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PubMed1996

Functional studies of the gvpACNO operon of Halobacterium salinarium reveal that the GvpC protein shapes gas vesicles.

Gas vesicle (Vac) synthesis in Halobacterium salinarium PHH1 involves the expression of the plasmid pHH1-encoded vac (p-vac) region consisting of 14 different gvp genes that are arranged in two clusters, p-gvpACNO and, oriented in the direction opposite to that of gvpA, p-gvpDEFGHIJKLM. The p-gvpACNO region was analyzed at the transcriptional and functional levels in H. salinarium and in Haloferax volcanii transformants containing subfragments of the p-vac region. The p-gvpACNO genes were transcribed as several mRNAs: the 270-nucleotide (nt) p-gvpA transcript, encoding the major structural protein, occurred in large amounts, and minor amounts of three different readthrough transcripts (p-gvpACN, and p-gvpACNO mRNA) were found. In addition, the p-gvpO gene gave rise to two separate mRNA species: a 550-nt mRNA starting at the ATG and spanning the entire reading frame and a 420-nt RNA encompassing the second half of the p-gvpO gene. The requirement of p-gvpC, p-gvpN, and p-gvpO gene expression for gas vesicle synthesis was assessed by transformation experiments using the VAC- species Haloferax volcanii as the recipient. A delta C transformant, harboring the p-vac region with a deletion of the p-gvpC gene, produced large amounts of irregularly shaped gas vesicles. A shape-forming function of p-GvpC was demonstrated by complementation of the delta C transformant with the p-gvpC gene, resulting in wild-type-shaped gas vesicles. In the delta N transformant, the level of gas vesicle synthesis was very low, indicating that the p-GvpN protein is not required for gas vesicle assembly but may enhance gas vesicle synthesis. The p-gvpN deletion did not affect accumulation of p-gvpACO mRNA but reduced the separate p-gvpO transcription. The delta O transformant was Vac- and had a strongly decreased level of p-gvpACN mRNAs, demonstrating that the p-GvpO protein is required for gas vesicle synthesis and may affect transcription of this DNA region.

Archaeal Proteins↗

PubMed1997

Role of the intergenic dinucleotide in vesicular stomatitis virus RNA transcription.

To investigate the role played by the intergenic dinucleotide sequence of the conserved vesicular stomatitis virus (VSV) gene junction in modulation of polymerase activity, we analyzed the RNA synthesis activities of bicistrionic genomic analogs that contained either the authentic N/P gene junction or gene junctions that had been altered to contain either the 16 possible dinucleotide combinations, single nucleotide intergenic sequences, or no intergenic sequence at all. Quantitative measurements of the amounts of upstream, downstream, and readthrough mRNAs that were transcribed by these mutant templates showed that the behavior of the viral polymerase was profoundly affected by the nucleotide sequence that it encountered as it traversed the gene junction, although the polymerase was able to accommodate a remarkable degree of sequence variation without altogether losing the ability to terminate and reinitiate transcription. Alteration or removal of the intergenic sequence such that the U tract responsible for synthesis of the upstream mRNA poly(A) tail was effectively positioned adjacent to the consensus downstream gene start signal resulted in almost complete abrogation of downstream mRNA synthesis, thus defining the intergenic sequence as an essential sequence element of the gene junction. Many genome analogs with altered intergenic sequences directed abundant synthesis of a readthrough transcript without correspondingly high levels of downstream mRNA, an observation inconsistent with the shunting model of VSV transcription, which suggests that polymerase molecules are prepositioned at gene junctions, awaiting a push from upstream. Instead, the findings of this study support a model of sequential transcription in which initiation of downstream mRNA can occur only following termination of the preceding transcript.

Animals↗

PubMed1997

Amy as a reporter gene for promoter activity in Nocardia lactamdurans: comparison of promoters of the cephamycin cluster.

Promoter probe vectors containing the pA origin of replication and the Streptomyces griseus promoterless amy gene (encoding alpha-amylase) as reporter have been constructed to study transcription initiation regions in Nocardia lactamdurans. In some of the promoter probe vectors the phage fd terminator has been introduced to avoid readthrough expression from upstream sequences. By using these vectors, four different transcription initiation regions of the cephamycin gene cluster have been studied in N. lactamdurans. The bla gene encoding a beta-lactamase has a relatively strong promoter. Two other separate promoters corresponding to the lat and cefD genes (encoding, respectively, lysine-6-aminotransferase and isopenicillin N-epimerase) showed weak transcription initiation ability. These two promoters are arranged in a bidirectional transcription initiation region located in the center of the cephamycin gene cluster. The cmcH gene (encoding 3-hydroxymethylcephem carbamoyltransferase) upstream region did not contain a functional promoter, suggesting that cmcH is transcribed as a part of a polycistronic mRNA. The native amy promoter is used very efficiently in N. lactamdurans, resulting in secretion of high levels of extracellular alpha-amylase.

