals with access to the Internet telecommunications network may obtain text files of the ribosomal RNA mutation databases by anonymous file transfer protocol. The ftp site is: Acad.FandM.edu; the directory is: /NAR . The databases are also available on the World Wide Web at the following URL: http://www.fandm.edu/Departments/Biology/Databases/RNA.html
Email inquiries should be addressed as follows: Table
Table
AVAILABILITY
Position
Alteration
Phenotype
Ref(s)
13
U->9A
Impaired growth
17
13
U13A/A914U
Impaired growth
17
18
C18A
Inhibits translation. Mutant 30S particles are impaired in forming 70S tight couples
17
23
C23U
Dominant cold-sensitive phenotype and a defective maturation of the 16S rRNA 5[prime] end
18
517
G->A
Increased sensitivity to streptomycin in S.cerevisiae
3
517
U->A
Polysome formation severely inhibited while tight couple formation was not disturbed
17
526
C->U
Extra PvuII site in region coding for 530-loop in N.plumbaginifolia
37
527
G->U
Lethal, found in all ribosome fractions
21
527
G527U/A1492C
Lethal, found in polysome
21
527
G527U/A1492G
Like G527U
21
527
G527U/A1492U
Lethal, found in polysome
21
527
G527U/A1493C
Like G527U
21
527
G527U/A1493G
Lethal, found in polysome
21
527
G527U/A1493U
Like G527U
21
529
G->U
Stimulates initiation from a non-AUG initiation codon
14
530
G530A/A531G
No increase in initiation from non-AUG codons
14
597
G597A/C643U
Slightly decreased affinity for S8 binding
13
597
G597C/U641A/ C643G
No effect on S8 binding
13
597
G597U/C643G
No binding of S8
13
597
G597U/U641A/C643G
No binding of S8
13
597
G597U/U641C/C643G
No effect on S8 binding
13
653
nU
No effect on B.stearothermophilus S15 binding
1
665
A665C/A668C
No effect on B.stearothermophilus S15 binding
1
740
U->C
Slight reduction in S15 binding
1
748
nA
30-fold reduction in S15 affinity
1
749
C->A
Little effect on S15 binding
1
752
G->C
Severely reduced affinity for S15
1
787
A->C
Produces ribosomes that are highly functional
8
787
A->G
Strongly inhibits ribosome function
8
787
A->U
Moderately inhibits ribosome function
8
787
A787C/C795A
Moderately inhibits ribosome function
8
787
A787C/C795G
Strongly inhibits ribosome function
8
787
A787C/C795U
Produces ribosomes that are highly functional
8
787
A787G/C795A
Moderately inhibits ribosome function
8
787
A787G/C795G
Moderately inhibits ribosome function
8
787
A787G/C795U
Produces ribosomes that are highly functional
8
787
A787U/C795A
Strongly inhibits ribosome function
8
787
A787U/C795G
Strongly inhibits ribosome function
8
787
A787U/C795U
Produces ribosomes that are highly functional
8
795
C->A
Produces ribosomes that are highly functional
8
795
C->G
Moderately inhibits ribosome function
8
795
C->U
Produces ribosomes that are highly functional
8
885
G->C
Interfere with 912·885 base pair and favored 912·888 conformation
10
885
G->A
Novel mutation for streptomycin resistance. Creates a StyI recognition sequence. Affects binding of S12. In N.plumbaginifolia
37
885
G->U
Favored the 912·885 conformation. Increases rates of readthrough errors and in-frame stop codons
10
888
G->A
Antisuppressor phenotype in Yeast. Increased base pairing in the 912·888 conformation
10
910
C->G
Favored the 912·888 conformation, but without cold-sensitivity. Lowers stop codon read-through rates, and elevated rate of frame-shifting.
10
910
C910G/G887C
Favored the 912·885 conformation. Increases rates of readthrough errors and in-frame stop codons
10
911
U->C
Favored the 912·885 conformation. Increases rates of readthrough errors and in-frame stop codons
10
912
C->G
Favored the 912·888 conformation, but without cold-sensitivity. Lowers stop codon read-through rates, and elevated rate of frame-shifting.
