In this review, we describe a variety of mechanisms that bacteria use to regulate transcription elongation in order to control gene expression in response to changes in their environment. Together, these mechanisms are known as attenuation and antitermination, and both involve controlling the formation of a transcription terminator structure in the RNA transcript prior to a structural gene or operon. We examine attenuation and antitermination from the point of view of the different biomolecules that are used to influence the RNA structure. Attenuation of many amino acid biosynthetic operons, particularly in enteric bacteria, is controlled by ribosomes translating leader peptides. RNA-binding proteins regulate attenuation, particularly in gram-positive bacteria such as Bacillus subtilis. Transfer RNA is also used to bind to leader RNAs and influence transcription antitermination in a large number of amino acyl tRNA synthetase genes and several biosynthetic genes in gram-positive bacteria.

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Attenuation is a regulatory mechanism used in bacterial operons to ensure proper transcription and translation. In bacteria, transcription and translation are capable of proceeding simultaneously.

The need to prevent unregulated and unnecessary gene expression can be prevented by attenuation, which is characterized as a regulatory mechanism. The process of attenuation involves the presence of a stop signal that indicates premature termination.

The stop signal, referred to as the attenuator, prevents the proper function of the ribosomal complex, stopping the process. The attenuator is transcribed from the appropriate DNA sequence and its effects are dependent on the metabolic environment.

In times of need, the attenuator within the mRNA sequence will be bypassed by the ribosome and proper translation will occur. However, if there is not a need for a mRNA molecule to be translated but the process was simultaneously initiated, the attenuator will prevent further transcription and cause a premature termination. Hence, attenuators can function in either transcription-attenuation or translation-attenuation.

These RNA structures dictate whether transcription will proceed successfully or be terminated early, specifically, by causing transcription-attenuation. The result is a misfolded RNA structure where the Rho-independent terminator disrupts transcription and produced a non-functional RNA product. This characterizes the mechanisms of transcription-attenuation. The other RNA structure produced will be an anti-terminator that allows transcription to proceed. Translation-attenuation is characterized by the sequestration of the Shine-Dalgarno sequence , which is a bacterial specific sequence that indicates the site for ribosomal binding to allow for proper translation to occur.

However, in translation-attenuation, the attenuation mechanism results in the Shine-Dalgarno sequence forming as a hairpin-loop structure. The formation of this hairpin-loop structure results in the inability of the ribosomal complexes to form and proceed with proper translation.

Hence, this specific process is referred to as translation-attenuation. Key Points Attenuators are characterized by the presence of stop signals within the DNA sequence that can result in either transcriptional- attenuation or translational-attenuation. Transcriptional-attenuation is characterized by the presence of an attenuator within the DNA sequence that results in formation of mRNA-stem loops that prevent further transcription from occurring.

The non-functional RNA produced prevents proper transcription. Translational-attenuation is characterized by the misfolding of the Shine-Dalgarno sequence. The Shine-Dalgarno sequence, responsible for ribosomal binding to allow proper translation, is inaccessible because it is folded into a hairpin-loop structure, thus, translation cannot occur.

Key Terms operons : A unit of genetic material that functions in a coordinated manner and is transcribed as one unit.


Transcription Attenuation

Metrics details. Many operons of biochemical pathways in bacterial genomes are regulated by processes called attenuation and antitermination. Though the specific mechanism can be quite different, attenuation and antitermination in these operons have in common the termination of transcription by a RNA 'terminator' fold upstream of the first gene in the operon. In the past, detecting regulation by attenuation or antitermination has often been a long process of experimental trial and error, on a case by case basis. We report here the prediction of over upstream regions of genes with attenuation or antitermination regulation structures in the completed genomes of Bacillis subtilis and Escherichia coli for which extensive experimental studies have been done on attenuation and antitermination regulation. These predictions are based on a computational method devised from characteristics of known terminator fold candidates and benchmark regions of entire genomes.



Antitermination is the prokaryotic cell's aid to fix premature termination of RNA synthesis during the transcription of RNA. It occurs when the RNA polymerase ignores the termination signal and continues elongating its transcript until a second signal is reached. Antitermination provides a mechanism whereby one or more genes at the end of an operon can be switched either on or off, depending on the polymerase either recognizing or not recognizing the termination signal. Antitermination is used by some phages to regulate progression from one stage of gene expression to the next. The lambda gene N, codes for an antitermination protein pN that is necessary to allow RNA polymerase to read through the terminators located at the ends of the immediate early genes.

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