Intragenic reorganization followed by vertical descent is therefore a more satisfactory explanation. Clustering may facilitate co-regulation of gene expression, although it is clearly not a prerequisite for this since expression of unlinked genes for other metabolic pathways can be readily co-regulated.
As the number of complete genome sequences of filamentous fungi increases, it should become possible to elucidate and perhaps model the mechanisms that drive cluster formation and maintenance, following approaches similar to those used to study the life and death of bacterial operons.
While this section has focused on gene clusters for the synthesis of secondary metabolites in filamentous fungi, it is noteworthy that clusters of diverse virulence genes with no obvious function in metabolism have recently been identified in the corn smut fungus Ustilago maydis following completion of the full genome sequence of this organism [ 74 ]. Clusters of genes of related function are relatively unusual in S. However, the S.
These include gene clusters for utilization of specific carbon sources [e. Studies of the distribution, origin, and fate of these gene clusters have provided important insights into the mechanisms underpinning adaptation of yeasts to new ecological niches.
The DAL gene cluster of S. These genes enable yeast to use allantoin a purine degradation product as a nitrogen source Fig. The DAL gene cluster is completely conserved in the four closest relatives of S. In less closely related species, the six genes are also clustered, but there are differences in the internal arrangement of gene order and the cluster is located in a different part of the genome although probably still subtelomeric.
The DAL cluster is not present in the genomes of more distantly related hemiascomycetes. However, homologues of the six DAL genes are found scattered around the genomes of these species. The species that possess a DAL cluster form a monophyletic group. Comparative analysis of the DAL genes and clusters in the genomes of different yeast species in combination with phylogenetic information has provided compelling evidence to suggest that the DAL cluster was assembled quite recently in evolutionary terms, after the split of the sensu stricto group of yeasts from other yeasts and hemiascomycetes [ 76 ].
Six of the eight genes involved in allantoin degradation, which were previously scattered around the genome, became relocated to a single subtelomeric site in an ancestor of S. This could have occurred by gene duplication followed by loss of the gene at the original locus. These genomic rearrangements coincided with a biochemical reorganization of the purine degradation pathway, which switched to importing allantoin instead of urate.
This change circumvented the need for urate oxidase, one of several oxygen-consuming enzymes lost by yeasts that can grow vigorously in anaerobic conditions Fig. It has therefore been proposed that selection for reduced dependence on oxygen led to a switch from urate to allantoin utilization in an ancestor of the sensu stricto group of yeasts [ 76 ]. Natural sources of allantoin for yeasts are plants [ 79 ] and insect excretion [ 80 ].
The allantoin degradation pathway—an adaptation to growth under oxygen-limiting conditions in Saccharomyces cerevisiae. In the classical purine degradation pathway, xanthine is converted to urate and then to allantoin, in two successive oxidation steps catalyzed by the peroxisomal enzymes xanthine dehydrogenase XDH and urate oxidase UOX. XDH genes are present in filamentous fungi but not in yeasts. To use purine derivatives as a nitrogen source yeasts must therefore import urate, allantoin or allantoate from outside the cell.
Yeasts that lack the DAL cluster e. In contrast, S. The Dal4 and Fur4 proteins are members of a purine-related transporter family. The subsequent degradation steps involve the same DAL pathway genes in all yeasts, but in S.
The reaction catalyzed by UOX requires molecular oxygen as a substrate and takes place in the peroxisome. Biochemical reorganization of the purine degradation pathway to enable import of allantoin instead of urate eliminates the oxygen-requiring step mediated by UOX and coincided with the formation of the DAL gene cluster. This biochemical reorganization may have been driven by selection for ability to grow under conditions of oxygen limitation.
Reproduced from [ 76 ]. The birth of the DAL gene cluster. The DAL gene cluster on S. The corresponding region in K. The K. The region of the K. Adapted from [ 76 ]. The selection for formation of new metabolic gene clusters such as the DAL gene cluster is likely to be intense, driven by the need to adapt to growth under different environmental conditions.
Gene clusters that have been formed by epistatic selection are expected to be recombination cold spots and so to be in linkage disequilibrium [ 81 ], and this is indeed the case for the DAL gene cluster [ 76 ]. Epistatic selection for linkage may in addition be driven by the need to select for combinations of alleles that interact well in order to avoid the accumulation of toxic pathway intermediates within cells.