Amino Acid Isomerases↗

PubMed1988

Transcriptional patterns for the thrS-infC-rplT operon of Escherichia coli.

The genes coding for threonyl-tRNA synthetase (thrS), translation initiation factor 3 (infC) and ribosomal protein L20 (rplT) are clustered in the Escherichia coli genome. Previous studies had suggested the possibility that the expression of these genes is coupled. The transcriptional events in this operon have now been examined by S1 nuclease mapping and promoter fusion studies. The results indicate that infC-containing mRNAs are initiated from three separate promoters. Two of these are located in the protein-coding region of thrS and one, P12, is the major promoter at all growth rates tested. In addition, there is co-transcription of thrS and infC from the thrS promoter (PT). A single promoter for thrS has been mapped approx. 170 nucleotides upstream from its translation initiation site. Another promoter has been located within the infC-coding region. It is separated from the next downstream gene, rplT, by a transcription end point. However, termination at this region is only 50-70% efficient and transcripts starting at this promoter can read through into rplT. These findings demonstrate that the pattern of transcription in this operon is highly complex and the mRNA levels for each of the genes is determined by a variety of factors, including multiple promoters, co-transcription and readthrough of transcription termination signals.

Amino Acyl-tRNA Synthetases↗

PubMed1984

Identification of a tenth mRNA of respiratory syncytial virus and assignment of polypeptides to the 10 viral genes.

Nine mRNAs, their cDNA clones, and a genome transcriptional map have been reported previously for respiratory syncytial virus (P. L. Collins and G. W. Wertz, Proc. Natl. Acad. Sci. U.S.A. 80:3208-3212, 1983). We report here the identification of a 10th viral mRNA, designated mRNA 2b (molecular weight [MW] ca. 0.39 X 10(6)), that was detected by RNA (Northern) blot hybridization with cDNA clones. Analysis of a polycistronic readthrough transcript was used to deduce the position in the viral transcriptional map of the gene encoding the newly identified mRNA. The polypeptide coding assignments of 9 of the 10 respiratory syncytial virus mRNAs were determined. Individual viral mRNAs were purified by hybridization selection with nine unique, nonoverlapping cDNA clones and analyzed by translation in vitro. Each of the nine mRNAs encoded a single polypeptide chain. The coding assignments were as follows: RNA 1a (MW ca. 0.24 X 10(6)), a 9,500-dalton (9.5K) protein; RNA 1b (MW 0.26 X 10(6)), an 11K protein; RNA 1c (MW 0.26 X 10(6)), a 14K protein; RNA 2a (MW 0.38 X 10(6)), the 34K phosphorylated (P) protein; RNA 2b (MW 0.39 X 10(6)), a 36K protein; RNA 3a (MW 0.40 X 10(6)), the 26K matrix (M) protein; RNA 3b (MW 0.40 X 10(6)), a 24K protein; RNA 4 (MW 0.47 X 10(6)), the 42K major nucleocapsid (N) protein; and RNA 5 (MW 0.74 X 10(6)), a 59K protein. The cDNA clones used for the hybridization selections were respiratory syncytial virus specific and did not hybridize with uninfected-cell mRNA; therefore the proteins synthesized with the selected mRNAs were virus specific. The 9.5K, 11K, 14K, 24K, M, P, 36K, N, and 59K proteins were encoded by different mRNAs; therefore these nine proteins are all unique. The 9.5K, 11K, 14K, 24K, M, P, and N proteins synthesized in vitro with hybrid-selected mRNAs each had counterparts with the same electrophoretic mobilities in extracts of virus-infected cells. The in vitro polypeptides and their authentic counterparts were shown to be closely related by limited digest peptide mapping. The 36K and 59K polypeptides lacked counterparts with the same electrophoretic mobilities in infected cells and therefore are candidates for the unprocessed precursors of the viral F and G glycoproteins. The 10th viral mRNA, the 2,500K RNA 7, was not tested directly but is the only known mRNA of the appropriate size to encode the 200K large (L) protein of the viral nucleocapsid. These assignments account for all 10 of the reported viral mRNAs and bring to 10 the number of known unique viral proteins.

