The metal response element is present in multiple copies in genes, such as the metallothionein genes, whose transcription is increased in response to treatment of cells with metals like zinc, copper, cadmium, and lead (1, 2). The metallothionein proteins are cysteine -rich metal-binding proteins that play a critical role in protecting cells from metal toxicity. Hence, increased levels of potentially toxic metals lead to enhanced transcription of the metallothionein genes. Inspection of the regulatory regions of the metallothionein genes reveals that they contain multiple copies of a 13- to 15-bp element with the consensus sequence 
where R = purine and N = any base. The core sequence of this motif (underlined above) is essential for the ability of the metallothionein gene to respond to metals. Thus mutagenesis of this sequence destroys the metal responsiveness of the metallothionein gene (3), while individual elements of this sequence can confer metal responsiveness upon a gene that is not normally induced in response to this treatment (4).
This element is thus a metal response element (MRE), which allows the transcription of specific genes to be activated in response to metals (see Response Element).