For example, glyoxylate, which is an intermediate in the DAL pathway Fig. Glyoxylate is produced by the Dal3 reaction and removed by the Dal7 reaction. The finding that Dal3 enzyme activity is reduced in a dal7 mutant is consistent with this channeling hypothesis [ 76 , 82 ]. Z Htz1 rather than with the normal histone H2A [ 83 ].
Htz1 preferentially associates with narrow regions within the promoters of genes that are normally maintained in repressed form but are strongly induced under specific growth conditions or during particular gene expression programmes.
A model has been proposed in which Hzt1 associates to specific nucleosomes in the promoters of inactive genes in order to poise, and perhaps organize, chromatin structure in a manner that is permissive to transcription initiation [ 84 ].
The genes in the DAL cluster are negatively regulated by the Hst-Sum1 system, which represses expression of mid-sporulation genes during mitotic growth Fig.
Assuming that there is a selective advantage to repressing DAL gene expression when nitrogen is not limiting, there would have been an incremental selective advantage to relocating each gene into the chromatin modification HZAD domain. Thus, one way in which alleles could interact well is by being amenable to the same type of chromatin modification [ 76 ]. Activation of expression of the DAL genes. The exchange of histone H2A for H2A.
Z is mediated by the Swr1 chromatin remodeling complex [ ]. Under new selection regimes, adaptations may evolve while established functions may become less important. The GAL genes, which are required for galactose utilization, are clustered in the genomes of every yeast species in which they are present [ 75 ]. This pathway converts galactose into glucosephosphate, a substrate for glycolysis.
Galactose utilization is widespread amongst yeasts and is likely to be ancestral. However, several yeast species have lost the ability to use this carbon source. Comparisons of the genomes of galactose-utilizing and non-utilizing yeast species have revealed that three out of the four non-utilizing species examined lack any trace of the pathway except for a single gene.
However, S. Thus, whilst a newly formed functional gene cluster confers a selective advantage in a new ecological niche, rapid and irreversible gene inactivation and pathway degeneration can occur under non-selective conditions. It has been suggested for S. The loss of genes and pathways through reductive evolution has been inferred for many organisms that have adapted to pathogenic or endosymbiotic lifestyles [ 85 — 92 ].
These capabilities may be lost either because they are no longer under selection neutral or because of a deleterious effect on fitness in a new niche [ 75 , 93 — 95 ]. Genes for metabolic pathways in plants are generally not clustered, at least for the majority of the pathways that have been characterized in detail to date. However, several examples of functional gene clusters for plant metabolic pathways have recently emerged.
These are the cyclic hydroxamic acid DIBOA pathway in maize [ 96 — 98 ], triterpene biosynthetic gene clusters in oat [ 99 , ] and Arabidopsis [ ] the avenacin and thalianol gene clusters, respectively , and the diterpenoid momilactone cluster in rice [ , ]. These gene clusters all appear to have been assembled from plant genes by gene duplication, acquisition of new function, and genome reorganization and are not likely to be a consequence of horizontal gene transfer from microbes.
The existence of these clusters, of which at least three are implicated in plant defense [ 98 , 99 , — ], implies that plant genomes are able to assemble functional gene clusters that confer an adaptive advantage. The selection for rapid and recent formation of such metabolic gene clusters is likely to be intense, driven by the need to adapt to growth under different environmental conditions, and implies remarkable genome plasticity.
The benzoxazinoids are defense-related compounds that occur constitutively as glucosides in certain members of the Gramineae and in some dicots.
In the Poaceae, the production of benzoxazinoids is developmentally regulated with highest levels being found in the roots and shoots of young seedlings. Induction of benzoxazinoid accumulation has also been reported in response to cis -jasmone treatment [ ].
The complete molecular pathway for benzoxazinoid biosynthesis has been elucidated in maize reviewed in [ 98 ]. Bx1 is likely to have been recruited from primary metabolism either directly or indirectly by duplication of the maize gene encoding TSA.
The glucosyltransferases BX8 and 9 catalyse glucosylation of benzoxazinoids. All the Bx genes with the exception of Bx9 are linked within 6 cM of Bx1 on maize chromosome 4 [ 97 , ]. The distribution of benzoxazinoids across the Gramineae is sporadic. Maize, wheat, rye, and certain wild barley species are capable of the synthesis of these compounds while oats, rice, and cultivated barley varieties are not [ , ]. The Bx gene cluster is believed to be of ancient origin. Wheat and rye have undergone a shared genomic event that has led to the splitting of the Bx gene cluster into two parts that are located on different chromosomes.
