Promoter regions mRNA synthesis

The promoter has been defined as the site for initiation of mRNA synthesis [61]. It has also been shown to be the site for catabolite repression [21]. With deletion mutants 719 and 1109, deletions which we have indicated excise the araO site, the ara structural genes cis to the deletions are activated in the presence of inducer and a C allele in the trans position. This indicates that, if there is a promoter site distinct from aral, it must exist between araO and araB. Whether aral is a unique promoter site requiring modification by the activator (or one requiring an activator-modified RNA polymerase) or whether there exists a separate promoter site in this region distinct from aral is not known. This region is also required for catabolite repression (see below). 

Mutations can also alter gene expression. For example, a mutated promoter region may lose the ability to bind a repressor. Consequently, gene expression always occurs. Such a cell is often called a constitutive mutant and the gene product is constitutively expressed. Alterations in the sequence that encodes for the repressor protein could also result in constitutive expression in that the altered repressor protein can no longer bind to the promoter region and block mRNA synthesis. 

The required template is a strand of DNA, for, as it will be recalled, during the process of transcription, the genetic message from the DNA storage form is transferred to the RNA polymer (so-called mRNA). Only one of the two DNA strands serves as a template. However, a RNA primer is not required to initiate synthesis. Instead, the enzyme binds to a specific region of the DNA strand and from this point proceeds with RNA synthesis the so-called promoter region. The reaction catalyzed may be represented as follows ... 

DNA complex, while the A subunit binds to purified DNA. As a consequence of these divergent specificities, it has been proposed that the B subunit locates the specific site at which to bind to chromatin, while A may cause a conformational change in a localized region of chroma-tin-DNA, thereby providing sites for RNA polymerase to initiate mRNA synthesis. An alternate view, proposed by Yamamoto and Alberts (1976), is that binding of the receptor causes a cascade of histone acetylation, which makes the genome accessible to RNA polymerase. Perhaps the receptor, in a manner analogous to the cAMP receptor protein of prokaryotes, influences formation of an open-promoter complex with RNA polymerase (Krakow and Kumar, 1977). 

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