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UGA Suppression by a Mutant RNA of the Large Ribosomal Subunit (Nonsense Suppression/Termination Defect/23S Rrna, Domain II/Conserved Nucleotide) DAVID K

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UGA Suppression by a Mutant RNA of the Large Ribosomal Subunit (Nonsense Suppression/Termination Defect/23S Rrna, Domain II/Conserved Nucleotide) DAVID K Proc. Natl. Acad. Sci. USA Vol. 92, pp. 12309-12313, December 1995 Biochemistry UGA suppression by a mutant RNA of the large ribosomal subunit (nonsense suppression/termination defect/23S rRNA, domain II/conserved nucleotide) DAVID K. JEMIOLO*, FRANCES T. PAGEL, AND EMANUEL J. MURGOLAt Department of Molecular Genetics. Box 11, The University of Texas M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030 Communicated by John Roth, University of Utah, Salt Lake City, UT, August 16, 1995 (received for review January 25, 1995) ABSTRACT A role for rRNA in peptide chain termination was indicated several years ago by isolation of a 16S rRNA (small subunit) mutant of Escherichia coli that suppressed UGA mutations. In this paper, we describe another interesting rRNA mutant, selected as a translational suppressor of the chain-terminating mutant trpA(UGA211) of E. coli. The find- ing that it suppresses UGA at two positions in trpA and does not suppress the other two termination codons, UAA and UAG, at the same codon positions (or several missense mutations, including UGG, available at one of the two posi- tions) suggests a defect in UGA-specific termination. The H indI' suppressor mutation was mapped by plasmid fragment ex- changes and in vivo suppression to domain II of the 23S rRNA SaLI gene of the rrnB operon. Sequence analysis revealed a single SphI base change of G to A at residue 1093, an almost universally conserved base in a highly conserved region known to have ;l {\E EcoRI specific interactions with ribosomal proteins, elongation fac- HpaI tor G, tRNA in the A-site, and the peptidyltransferase region SacI of 23S rRNA. Several avenues of action of the suppressor Bgl I I rsp45 I mutation are suggested, including altered interactions with FIG. 1. Map of plasmid pDJ100. Open bars (from HindIlI clock- release factors, ribosomal protein L1I, or 16S rRNA. Regard- wise to BamHI), pBR322; stippled bars, phage A DNA; hatched bar, less of the mechanism, the results indicate that a particular unidentified 300-bp insertion; solid and shaded bars, E. coli chromo- residue in 23S rRNA affects peptide chain termination, spe- somal DNA containing the rrnB operon (solid bars represent coding cifically in decoding of the UGA termination codon. regions for the three rRNAs and tRNAGIu); PL, promoter-operator region from phage A; bent arrow, start site and direction of transcrip- A role for rRNA in peptide chain termination was indicated tion of rRNA genes. Unique restriction sites: Kpn I, Csp45I, Sac I, Hpa I, BamHI; double sites: Sph I, Bgl II. HindlIl is shown only for several years ago by isolation of a 16S rRNA (small subunit) reference; there are two other Hindlll sites in pDJ100, both in the 16S mutant ofEscherichia coli that suppressed UGA mutations and rRNA gene. implicated in particular the universally conserved nucleotide C1054, located in the conserved helix 34 (1). A key role for 23S was moved into our strains by way of the closely linked rRNA (large ribosomal subunit) in peptide bond formation, transposon zad-981::mini-kan. We have previously described translocation, and translational accuracy has been clearly the methods for screening prototrophic derivatives of a Trp- established (refs. 2-5 and references therein). The small auxotroph to distinguish suppressed mutants from revertants ribosomal subunit, on the other hand, has generally been (10) and for comparing growth of suppressor-containing thought to be the subunit involved in codon-specific transla- strains on plates (11). The main plasmids used in this study tional events in both elongation and termination. Indeed, until were as follows. pc1857 was derived from pACYC177 and recently, the majority of rRNA suppressors of nonsense (ter- contains a temperature-sensitive bacteriophage A repressor mination codon) mutations obtained were associated with 16S gene (12). pDJ100 was derived from pBR322 and contains the rRNA (6). In this paper, however, we describe a 23S rRNA wild-type rRNA operon, rrnB, under the control of the A PL nonsense suppressor that works at UGA mutant codons in trpA promoter. It is a spontaneous derivative of pNO2680 (13) and but not at UAA or UAG mutations at the same codon contains an '300-bp insertion in the PL region between the positions. A preliminary report of these results was presented two Bgl II sites of pNO2680 (unpublished observations; Fig. 1). at the Cold Spring Harbor Laboratory meeting on the Mo- pDJ101 is the original rrlB(SuUGA)-containing plasmid re- lecular Genetics of Bacteria and Phages, August 18-23, 1992. ported in this study (that is, pDJ100 with the new suppressor mutation). pDJ101[4a] is pDJ101 with an uncharacterized MATERIALS AND METHODS secondary mutation, outside of rrnB, that was found in this The bacterial strains were derived from E. coli K-12. The study to affect plasmid copy number or level of transcription