Animals↗

PubMed2004

Anxiety and panic: from human studies to animal research and back.

The role of learning and conditioning varies across human anxiety disorders, and distinguishing between fear and panic is important to guide investigation in panic disorder. By reminding that some psychological and psychobiological theories view panic attacks as false alarms of unconditioned biological origin, we suggest that employing endophenotypes of biological and evolutionary relevance--such as the respiratory responses to suffocative stimuli--can be fruitful for both human research and animal models of panic, and can help keeping unconditioned components of the clinical picture separate from the conditioned components in the experimental setting. We present a review of a model of panic disorder by which idiosyncratic environmental adverse events can promote unconditioned and unexpected spells of physical alarm. Along the proposed causal pathway the alternative splicing expression of polymorphic genes of the cholinergic system play an important role. The overproduction of the Acetylcholinesterase readthrough splice variant after minor stress can promote passive avoidance and learning through action at the level of the corticolimbic circuitries, as well as heightened sensitivity to suffocative stimuli by action upon the cholinergic components of chemoception. When a component of anticipatory anxiety complicates the clinical picture of recurrent panic attacks, and the HPA becomes activated, the glucocorticoid response element 17 kb upstream of the Acetylcholinesterase gene transcription initiation site may sustain sensitivity to suffocative stimuli for prolonged time. Finally, we review how animal models of human panic based on unconditioned provocation of alarm reactions by the same respiratory panicogens that are employed in man are viable and promising.

Acetylcholinesterase↗

PubMed2002

Gene overexpression as a tool for identifying new trans-acting factors involved in translation termination in Saccharomyces cerevisiae.

In eukaryotes, translation termination is dependent on the availability of both release factors, eRF1 and eRF3; however, the precise mechanisms involved remain poorly understood. In particular, the fact that the phenotype of release factor mutants is pleiotropic could imply that other factors and interactions are involved in translation termination. To identify unknown elements involved in this process, we performed a genetic screen using a reporter strain in which a leaky stop codon is inserted in the lacZ reporter gene, attempting to isolate factors modifying termination efficiency when overexpressed. Twelve suppressors and 11 antisuppressors, increasing or decreasing termination readthrough, respectively, were identified and analyzed for three secondary phenotypes often associated with translation mutations: thermosensitivity, G418 sensitivity, and sensitivity to osmotic pressure. Interestingly, among these candidates, we identified two genes, SSO1 and STU2, involved in protein transport and spindle pole body formation, respectively, suggesting puzzling connections with the translation termination process.

Cytoskeleton↗

PubMed1990

Conservation of a dual-start motif in P22 lysis gene regulation.

Gene 13 of bacteriophage P22 is functionally equivalent to lambda lysis gene S. Gene S codes for two products, the polypeptides S105 and S107, produced from translational initiation events at the third and first codon, respectively. We have shown that the two polypeptides have opposing functions in lysis: S105 is the lethal lysis effector, and S107 acts as an inhibitor of lysis (U. Bläsi, K. Nam, D. Hartz, L. Gold, and R. Young, EMBO J. 11:3501-3510, 1989). Gene 13 has a 108-codon reading frame and its product begins with a similar motif: Met-1-Lys-2-Lys-3-Met-4. Here, we present in vivo and in vitro evidence for the expression of a 13(108) and a 13(105) product and show that the lambda lysis control mechanisms is evolutionarily conserved in phage P22. In this case 13(108), like S107 in lambda, functions as the inhibitor of the lysis effector 13(105). Although the DNA sequences upstream of the S and 13 gene starts showed less homology, the same structural characteristics, i.e., stem-loop structures immediately upstream and about 10 codons downstream of the start region, were present in both reading frames. Using in vitro mutagenesis and toeprinting, we show that the upstream stem-loop structures of genes 13 and S, containing the Shine-Dalgarno sequence for initiations at Met-1, are interchangeable. Moreover, our data indicate that the stability of the secondary structures present in the translational initiation regions of genes S and 13 is set to create a particular ratio of initiation events at Met-1 and Met-3 or Met-4. The ratio of effector to inhibitor was much higher in P22 than in lambda. We propose that this reflects less transcriptional readthrough at the late terminator t(R) and suggests that the dual-start motif in genes 13 and S may be important for establishment of maintenance of the lysogenic state.