This can be explained by a reciprocal translocation in the ancestor of wheat and rye [ ]. Bx-deficient variants of a diploid accession of wild wheat Triticum boeoticum have recently been identified. Molecular characterization suggests that Bx deficiency in these accessions arose by disintegration of the Bx1 coding sequence, followed by degeneration and loss of all five Bx biosynthetic genes examined [ ].
Barley species that do not produce benzoxazinoids have also lost all Bx genes [ , ]. The precise physical distances between all of the genes within the Bx cluster are not known. However, in maize, Bx1 and Bx2 genes are 2. In hexaploid wheat, the Bx3 and Bx4 genes are 7—11 kb apart within the three genomes [ ]. Although several of the Bx genes are in close physical proximity this gene cluster appears to be less tightly linked than the other examples that have been considered so far in this review.
Interestingly, barley lines that produce benzoxazinoids do not synthesize gramine, a defense compound that is also derived from the tryptophan pathway. Conversely, gramine-accumulating barley species are deficient in benzoxazinoids. This has led to the suggestion that the biosynthetic pathways for these two different classes of defense compound are mutually exclusive, possibly due to competition for common substrates [ ].
Outside the Poaceae, benzoxazinoids in particular DIBOA and its glucoside are found in certain isolated eudicot species belonging to the orders Ranunculales e. Comparison of the BX1 enzymes of grasses and benzoxazinone-producing eudicots indicates that these enzymes do not share a common monophyletic origin.
Furthermore, the CYP71C family of CYPs to which BX belong is not represented in the model eudicot, thale cress Arabidopsis thaliana , and all members of this family described to date originate from the Poaceae. It therefore seems likely that the ability to synthesize benzoxazinones has evolved independently in grasses and eudicots. Investigation of triterpene biosynthesis in plants has led to the discovery of two other examples of operon-like metabolic gene clusters, namely the avenacin gene cluster in oat Avena species and the thalianol gene cluster in A.
Avenacins are antimicrobial triterpene glycosides that confer broad spectrum disease resistance to soil-borne pathogens [ , ]. Analysis of the genes and enzymes for avenacin synthesis has revealed that the pathway has evolved recently, since the divergence of oats from other cereals and grasses [ 99 , , , , ]. Transferal of genes for the synthesis of antimicrobial triterpenes into cereals such as wheat holds potential for crop improvement but first requires the necessary genes and enzymes to be characterized.
Synthesis of avenacins is developmentally regulated and occurs in the epidermal cells of the root meristem. The major avenacin, A-1, has strong fluorescence under ultra-violet light and can be readily visualized in these cells.
This fluorescence, which is an extremely unusual property amongst triterpenes, has enabled isolation of over 90 avenacin-deficient mutants using a simple screen for reduced root fluorescence [ , ]. This mutant collection has facilitated gene cloning and pathway elucidation. Sad1 encodes an oxidosqualene cyclase enzyme that catalyses the first committed step in the avenacin pathway [ 99 , ], while Sad2 encodes a second early pathway enzyme—a novel cytochrome P enzyme belonging to the newly described monocot-specific CYP51H subfamily [ ].
Sterols and avenacins are both synthesized from the mevalonate pathway [ ]. While the genes for sterol synthesis are generally regarded as being constitutively expressed throughout the plant, the expression of Sad1 , Sad2 , and other cloned genes for avenacin biosynthesis is tightly regulated and is restricted to the epidermal cells of the root meristem [ 99 , , ]. Recruitment of Sad1 and Sad2 from the sterol pathway by gene duplication has therefore involved a change in expression pattern as well as neofunctionalisation.
A third gene has recently been cloned and shown to encode a serine carboxypeptidase-like acyltransferase that is required for avenacin acylation. Four other loci that are required for avenacin synthesis also co-segregate with these cloned genes, indicating that most of the genes for the pathway are likely to be clustered [ 99 ].
Since avenacins confer broad spectrum disease resistance, the gene cluster is likely to have arisen through strong epistatic selection for maintenance and co-inheritance of this gene collective. In addition, interference with the integrity of the gene cluster can in some cases lead to the accumulation of toxic intermediates, with detrimental consequences for plant growth, so providing further selection for cluster maintenance [ ].