nomenclature for trpA mutations and suppressor genes has from PL. Plasmid DNA preparation and transformations were been described (7). Specific strains are described at first carried out essentially as described by Sambrook et al. (14). mention in Results. Some strains contained a pcnB mutation, Plasmid mutagenesis was performed in vivo. The plasmid was which reduces colEl-type plasmids to a few copies per cell (8, 9). pcnBl, obtained from J. S. Parkinson in strain RP7947 (9), Abbreviations: AmpR, ampicillin resistance (resistant); Ind, indole; 5MT, 5-methyl-DL-tryptophan; EF, elongation factor; RF, release factor. The publication costs of this article were defrayed in part by page charge *Permanent address: Department of Biology, Vassar College, Pough- payment. This article must therefore be hereby marked "advertisement" in keepsie, NY 12601. accordance with 18 U.S.C. §1734 solely to indicate this fact. tTo whom reprint requests should be addressed. Downloaded by guest on September 29, 2021 12309 12310 Biochemistry: Jemiolo et al. Proc. Natl. Acad. Sci. USA 92 (1995) introduced into a strain containing the mutator mutDS (15) on functional and transcription of the mutant rrnB increases. In supplemented minimal medium; the strain was then grown in this way, we demonstrated that at 42°C, the suppressor muta- L broth plus thymidine to allow the mutator to work. The tion, present in pDJ101, is lethal to the cell. In the second mutD5-exposed plasmid was harvested and used to transform instance, we used a plasmid preparation of the suppressor various trpA mutant strains to obtain plasmid-associated sup- mutant to transform pairs of isogenic strains containing each pressors. Media and other genetic procedures have been offour trpA UGA mutations. Each pair contained a PcnB+ and described elsewhere (7, 16) or are presented in Results. Most a PcnB- member. In both members of each pair, the rrnB biochemical procedures were performed essentially according operon was maximally transcribed. They differed, however, in to ref. 14. For DNA sequence analyses, small fragments from their plasmid copy numbers by virtue of the status of thepcnB the mutant rrnB operon were separated by agarose gel elec- allele. Table 1 highlights the UGA suppression ability of the trophoresis, purified using the Prep-A-Gene DNA purification suppressor (in pDJ101) and indicates the suppressor's lethality kit (Bio-Rad), and recloned into a vector containing multiple at higher copy number. cloning sites bracketed by T3 and T7 promoters. Plasmid Transformation of PcnB+ strains with pDJ101 yielded ex- preparations were analyzed by automated sequence analysis tremely sick looking, nonviable "colonies." Among them, using T3 and T7 complementary primers, Applied Biosystems however, were a few fast-growing, healthy colonies, so several reaction protocols, and a model 373A DNA sequencer. were purified and examined for a secondary mutation in the plasmid. In two cases, back transformation demonstrated that RESULTS a secondary mutation accounting for healthy growth was plasmid associated. Fragment exchanges between one of the Suppressor Selection. mutD5-treated pDJ100 (see Fig. 1) nondetrimental plasmids, pDJ101[4a], and wild-type pDJ100, was used to transform strain MDA6655 to ampicillin resistance followed by transformations of PcnB+ and PcnB- strains, on minimal containing 50 (AmpR) and Trp+ glucose medium indicated that the secondary, remedial mutation was not in the of per ml Amp-50). MDA6655 is Trp- due to Ag Amp (Min rRNA operon (between Kpn I and, counterclockwise, a UGA nonsense mutation at codon 211 of the trpA gene. It BamHI). Presumably, it lowers the effectiveness of the sup- also contains apcnB mutation, which lowers the copy number pressor (Table 1), and hence its detrimentality, either by of colEl-type plasmids (8, 9), to allow us to obtain rRNA copy number or by lowering transcription mutations that, when highly expressed, might be detrimental to decreasing plasmid from the PL promoter. gene was found the cell. After single-colony isolations, the trpA and Nucleotide Analysis of to still contain the original UGA mutation, indicating that the Molecular Mapping Sequence the Suppressor Mutation. To localize the suppressor mutation Trp+ phenotype was due to suppression. Plasmid extracted to a convenient for DNA sequence analysis and to from the suppressor strain was used to retransform the original fragment recipient strain (MDA6655) to AmpR. All the AmpR trans- exclude the possibility that secondary mutations outside the were in we cut both the wild-type formants were Trp+ (i.e., suppressor positive), indicating that region involved suppression, with appro- the new suppressor was plasmid associated (and presumably in plasmid and the suppressor-containing plasmid the rrnB operon). priate restriction enzymes (see Fig. 1), exchanged the frag- High Expression Detrimentality and Its Reversal by a ments, religated them, and transformed appropriate cells for Vector Mutation. Overproduction of a mutant rRNA encoded the functional test (UGA suppression). The results of several by a cloned rrn operon may be detrimental to cell growth or pairwise cuts established that the suppressor was in the gene even result in lethality.
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