10
912
C->U
High-level streptomycin resistance in N.plumbaginifolia
37
912
C912G/G885C
Favored the 912·885 conformation. Increases rates of readthrough errors and in-frame stop codons
10
Position
Alteration
Phenotype
Ref(s)
912
C912G/G885C
Favored the 912·885 conformation. Increases rates of readthrough errors and in-frame stop codons
10
912
C912G/G885U
Allowed base pairing at 912·885 but interfered with 912·888 base pairing
10
912
C912G/G888C
Favored the 912·888 conformation and cold sensitivity, but does not increase reactivity to kethoxal
10
912
C912G/G888U
Favored 912·888 conformation but cold-sensitive
10
912
U->C
Decreases resistance to streptomycin and increases resistance to paromomycin and inhibits nonsense suppression induced by paromomycin in S.cerevisiae
3
913
A->G
Moderate effect of streptomycin binding in N.plumbaginifolia
37
914
A->U
Impaired growth
17
915
A->G
Increased streptomycin binding in N.plumbaginifolia
37
1054
C->A
Lethal above 37°C or high expression. UGA suppression
15
1054
C->G
Slight defect in subunit association. Suppresses all three termination codons
15
1054
C->U
Temperature sensitive lethality; slow growth rate at 37°C and when highly expressed. Defective ability to enter polysome
15
1054
nC
Lethal at 31°C, No suppression of trpA nonsense mutation. Affects 30S subunit assembly and subunit association
15
1065
U1065C/A1191G
Inhibits translation, increased level of acetylation, and does not allow S5 to bind. Causes an accumulation of free 30S subunits
18
1192
C->G
Gain resistance to spectinomycin and macrolides in Mycobacterium smegmatis
20
1192
C->U
Spectinomycin resistance, but no effect on stop codon, readthrough, frameshifting, or initiation events
14
1199
U1199C/C1200U
Stimulates initiation from a non-AUG initiation codon
14
1199
U1199G/C1200G
Stimulates initiation from a non-AUG initiation codon
14
1341
U->C
No effect on growth rate
4
1341
U1341C/C1192U
No effect on growth rate
4
1351
A1351C/C1192U
Counteracts mutation C1192U and restores spectinomycin binding. No cell growth
4
1351
U->C
No effect on growth rate
4
1357
A->C
No effect on growth rate
4
1357
A1357C/C1192U
Severely decreased growth rate due to defect in elongation
4
1386
G->A
Spectinomycin resistance in N.tabacum
25
1395
C1395U/G1505U
Viable cells, suppresses lethality. Stimulates initiation from a non-AUG initiation codon. Increased growth rate over C1395U alone
14
1400
nC1400/G1505U
Viable cells, suppresses lethality. Stimulates initiation from a non-AUG initiation codon. Increased growth rate over nC1400 alone
14
1405
G->C
Significantly reduced interaction with Paromomycin at positions 1491 and 1494
12
1405
G1405C/C1496G
No affect on Paromomycin binding
12
1406
U->A or C
No affect on Paromomycin binding
12
1406
U1406G/U1495G
No effect on Paromomycin binding
12
1407
C->G
Severely impaired Paromomycin binding
12
1407
C1407G/G1494C
Severely impaired Paromomycin binding
12
1407
C1407U/G1494G
Severely impaired Paromomycin binding
12
1407
C1407U/G1494A
Severely impaired Paromomycin binding
12
1407
C1407U/G1505U
Viable cells, suppresses lethality. Stimulates initiation from a non-AUG initiation codon. Increased growth rate over C1407U alone
14
1408
A->C
Moderate reduction of Paromomycin binding
12
1408
A->G
Gain resistance to gentamicin, amikacin, or tobramycin in Mycobacterium smegmatis
20
1408
A->G
High level neamine and kanamycin resistance in C.reinhardtii
6
1408
A->G
Weak reduction of Paromomycin binding
12
1408
A->U
Large reduction of Paromomycin binding
12
1409
C->U
Low level neamine and kanamycin resistance in C.reinhardtii
6
1409
C1409A/G1491U
Slightly reduced interaction with Paromomycin
12
1409
C1409G/G1491C
Slightly reduced interaction with Paromomycin
12
1491
G->U
Weakened interaction with Paromomycin
12
1492
A1492C/A1493C
No effect on Paromomycin binding
12
1494
G->C
Severely impaired Paromomycin binding
12
1495
U->A or C
Greatly reduced affinity for Paromomycin binding
12
1495
U->G
No effect on Paromomycin binding
12
1495
U1495G/U1406G
No effect on Paromomycin binding
12
1496
C->G
Significant reduction of paromomycin binding at positions 1405 and 1491. Slight reduction of Paromomycin binding at position 1494
12
1505
G1505U/G791A
Slower growth rate than G791A alone
14
Position
Alteration
Phenotype
Ref(s)
1067
A1067U
Normal growth
22,23
1093
G->U
trpA UGA suppressor; temperature sensitive
36
G->C