Gene clustering may also facilitate co-ordinate regulation of gene expression at the level of chromatin [ 2 ]. The thalianol gene cluster in A. The BAHD acyltransferase gene is predicted to be part of the cluster based on its location and expression pattern, but an acylated downstream product has not as yet been identified.
In the related crucifer, A. This may be indicative of paralogy rather than orthology [ ]. Alternatively it may indicate that the BAHD acyltransferase genes are not under strong selection and so are divergent. The thalianol gene cluster in Arabidopsis. The A. The organization of the equivalent region from the related crucifer, A. Adapted from Ref. Simultaneous Gene Transcription and Translation in Bacteria. Chromatin Remodeling and DNase 1 Sensitivity. Chromatin Remodeling in Eukaryotes. RNA Functions.
Citation: Ralston, A. Nature Education 1 1 How do bacteria adapt so quickly to their environments? Part of the answer to this question lies in clusters of coregulated genes called operons.
Aa Aa Aa. The lac Operon. References and Recommended Reading Jacob, F. Article History Close. Share Cancel. Revoke Cancel. Keywords Keywords for this Article. Save Cancel. Flag Inappropriate The Content is: Objectionable.
Flag Content Cancel. Email your Friend. Submit Cancel. This content is currently under construction. Explore This Subject. Consequences of Gene Regulation. Gene Responses to Environment. Regulation of Transcription.
Transcription Factors. From DNA to Protein. Organization of Chromatin. Topic rooms within Gene Expression and Regulation Close. No topic rooms are there. Or Browse Visually.
Other Topic Rooms Genetics. In this study, we considered operons that are new to the Enterobacteria or are shared with somewhat more distant relatives Haemophilus, Pasteurella, Vibrio, or Shewanella species—see Figure 2. ORFans are genes that lack identifiable homologs outside of a group of closely related bacteria [ 23 ].
Most ORFans are functional protein-coding genes that contribute to the fitness of the organism they are under purifying selection , and they were probably acquired from bacteriophage [ 22 ]. Distant relatives other Proteobacteria, Bacteria, and Archaea are not shown. The tree is based on highly conserved proteins see Materials and Methods and is consistent with that of [ 42 ] but contains more taxa.
A similar pattern was found in B. The most parsimonious evolutionary scenario for constructing a native—ORFan pair is a single insertion event that transfers the ORFan into the genome and places it adjacent to the native gene. To test this hypothesis, we compared the evolutionary age of the new operon to that of the ORFan. The age was determined from the most distant relative that contained the new operon or ORFan see Materials and Methods.
This arrangement may be selected for because the ORFan gene is transcribed from a native promoter without perturbing the expression of a native gene. However, in B. A Types of genes in new operon pairs and in other operon pairs.
C Validation of predicted new operon pairs of each of the three major types. We quantified the similarity of expression patterns in microarray data using the Pearson correlation.
As a negative control, we also tested non-operon pairs adjacent genes on the same strand that are known not to be co-transcribed from [ 48 ].
For both E. Indeed, because phages have compacted operon-rich genomes, it is surprising that more ORFans are not in such pairs, and that ORFans are less likely to be in operons than other genes [ 14 ].
Perhaps the phage operon benefits the phage, whereas only one gene in the operon would benefit the host. Because new operons are not, by definition, conserved across many genomes, these operon predictions may be less reliable. However, new operon pairs of each of the three major types discussed above tend to have strongly correlated expression patterns Figure 3 C and Figure S1 C.
Therefore, most of these predictions are probably accurate. If new operons containing ORFans often form by insertion, how do new operon pairs containing only native genes form? Although we cannot examine the ancestor of E. Specifically, we examined new operon pairs that were shared by E. Among the ten E. Within each of these Vibrio pairs, the genes are on the same strand. For four of these pairs, the intervening genes are on the opposite strand, so we are confident that these are not operons in Vibrio.
In principle, operons could contain within themselves transcripts on the opposite strand, but this has never been observed in E. In rare cases, B. For these six new operon pairs, the most parsimonious scenario is that the operon formed by deleting the intervening genes one event.
Because these operons are unique to the Enterobacteria, insertion within the operon in the ancestor of Vibrio would require two events operon formation followed by insertion. Other features of these pairs, such as the absence of homologs for the intervening genes in the Enterobacteria, are consistent with deletion see Protocol S1.
