Why Are sRNAs Used Everywhere?
This review, as many others, shows that RNA-mediated regulation occurs everywhere. Focusing on sRNAs, we can ask why they have been recruited into essentially all types of regulatory motifs, and why almost all global regulatory networks use transcriptional as well as posttranscriptional control. A null hypothesis might state that sRNAs can simply fill the same regulatory niches than TFs. Regulation of the same pathway in different bacteria indeed sometimes shows TF-, and sometimes RNA-mediated control. A second reason could be that two layers of control are better than one. However, we believe that this only makes sense if the properties of control differ. For instance, regulation of the trp operon in enterobacteria uses transcriptional control with the Trp repressor (TrpR), and attenuation as a second posttranscriptional mechanism. Here, TrpR uses the amino acid tryptophan as corepressor, whereas attenuation relies on sensing of the levels of Trp-tRNATrp. The combination of the two signals used in the two control layers adds information and fine-tunes regulation. For sRNAs, an attractive argument lies in the different response curves and the rapid removal of the regulator once it has done its job (Massé et al., 2003). Depending on the specific requirements of control of a give gene (or genes), a TF- or sRNA-mode may be appropriate. An important distinguishing feature between TFs and sRNA is sensitivity to transcriptional noise. TFs are bad at keeping a noise-free silent state, because transcriptional burstiness is characteristic of transcription per se in all organisms (Golding et al., 2005). Additional amplification by multiple translation events causes significant and unavoidable cell-to-cell variations in protein output. As shown above, high levels of sRNAs counteract this noise, and in particular stabilize OFF-states (Section 8). A maybe minor mechanism that is open to sRNAs, but less so to TFs, enables discoordinate regulation of genes within an operon, as exemplified by SpoT/galK(Section 4.5).
Energy arguments have sometimes been evoked but may not fly. Though it is indeed “cheaper” to make an RNA than a protein, the contribution to total energy consumption in the cell is probably negligible. Many TFs are only present in a few copies per cell and are stable, and sRNAs may be up to 1000 copies, and are consumed upon their action. So far, there are simply no data that compare growth rate effects in the two regimes.
An interesting aspect, related to evolution of sRNA–mRNA pairs, is target space. TFs have relatively few, and short, recognition sites. By contrast, there are many potential target sites that can be “selected” by sRNAs, since—as discussed above (Section 5.1)—essentially the entire mRNA can be targeted; evidence for 5′-UTR, CDS, and 3′-UTR targeting has been documented. On top of that, the outcome of regulation depends on the location of the sRNA binding site. An sRNA can bind to an RBS site to inhibit translation, and can activate translation by binding upstream (Section 5.1). Conversely, two regions within one sRNA can target two mRNAs (Lease et al., 1998). All this gives versatility and flexibility in evolving interactions that, if adaptive, may be fixed.
A further benefit might be the high rates at which sRNA/target systems can evolve—and this also applies to miRNAs. Numerous sRNAs do not branch deeply, but are present in only some bacterial relatives, or even in single isolates. This suggests that de novo evolution is easy, and gene duplications, like omrA/omrB (Section 4.2 and 4.3), ryhB-1/ryhB-2 (Section 4.1), and qrr1-4 (Section 4.7), might facilitate further diversification. Suppose that single mutations/genetic rearrangements create a (weak) promoter element that drives transcription. If the generated RNA has an adaptive phenotypic effect by matching a target, selection may fix this regulatory pair. In comparison, evolving a new TF may be more difficult (however, see Taylor et al., 2015). Both bacterial sRNAs and eukaryotic miRNAs indeed often show signs of being recently “invented” (Cuperus, Fahlgren, & Carrington, 2011). Major horizontal transfer and gene loss contribute to the patchy pattern of free sRNA genes in comparisons between bacteria (Hershberg, Altuvia, & Margalit, 2003; Peer & Margalit, 2014; Skippington & Ragan, 2012), and sRNAs can also be derived from coding genes (Section 2.3). A recent analysis in E. coli strains suggests how sRNA genes may become fixed after successive acquisition of target sequences in genes (Peer & Margalit, 2014).
Lac vs Trp Operon
Operon is a special gene alignment in prokaryotes. In one operon, it aligns all the genes needed for a specific function. This organization allows one single promoter to activate, deactivate, and regulate all the genes participating in one particular function. Due to this nature, operon is called the functional unit of prokaryotic gene expression. Lac operon and Trp operon are two operons found in E.coli bacterial genome, and in many other bacteria. These operons control different functions. Operon is the functional unit of prokaryotic gene expression.
Lac operon is the cluster of genes responsible for lactose transportation and metabolism in E.coli bacteria. The operon has one promoter region and genes lac Z, lac Y, lac A, and lac I. The operon is activated by the presence of lactose. The lac Z, lac Y, lac A produce beta galactosidase, lactose permease, and thiogalactoside transacetylase enzymes.
Permease enzyme allows lactose to come into the cell, and beta galactosidase hydrolyzes lactose to glucose and galactose. Transacetylase is used to functionalize substrates. If a more preferable substrate is present or lactose is absent, lac I gets activated. This produces an allolactose binding protein. In the presence of allolctose, the repressor protein molecules bind to allolactose molecules. This allows the transcription to continue without getting disturbed. In the absence of lactose, this protein binds to the promoter region (control unit) of the lac operon blocking and stopping gene transcription. When this happens no lactose permease or beta galactosidase are produced. Therefore, lactose catabolism is stopped.
Trp operon is also a cluster of genes controlled by a single promoter. This operon contains all the genes required for Trp synthesis. Tryptophan commonly abbreviated as Trp is an unusual amino acid. The operon consists of trp E, trp D, trp C, trp B, and trp A, which collectively code tryptophan synthetase; the enzyme which produces tryptophan.
The trp operon also contains trp R that produces a repressor when needed. In the presence of tryptophan this operon stays deactivated because the repressor changes its conformation to active form and is bound to the promoter region. In the absence of tryptophan, the repressor protein gets released from the promoter region or is in the inactive conformation, which cannot bind to the promoter region, and thereby transcription of the genes is initiated making tryptophan, as a result. Unlike the lac operon this operon is deactivated in the presence of tryptophan, this mechanism is referred to as “negative repressive feedback mechanism”.
What is the difference between Lac operon and Trp operon?
• Lac operon is involved with the catabolic process of a sugar, but Trp operon is involved in the anabolic process of an amino acid.
• Lac operon gets activated in the presence of lactose, but Trp operon gets deactivated in the presence of tryptophan.
• Lac operon consists of three structural genes and a repressor gene, but Trp operon consists of five structural genes and a repressor gene.
• Lac operon does not use “attenuation” mechanism, but Trp operon uses “attenuation” mechanism.
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Filed Under: BiologyTagged With: Lac Operon, Lactose Operon, Operon, Trp Operon, Tryptophan Operon