Base Sequence↗

PubMed2003

RNA editing and regulation of Drosophila 4f-rnp expression by sas-10 antisense readthrough mRNA transcripts.

We have previously described an example of extensively A-to-G edited cDNA derived from adult heads of the fruitfly Drosophila melanogaster. In that study, the source of the predicted antisense RNA pairing strand for template recognition by dADAR editase was not identified, and the biological significance of the observed hyperediting was not known. Here, we address each of these questions. 4f-rnp and sas-10 are closely adjacent X-linked genes located on opposite DNA strands that produce convergent transcripts. We show that developmentally regulated antisense sas-10 readthrough mRNA arises by activation of an upstream promoter P2 during the late embryo stage of fly development. The sas-10 readthrough transcripts pair with 4f-rnp mRNA to form double-stranded molecules, as indicated by A-to-G editing observed in both RNA strands. It would be predicted that perfect RNA duplexes would be targeted for modification/degradation by enzyme pathways that recognize double-stranded RNAs, leading to decline in 4f-rnp mRNA levels, and this is what we observe. The observation using quantitative RT-PCR that sas-10 readthrough and 4f-rnp transcript levels are inversely related suggests a role for the antisense RNA in posttranscriptional regulation of 4f-rnp gene expression during development. Potential molecular mechanisms that could lead to this result are discussed, one of which is targeted transcript degradation via the RNAi pathway. Insofar as the dADAR editase and RNAi pathways are known to be constitutive in this system, it is likely that control of antisense RNA transcription is the rate-limiting factor. The results provide insight into roles of naturally occurring antisense RNAs in regulation of eukaryotic gene expression.

Amino Acid Sequence↗

PubMed2000

Construction of full-length cDNA clones to Soil-borne wheat mosaic virus RNA1 and RNA2, from which infectious RNAs are transcribed In vitro: virion formation and systemic infection without expression of the N-terminal and C-terminal extensions to the capsid protein.

The 19-kDa capsid protein (CP) of Soil-borne wheat mosaic furovirus (SBWMV) is encoded in the 5'-terminal region of RNA2. In addition to CP, two CP-related proteins are translated from SBWMV RNA2: (1) a 24-kDa protein (N-CP) with an N-terminal 40-amino-acid extension initiated at an upstream in-frame CUG codon; and (2) an 83-kDa protein (CP-RT) with an about 580-amino-acid, C-terminal extension by partial translational readthrough at the UGA termination codon at the end of the CP gene. We examined requirements for N-CP and CP-RT on virion formation and systemic infection in wheat plants using full-length cDNA clones, from which infectious RNA can be transcribed in vitro. RNA2 mutants, which could not synthesize N-CP, CP-RT, or either infected wheat plants systemically in combination with the wild-type RNA1 transcripts, produced rod-shaped virus particles in uninoculated upper leaves. Original mutations which abolished translation of N-CP and CP-RT were confirmed on RNA2 extracted from purified virus from the upper leaves by nucleotide sequence analysis. These results indicate that neither N-terminal nor C-terminal extensions to the CP are required for virion formation and systemic infection of SBWMV in wheat plants.

Base Sequence↗

PubMed1989

Structure and transcription of the glycoprotein gene of attenuated HEP-Flury strain of rabies virus.

The mRNA-encoding G protein of the attenuated HEP-Flury strain of rabies virus was sequenced by the cDNA cloning technique. The G-mRNA was composed of 2059 nucleotides, with the coding region located from the 28th to 1602nd nucleotide, and was capable of encoding a polypeptide of 524 amino acids. Although the coding region was highly homologous (90% or more) to that of ERA and PV strains, the 3' noncoding region of the HEP virus G-mRNA was longer than that reported for other strains by some 400 nucleotides. The extra sequence was homologous to the long G-L intergenic sequence of the PV viral genome. The HEP virus genome lacked the postulated polyadenylating signal (TG-AAAAAAAA) that should have been found just before the "long G-L intergenic region," which indicates that the long G-L intergenic region of the HEP virus is integrated into the preceding G gene, and is transcribed only as a portion of the G-mRNA molecule. In the ERA virus-infected cells, however, two species of G-mRNA (1.9 and 2.3 kb long) were produced. The longer G-mRNA also contained the sequence complementary to the long G-L intergenic region and the shorter one did not. These findings suggest that two different poly(A)-tailing signals (one is present just before and another at the end of the long G-L intergenic region) work toward terminating the transcription of the ERA virus G gene and that the longer G-mRNA is produced as a readthrough product.