For example, in E. These residues are not present in bacteria that lack the operon unpublished data; evidence that the predicted start codon for murI is correct is discussed in Protocol S1. This overlap suggests that the operon formed by deletion in a single event that destroyed the original ribosome binding site of btuB as well as other intervening DNA such as promoters and terminators. In general, however, it is possible that the deletion involves several steps e. In another four cases, the Vibrio genes were distant from each other, so we suspect that the E.
In general, we cannot rule out more complicated scenarios that involve deletion, such as: 1 a rearrangement that placed the genes in proximity that was then followed by a deletion; or 2 a rearrangement in the ancestral Vibrio that masked the pre-existing proximity of the genes.
However, for ptr—recB, we can rule out deletion, as the native gene ptr was inserted into and destroyed the ancestral operon recC—recB. In summary, operons containing native genes form both by deleting intervening genes and by rearrangements that bring more distant genes into proximity.
In contrast, many new ORFan—native operons probably arise from the insertion of the new gene, and often allow expression of the ORFan gene from a native promoter. We examined the new operon pairs—adjacent genes that are predicted to be in the same operon in E. Such modifications appear to be much less common than the formation of new operons: we identified new operon pairs but only 81 modification events.
However, in a surprisingly large number of cases, two or more new operon pairs are adjacent and furthermore of the same age, so that the operon has undergone rapid evolution Figure 4 A. This was also observed in B. Adjacent new operon pairs of the same age occur significantly more often than under a completely random model of operon evolution see Materials and Methods.
In other words, some operons are evolving more rapidly than the average operon. Although it is possible for insertions within pre-existing operons to create two or more new operon pairs with a single event, insertions are much less common than additions at the beginning or end of pre-existing operons Figure 4 B. Also, there is a slight preference for appending a new gene to the end of a pre-existing operon instead of prepending a gene to the beginning Figure 4 B , so that the majority of genes retain the original promoter instead of acquiring a new one.
A New operon pairs are more likely to be adjacent to each other than expected by chance. The surplus of adjacent pairs of the same age is particularly striking. The model for random evolution is detailed in Materials and Methods.
B The frequency of different types of modifications to pre-existing operons. To confirm that some operons are undergoing rapid evolution, we manually examined the modified operons in E. The complete results of this analysis are given in Table S1. We found many cases where two or more changes had occurred to the original operon s. We also observed several cases where a single gene in an operon has been replaced by a non-homologous gene Table S1. This supports a previous finding that genes in operons are occasionally replaced by horizontally transferred homologs that are too diverged for homologous recombination to occur [ 16 ], although the mechanism by which genes can be replaced or inserted into operons remains unclear.
As the modified operons are evolving more rapidly than the average operon, we considered that these operons might be under positive selection. Proof of positive selection is provided by evolution that is faster than the neutral rate for example, when changes in a protein-coding sequence that change the protein sequence are more likely than other changes. Unfortunately, the neutral rate of operon evolution is not known, and so we do not see how to perform an analogous test for adaptive operon evolution.
Instead, we tested whether rapid evolution of these operons could be due to weak selection. First, under a neutral model, the ages of the adjacent new operon pairs should be independent, whereas we found that they have a significant tendency to match. Second, we reasoned that if these operons were under weak selection, then the protein sequences of their genes would be evolving rapidly.
Instead, we found that genes in modified operons have about the same average level of amino acid identity between E. Adjacent new operon pairs i. As the rapid evolution of these operons does not seem consistent with neutral processes, it may result from positive selection. Genes in the same operon are usually separated by 20 bases or fewer of DNA [ 8 ].
Furthermore, the stop codon of the upstream gene often overlaps the start codon of the downstream gene [ 25 ], which gives the impression that the genes are packed together as tightly as possible. Why are genes within operons so closely spaced? Close spacing could arise without selection because of the bias of bacterial genomes toward small deletions [ 26 ].
Alternatively, close spacings may be preferred because of translational coupling—the ribosome can move directly from the upstream gene's stop codon to a downstream gene's start codon, which can increase translation from the downstream gene and may also ensure that similar amounts of protein are made from the two genes reviewed by [ 27 , 28 ].
