Genetic and biochemical basis of weed resistance to ALS-inhibiting herbicides

Abstract

Genetic and biochemical bases of resistance of weed plants to herbicides that inhibit acetolactate synthetase (ALS) are reviewed. Resistance to sulfonyl urea and imidazolinone herbicides and their new derivative products, namely triazolopyrimidin sulfoanilide, pyrimidinil oxybenzoi acid, non-aromatic imidazolinone and sulphonyl carboxiamide is discussed. The main biosynthetic pathway of amino acids with branching chains (valine, isoleucine and leucine) is shown, as well as the herbicides' mechanisms of inhibition of ALS enzyme. Mechanisms of weed resistance to ALS inhibitors are discussed from the aspects of mechanism of resistance located on the primary site of activity, mechanism of resistance based on metabolism of herbicides, mechanism of resistance based on cross-resistance located on the primary site of activity and outside the primary site. Special attention is focused on the mechanism of resistance based on multiple resistance. For all cases of developing resistance, examples are cited of instances of change and mutation on the primary site of activity in region A of the ALS gene leading to an exchange of individual amino acids within ALS molecules. Special attention is focused on natural plant tolerance to ALS inhibitors, which is attributed to herbicide metabolism, brief lif span of created intermediaries during the metabolic process and forming of conjugates with significantly reduced herbicide activity.