Amino Acid Sequence↗

PubMed1998

Structure and expression of the human septin gene HCDCREL-1.

Septins are a family of highly conserved filament-forming proteins that have been shown to mediate cytokinesis and cytoskeletal organization in fungi and Drosophila. The gene encoding the human septin family member HCDCREL-1 has been shown to be transcribed from a locus immediately adjacent to that of the platelet glycoprotein (GP) Ib b. The HCDCREL-1 gene possesses a non-consensus polyadenylation signal that apparently is not efficiently utilized, resulting in the expression of a readthrough transcript also containing the platelet GPIb beta coding region. As a first step in understanding the regulation and function of HCDCREL-1, we have analyzed the structure of this gene and characterized its expression in a variety of human cells. Our results indicate that the gene is expressed at high levels in platelets and neural tissue, and is transcriptionally complex.

Base Sequence↗

PubMed2001

Aminoglycoside antibiotics and autism: a speculative hypothesis.

BACKGROUND: Recently, it has been suspected that there is a relationship between therapy with some antibiotics and the onset of autism; but even more curious, some children benefited transiently from a subsequent treatment with a different antibiotic. Here, we speculate how aminoglycoside antibiotics might be associated with autism. PRESENTATION: We hypothesize that aminoglycoside antibiotics could a)trigger the autism syndrome in susceptible infants by causing the stop codon readthrough, i.e., a misreading of the genetic code of a hypothetical critical gene, and/or b) improve autism symptoms by correcting the premature stop codon mutation in a hypothetical polymorphic gene linked to autism. TESTING: Investigate, retrospectively, whether a link exists between aminoglycoside use (which is not extensive in children) and the onset of autism symptoms (hypothesis "a"), or between aminoglycoside use and improvement of these symptoms (hypothesis "b"). Whereas a prospective study to test hypothesis "a" is not ethically justifiable, a study could be designed to test hypothesis "b". IMPLICATIONS: It should be stressed that at this stage no direct evidence supports our speculative hypothesis and that its main purpose is to initiate development of new ideas that, eventually, would improve our understanding of the pathobiology of autism.

Aminoglycosides↗

PubMed1994

Selenocysteine insertion or termination: factors affecting UGA codon fate and complementary anticodon:codon mutations.

Translation of UGA as selenocysteine instead of termination occurs in numerous proteins, and the process of recording UGA requires specific signals in the corresponding mRNAs. In eukaryotes, stem-loops in the 3' untranslated region of the mRNAs confer this function. Despite the presence of these signals, selenocysteine incorporation is inefficient. To investigate the reason for this, we examined the effects of the amount of deiodinase cDNA on UGA readthrough in transfected cells, quantitating the full-length and UGA terminated products by Western blotting. The gene for the selenocysteine-specific tRNA was also cotransfected to determine if it was limiting. We find that the concentrations of both the selenoprotein DNA and the tRNA affect the ratio of selenocysteine incorporation to termination. Selenium depletion was also found to decrease readthrough. The fact that the truncated peptide is synthesized intracellularly demonstrates unequivocally that UGA can serve as both a stop and a selenocysteine codon in a single mRNA. Mutation of UGA to UAA (stop) or UUA (leucine) in the deiodinase mRNA abolishes deiodinase activity; but activity is partially restored when selenocysteine tRNAs containing complementary mutations are contransfected. Thus, UGA is not essential for selenocysteine incorporation in mammalian cells, provided that codon:anticodon complementarity is maintained.

Anticodon↗

PubMed1985

Upstream activation of ribosomal RNA biosynthesis in Saccharomyces cerevisiae.

