Effect of catabolite repression on the mer operon

Area of Science:

• Microbiology
• Molecular Biology
• Environmental Science

Background:

• The plasmid-determined mer operon confers resistance to inorganic mercury compounds.
• Catabolite repression is a regulatory mechanism affecting gene expression in bacteria.

Purpose of the Study:

• To investigate the effect of glucose-mediated catabolite repression on the expression of the mer operon.
• To determine the role of cyclic AMP (cAMP) and specific regulatory proteins in this process.
• To examine the impact of catabolite repression on both mercury uptake and mercury reductase enzyme activity.

Main Methods:

• Studied mer operon expression in wild-type and mutant strains (cya, crp) under varying conditions (glucose, HgCl2, cAMP).
• Assayed mercuric ion [Hg(II)] reductase enzyme activity in cell extracts.
• Examined the Hg(II) uptake system in a mutant strain lacking reductase activity.

Main Results:

• Glucose caused a 2.5-fold decrease in mer operon expression, which was overcome by cAMP.
• Mutants lacking adenyl cyclase (cya) or catabolite activator protein (crp) showed 1.6- to 1.9-fold decreased expression.
• Catabolite repression reduced Hg(II) reductase enzyme activity by two- to threefold but did not affect the Hg(II) uptake system.

Conclusions:

• Glucose-induced catabolite repression transiently inhibits the mer operon, with cAMP reversing this effect.
• Constitutive catabolite repression in cya or crp mutants also downregulates mer operon expression.
• The Hg(II) reductase enzyme is subject to catabolite repression, while the Hg(II) uptake system is not.