Herbicide-binding Sites Revealed in the Structure of Plant Acetohydroxyacid Synthase

The sulfonylureas and imidazolinones are potent commercial herbicide families. They are among the most popular choices for farmers worldwide, because they are nontoxic to animals and highly selective. These herbicides inhibit branched-chain amino acid biosynthesis in plants by targeting acetohydroxyacid synthase (AHAS, EC 2.2.1.6). This report describes the 3D structure of Arabidopsis thaliana AHAS in complex with five sulfonylureas (to 2.5 angstrom resolution) and with the imidazolinone, imazaquin (IQ; 2.8 angstrom). Neither class of molecule has a structure that mimics the substrates for the enzyme, but both inhibit by blocking a channel through which access to the active site is gained. The sulfonylureas approach within 5 angstrom of the catalytic center, which is the C2 atom of the cofactor thiamin diphosphate, whereas IQ is at least 7 angstrom from this atom. Ten of the amino acid residues that bind the sulfonylureas also bind IQ. Six additional residues interact only with the sulfonylureas, whereas there are two residues that bind IQ but not the sulfonylureas. Thus, the two classes of inhibitor occupy partially overlapping sites but adopt different modes of binding. The increasing emergence of resistant weeds due to the appearance of mutations that interfere with the inhibition of AHAS is now a worldwide problem. The structures described here provide a rational molecular basis for understanding these mutations, thus allowing more sophisticated AHAS inhibitors to be developed. There is no previously described structure for any plant protein in complex with a commercial herbicide.

Heterotrimeric G proteins facilitate Arabidopsis resistance to necrotrophic pathogens and are involved in jasmonate signaling

Heterotrimeric G proteinshave been previously linked to plant defense; however a role for the G beta gamma dimer in defense signaling has not been described to date. Using available Arabidopsis (Arabidopsis thaliana) mutants lacking functional G alpha or G beta subunits, we show that defense against the necrotrophic pathogens Alternaria brassicicola and Fusarium oxysporum is impaired in G beta- deficient mutants while G alpha-deficient mutants show slightly increased resistance compared to wild-type Columbia ecotype plants. In contrast, responses to virulent (DC3000) and avirulent (JL1065) strains of Pseudomonas syringae appear to be independent of heterotrimeric G proteins. The induction of a number of defense-related genes in G beta-deficient mutants were severely reduced in response to A. brassicicola infection. In addition, G beta-deficient mutants exhibit decreased sensitivity to a number of methyl jasmonate- induced responses such as induction of the plant defensin gene PDF1.2, inhibition of root elongation, seed germination, and growth of plants in sublethal concentrations of methyl jasmonate. In all cases, the behavior of the G alpha- deficient mutants is coherent with the classic heterotrimeric mechanism of action, indicating that jasmonic acid signaling is influenced by the Gbg functional subunit but not by G alpha. We hypothesize that G beta gamma acts as a direct or indirect enhancer of the jasmonate signaling pathway in plants.

Summer dormancy in perennial temperate grasses

Background and Aims Dormancy has been extensively studied in plants which experience severe winter conditions but much less so in perennial herbaceous plants that must survive summer drought. This paper reviews the current knowledge on summer dormancy in both native and cultivated perennial temperate grasses originating from the Mediterranean Basin, and presents a unified terminology to describe this trait. Scope Under severe drought, it is difficult to separate the responses by which plants avoid and tolerate dehydration from those associated with the expression of summer dormancy. Consequently, this type of endogenous (endo-) dormancy can be tested only in plants that are not subjected to moisture deficit. Summer dormancy can be defined by four criteria, one of which is considered optional: (1) reduction or cessation of leaf production and expansion; (2) senescence of mature foliage; (3) dehydration of surviving organs; and (4, optional) formation of resting organs. The proposed terminology recognizes two levels of summer dormancy: (a) complete dormancy, when cessation of growth is associated with full senescence of foliage and induced dehydration of leaf bases; and (b) incomplete dormancy, when leaf growth is partially inhibited and is associated with moderate levels of foliage senescence. Summer dormancy is expressed under increasing photoperiod and temperature. It is under hormonal control and usually associated with flowering and a reduction in metabolic activity in meristematic tissues. Dehydration tolerance and dormancy are independent phenomena and differ from the adaptations of resurrection plants. Conclusions Summer dormancy has been correlated with superior survival after severe and repeated summer drought in a large range of perennial grasses. In the face of increasing aridity, this trait could be used in the development of cultivars that are able to meet agronomic and environmental goals. It is therefore important to have a better understanding of the genetic and environmental control of summer dormancy.