Yeast was transformed with eight recombinants that contained an rRNA minigene and upstream elements of rDNA in different orientations in the multi-copy yeast-Escherichia coli shuttle vector, pJDB207. The effect of these elements of upstream rDNA on the initiation of transcription of the minigene at the site for rRNA biosynthesis was determined by using an S1 nuclease mapping procedure to measure the abundance of the minigene transcript in RNA from the yeast transformants. Transcription of the minigene was enhanced 3-fold by DNA within a 2.2 kb element more than 1.5 kb upstream from the initiation site. Inversion of the 2.2 kb element decreased expression of the minigene by 40%. This 2.2 kb element contained approx. 500 bp from the 25S rRNA coding region at the 3' end of the preceding rRNA gene and 1 kb of adjacent nontranscribed spacer rDNA. The enhancing activity was independent of interference from readthrough that might have contributed to the 7-fold decrease in minigene expression caused by removing all rDNA upstream from -209 bp.

DNA, Ribosomal↗

PubMed1993

Growth and translation elongation rate are sensitive to the concentration of EF-Tu.

We have used quantitative immunoblotting to estimate the amount of EF-Tu in a variety of S. typhimurium strains with wild-type, mutant, insertionally inactivated or plasmid-borne tuf genes. In the same strains we have measured translation elongation rate, exponential growth rate and the level of nonsense codon readthrough. In the wild-type strain, at moderate to fast growth rates, our data show that EF-Tu makes up 8-9% of total cell protein. Strains with either of the tuf genes insertionally inactivated have 65% of the wild-type EF-Tu level, irrespective of which tuf gene remains active, or whether that gene is wild-type or a kirromycin-resistant mutant. Strains with only one active tuf gene have reduced growth and translation elongation rates. From the magnitude of the reduction in elongation rate relative to the level of EF-Tu we calculate that in glucose minimal medium the in vivo saturation level of wild-type ribosomes by ternary complexes is only 63%. Strains with a ribosome mutation causing a poor interaction with ternary complex are non-viable on minimal medium when the level of EF-Tu is reduced.

Cell Division↗

PubMed1991

Gene organization and nucleotide sequence of the primase region of IncP plasmids RP4 and R751.

The primase genes of RP4 are part of the primase operon located within the Tra1 region of this conjugative plasmid. The operon contains a total of seven transfer genes four of which (traA, B, C, D) are described here. Determination of the nucleotide sequence of the primase region confirmed the existence of an overlapping gene arrangement at the DNA primase locus (traC) with in-phase translational initiation signals. The traC gene encodes two acidic and hydrophilic polypeptide chains of 1061 (TraC1) and 746 (TraC2) amino acids corresponding to molecular masses of 116,721 and 81,647 Da. In contrast to RP4 the IncP beta plasmid R751 specifies four large primase gene products (192, 152, 135 and 83 kDa) crossreacting with anti-RP4 DNA primase serum. As shown by deletion analysis at least the 135 and 83 kDa polypeptides are two separate translational products that by analogy with the RP4 primases, arise from in-phase translational initiation sites. Even the smallest primase gene products TraC2 (RP4) and TraC4 (R751) exhibit primase activity. Nucleotide sequencing of the R751 primase region revealed the existence of three in-phase traC translational initiation signals leading to the expression of gene products with molecular masses of 158,950 Da, 134,476 Da, and 80,759 Da. The 192 kDa primase polypeptide is suggested to be a fusion protein resulting from an in frame translational readthrough of the traD UGA stopcodon. Distinct sequence similarities can be detected between the TraC proteins of RP4 and R751 gene products TraC3 and TraC4 and in addition between the TraD proteins of both plasmids. The R751 traC3 gene contains a stretch of 507 bp which is unrelated to RP4 traC or any other RP4 Tra1 gene.

Amino Acid Sequence↗

PubMed1983

Repression of cointegration ability of insertion element IS1 by transcriptional readthrough from flanking regions.

We describe a repression mechanism in which read-through messages transcribed from a gene into an IS1 sequence inhibit its ability to mediate plasmid cointegration. This mechanism was derived from the demonstration that removal of the promoter region of the chloramphenicol resistance gene in transposon Tn9, or introduction of a strong transcription terminator of phage T7 downstream of the chloramphenicol resistance gene, increases the cointegration ability of the downstream IS1 sequence when in a particular orientation. The cointegration ability of an IS1 sequence downstream of the chloramphenicol resistance gene but in an orientation opposite that of the above-mentioned IS1 sequence also can be repressed. Analysis of transcripts synthesized in vitro showed that the transcripts of the chloramphenicol resistance gene were read through into the IS1 sequence located downstream of the gene in either orientation. Repression of this type may be one mechanism that controls the rate of transposition of the IS1 element, which apparently does not encode a structural gene for repressor.

Chloramphenicol↗