To study the evolution of close spacing, we first compared spacings within orthologous operons between E. Because spacing is a major factor in operon predictions, we examined only experimentally characterized operons. The spacing within operons evolves very rapidly—in the close relative S. Even in another strain of E. Canonical spacings are also often different between E.
A Known operon pairs in E. For each class of spacing in E. Because operon predictions rely heavily on spacing, only known E. To see how canonical spacings form, we compared the DNA sequences of operon pairs that are at canonical spacings in E. The canonical overlap of the start and stop codons can easily form by deletion Table 2.
Spacing changes are often accompanied by small insertions or deletions at the ends of the protein sequences e. We also noticed that canonical overlaps can easily turn into larger overlaps by disrupting the stop codon cysNC and cstC — astA. These results are consistent with previous reports that overlapping genes often form by disrupting the upstream gene's stop codon and that this sometimes results in the addition of new coding sequence [ 29 , 30 ].
Because greater overlaps are less common than the canonical overlaps, at least for old operons Figure 5 B , this also suggests that there is selection against greater overlaps.
Greater overlaps can eliminate translational coupling reviewed by [ 28 ] or they might otherwise interfere with translation. It has also been suggested that the canonical spacing might be common because it stabilizes the transcript—with such close spacings, there is no intergenic region that is free of ribosomes and exposed to RNAses [ 8 ].
To test this hypothesis, we examined three genome-wide datasets of mRNA half-lives [ 31 , 32 ]. Operon pairs with canonical separations tended to have slightly longer half-lives for both downstream and upstream genes in all three datasets, but the effect was not consistently statistically significant unpublished data.
We concluded that spacing is not a major determinant of mRNA half-lives and that transcript stability is unlikely to explain the prevalence of overlapping start and stop codons. Overall, we argue that canonical overlaps form by neutral deletion and are maintained by selection against greater overlaps. However, changes to the spacing are likely accompanied by changes to the translation initiation rates of the downstream gene e.
We would expect these changes to expression levels to be under selection. Indeed, in laboratory experiments, the expression level of the lac operon evolves to optimality in a few hundred generations [ 33 ]. Thus, changes in operon spacing could reflect fine-tuning of expression levels.
Although genes in operons tend to be closely spaced, genes in highly expressed operons, as identified by codon adaptation, tend to be widely spaced [ 25 , 34 ]. We confirmed with microarray data that highly expressed operons in E.
The correlation of spacings with mRNA levels is stronger than with codon adaptation unpublished data —we suspect that this is because the empirical mRNA levels are less noisy estimates of expression levels than codon adaptation see Materials and Methods.
The wide spacings within highly expressed operons seem surprising, both because they reduce translational coupling [ 28 ] and because the additional RNA in highly expressed transcripts would waste the cell's resources. However, wide spacings are particularly common for alternatively transcribed operon pairs that have internal promoters or terminators Figure 5 B and Figure S3 B.
To see if the sequences between the widely spaced E. These conserved sequences averaged a total of 37 bases per pair median 32 , which is considerably larger than Shine—Dalgarno sequences. We searched the literature for evidence of function for the first 15 pairs with footprints, and found five attenuators or partial terminators, three internal promoters, two translation leader sequences, one small RNA not included in our database, two conserved REP sequences of unknown function, and only two cases with no information in the literature.
Thus, most of these footprints correspond to functional regulatory sequences, and by extension, most widely spaced operons are subject to complex regulation. This suggests that unidentified alternative transcripts are very common in E. Thus, in both organisms, wide spacings indicate complex regulation.
The correlation of these wide spacings with expression levels suggests regulatory fine-tuning, because making unnecessary proteins would be more costly in materials or energy or more deleterious in undesired protein activity if the proteins are highly expressed. Here, we focus on cases where a conserved operon has split apart, so that E. In particular, we ask by what mechanisms the operons die, and whether certain types of operons are more likely to die.
To identify dead operons in E. We considered conserved operon pairs that were predicted in more than one group of related bacteria and for which orthologous genes were present in E. To avoid cases of unclear orthology, we required both genes to be the only members of their respective COGs conserved orthologous groups [ 36 ] in E.
We then asked whether these E. Using these criteria, we identified 66 dead operon pairs that were split apart and live operon pairs that were still co-transcribed. When we examined the functions of these dead operon pairs, we found 15 functionally related dead operons and six functionally unrelated genes that are probably growth-rate regulated Table 3. Growth-related genes are often found together in operons even when there is no close functional relationship [ 5 ].