trpA UGA suppressor; temperature sensitive
36
G->A
trpA UGA suppressor; temperature sensitive
36
G1093A/A1098G
trpA UGA suppressor; temperature sensitive
36
1098
A->U
Normal growth phenotpye
36
A->G
Normal growth phenotpye
36
A->C
trpA UGA suppressor; temperature sensitive
36
A1098G/G1093A
trpA UGA suppressor; temperature sensitive
36
2057
G->A
Eryr in Chlamydomonas chloroplasts
6
2058
A->G
Eryr, Lincomycin and clindamycin resistance in Chlamydomonas chloroplasts
6
A->G
Lincomycin resistance in Solanum nigrum chloroplasts
7
A->G
Clarithromycin resistance in Helicobacter pylori
34
2059
A->G
Clarithromycin resistance in H.pylori
34
2061
G->A
Chloramphenicol resistance in rat mitochondria
35
2062
A->C
Chloramphenicol resistance in Halobacterium halobium
11
2249
U2249C
Normal growth
22,23
2250
G2250A
Normal growth
22,23
G2250A/C2254U
Normal growth
22,23
2251
G->A
Dominant lethal; Abolished both binding of tRNA and peptidyl transferase activity
5
G->U
Dominant lethal; Abolished both binding of tRNA and peptidyl transferase activity
5
2252
G->A, C or U
Less than 5% of control level peptidyl transferase activity
19
2253
G2253A
19% of control level peptidyl transferase activity
19
G2253C
42% control level peptidyl transferase activity
19
G2253U
Less than 5% control level peptidyl transferase activity
19
2254
C2254U
Normal growth
22,23
2438
U->C
Amicetin resistance in H.halobium
9
U->A
Amicetin resistance and reduced growth rate in H.halobium
9
U->G
Unstable in presence or absence of amicetin in H.halobium
9
2452
C->A
Chloramphenicol resistance in human mitochondria
2
C->U
Anisomycin resistance in Tetrahymena thermophila
26
C->U
Chloramphenicol resistance in H.halobium
C->U
Low level sparsomycin resistance in H.halobium
27
2499
C->U
Sparsomycin resistance in H.halobium
27
2505
G->A
14% activity of 70S ribosomes
19
G->C
Excluded from 70S ribosomes; 17% activity of 70S ribosomes
19
G->U
<5% activity of 70S ribosomes
19
2506
U->A
Dominant lethal; 5% activity of 70S ribosomes
19
U->C
20% activity of 70S ribosomes
19
U->G
<5% activity of 70S ribosomes
19
2507
C2507U
Dominant lethal
22,23
C2507U/G2581A
Dominant lethal; Inhibition of puromycin in reaction
22,23
[Delta]507/G2581A
Dominant lethal; Inhibition of puromycin in reaction
22,23
2508
G2508U
Control level peptidyl transferase activity
18,19
2580
U2580A
Deleterious; <5% activity of 70S ribosomes
19
U2580C
Dominant lethal; 12% activity of 70S ribosomes
19
U2580G
Deleterious; 6% activity of 70S ribosomes
19
Table 2. continued
Position
Alteration
Phenotype
Ref(s)
U2580C
Reduced growth
22,23
2581
G2581A
Deleterious; 22% activity of 70S ribosomes
22,23
G2581A
Dominant lethal inhibition of puromycin in reaction
22,23
G2581C
Deleterious; 13% activity of 70S ribosomes
22,23
G2581U
Deleterious; 18% activity of 70S ribosomes
22,23
2582
G2582A
<5% of control level peptidyl transferase activity
22,23
G2582C
<5% of control level peptidyl transferase activity
22,23
G2582U
<5% of control level peptidyl transferase activity
22,23
2583
G->A
<5% of control level peptidyl transferase activity
19
G->C
<5% of control level peptidyl transferase activity
19
G->U
Dominant lethal; <5% of control level peptidyl transferase activity
19
2584
U->A
Deleterious; 20% activity of 70S ribosomes
19
U->C
Deleterious; 20% activity of 70S ribosomes
19
U->G
Dominant lethal
19
2585
U->A
Dominant lethal; <6% of control level peptidyl transferase activity; disrupted binding of tRNA fragment, Decreased peptidyl transferase activity
19, 5
U->C
Dominant lethal; <6% of control level peptidyl transferase activity; disrupted binding of tRNA fragment, Decreased peptidyl transferase activity
19, 5
U->G
Dominant lethal; 36% of control level peptidyl transferase activity; disrupted binding of tRNA fragment, Decreased peptidyl transferase activity
19, 5
2611
C->U or G
Eryr and low level lincomycin and clindamycin resistance in Chlamydomonas chloroplasts
6
ACKNOWLEDGEMENTS
We are grateful to Janan Eppig from the Bioinformatics Group at the Jackson Laboratory for her expert advice on the use of appropriate database software. Steven Vavoulis assisted in the preparation of the manuscript. This work was supported by the National Science Foundation (MCB-9315443).
REFERENCES
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Last modification: 17 Dec 1997
Copyright© Oxford University Press, 1998.
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