Of the remaining dead operon pairs, 16 are functionally unrelated and 29 contain uncharacterized genes. For 11 of the 66 dead operon pairs, the genes are still near each other on the chromosome. In these cases, the operon was probably destroyed by an insertion event.
For example, the insertion of ptr discussed in a previous section appears to have both created the new ptr—recB operon pair and destroyed the ancestral recCBD operon. In the other 55 cases, the operon may have been destroyed by genome rearrangements. For example, the dead operon pair yebI—yebL is divergently transcribed in E. In many of its relatives, lysA is in an operon with dapF see Figure 6 , specifically Figure 6 A and is not regulated by lysine [ 38 ].
In phylogenetic analyses, lysR -associated lysA from diverse species constitutes a distinct clade unpublished data , which we term lysA2. This suggests horizontal transfer, as does the presence of both dapF—lysA and lysR—lysA2 in some species. Thus, the parsimonious reconstruction is that E. Mechanisms of Microbial Genetics. Search for:. Gene Regulation: Operon Theory Learning Objectives Compare inducible operons and repressible operons Describe why regulation of operons is important.
What types of regulatory molecules are there? Watch this video to learn more about the trp operon. Watch an animated tutorial about the workings of lac operon here. Think about It What affects the binding of the trp operon repressor to the operator? How and when is the behavior of the lac repressor protein altered?
In addition to being repressible, how else is the lac operon regulated? Think about It What is the name given to a collection of operons that can be regulated as a group? This video describes how epigenetic regulation controls gene expression. Think about It What stops or allows transcription to proceed when attenuation is operating? What determines the state of a riboswitch?
Describe the function of an enhancer. Describe two mechanisms of epigenetic regulation in eukaryotes. Key Concepts and Summary Gene expression is a tightly regulated process. Gene expression in prokaryotes is largely regulated at the point of transcription. Gene expression in eukaryotes is additionally regulated post-transcriptionally. Prokaryotic structural genes of related function are often organized into operons , all controlled by transcription from a single promoter.
The regulatory region of an operon includes the promoter itself and the region surrounding the promoter to which transcription factors can bind to influence transcription. Although some operons are constitutively expressed , most are subject to regulation through the use of transcription factors repressors and activators.
A repressor binds to an operator , a DNA sequence within the regulatory region between the RNA polymerase binding site in the promoter and first structural gene, thereby physically blocking transcription of these operons.
An activator binds within the regulatory region of an operon, helping RNA polymerase bind to the promoter, thereby enhancing the transcription of this operon.
An inducer influences transcription through interacting with a repressor or activator. The trp operon is a classic example of a repressible operon. When tryptophan accumulates, tryptophan binds to a repressor, which then binds to the operator, preventing further transcription. The lac operon is a classic example an inducible operon. When lactose is present in the cell, it is converted to allolactose. Allolactose acts as an inducer, binding to the repressor and preventing the repressor from binding to the operator.
This allows transcription of the structural genes. The lac operon is also subject to activation. When glucose levels are high, its presence prevents transcription of the lac operon and other operons by catabolite repression. Small intracellular molecules called alarmones are made in response to various environmental stresses, allowing bacteria to control the transcription of a group of operons, called a regulon.
Prokaryotes have regulatory mechanisms, including attenuation and the use of riboswitches , to simultaneously control the completion of transcription and translation from that transcript. There are additional points of regulation of gene expression in prokaryotes and eukaryotes. In eukaryotes, epigenetic regulation by chemical modification of DNA or histones, and regulation of RNA processing are two methods. Multiple Choice An operon of genes encoding enzymes in a biosynthetic pathway is likely to be which of the following?
An operon of genes encoding enzymes in a biosynthetic pathway is likely to be repressible. Show Answer Answer c. This type of operon is said to be constitutive. Show Answer Answer a. Lactose present and glucose absent leads to maximal expression of the lac operon.
Chemical modification of histones is a type of regulation of gene expression unique to eukaryotes. Show Answer The DNA sequence, to which repressors may bind, that lies between the promoter and the first structural gene is called the operator. Show Answer The prevention of expression of operons encoding substrate use pathways for substrates other than glucose when glucose is present is called catabolite repression.
Think about It What are two ways that bacteria can influence the transcription of multiple different operons simultaneously in response to a particular environmental condition?
0コメント