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The production of complex mixtures of secondary metabolites is a ubiquitous feature of plants. Several evolutionary hypotheses seek to explain how phytochemical diversity is maintained, including the synergy hypothesis, the interaction diversity hypothesis, and the screening hypothesis. We experimentally tested a set of predictions derived from these hypotheses by manipulating the richness and structural diversity of phenolic metabolites in the diets of eight plant consumers. Across 3940 total bioassays, there was clear support for the interaction diversity hypothesis over the synergy or screening hypotheses. The number of consumers affected by a particular phenolic composition increased with increasing richness and structural diversity of compounds. Furthermore, the bioactivity of phenolics was consumer-specific. All compounds tested reduced the performance of at least one consumer, but no compounds affected all consumers. These results show how phytochemical diversity may be maintained in nature by a complex selective landscape exerted by diverse communities of plant consumers.

Plants can alter nutritional availability, structure, and chemistry of the soil they grow in. These soil changes can positively or negatively influence the growth and metabolism of other plants that co-occur or grow later in the conditioned soil. Plant-soil feedbacks could affect community interactions and dynamics but also be applied in sustainable agriculture to promote plant growth and resistance to pests. In this study, we use a maize companion cropping system, commonly known as "push-pull," as a model to investigate soil-mediated effects of functional biodiversity, on maize plant growth, and resistance against insect herbivores. We grew maize in soils collected from push-pull (polyculture) and non-push-pull (monoculture) fields. We evaluated maize performance by measuring plant growth, as well as resistance traits (herbivore oviposition and larval feeding, production of defense-related volatile, and non-volatile secondary defense metabolites). Maize plants grown in soil conditioned by push-pull companion cropping had a higher growth rate compared to those grown in soil from non-push-pull monoculture fields. In addition, soil from push-pull fields induced a constitutively higher and qualitatively different emission of volatile organic compounds than soil from non-push-pull fields. Moreover, secondary defense metabolites such as 2,4-dihydroxy-7-methoxy-2H-1,4-benzoxazin-3(4H)-one (DIMBOA), were produced in larger quantities in plants grown in soil from push-pull fields compared to those from monoculture fields. These soil-mediated alterations in plant secondary metabolism were associated with reduced herbivory by larvae of the stemboring pest Chilo partelllus. This study provides novel evidence that plant-soil feedbacks can affect plant metabolism, growth, and resistance to pests. The observed soil-mediated effects on maize plant secondary metabolism can be viewed as emergent properties of plant community composition as well as a potent mechanism of associational resistance. In addition, these soil-conditioning effects provide a novel pest control mechanism of push-pull companion cropping.

We have studied a series of human acetyl-CoA carboxylase (ACC) 1 and ACC2 proteins with deletions and/or Ser to Ala substitutions of the known phosphorylation sites. In vitro dephosphorylation/phosphorylation experiments reveal a substantial level of phosphorylation of human ACCs produced in insect cells. Our results are consistent with AMPK phosphorylation of Ser , Ser , Ser , and Ser . Phosphorylation of the N-terminal regulatory domain decreases ACC1 activity, while phosphorylation of residues in the ACC central domain has no effect. Inhibition of the activity by phosphorylation is significantly more profound at citrate concentrations below 2 mm. Furthermore, deletion of the N-terminal domain facilitates structural changes induced by citrate, including conversion of ACC dimers to linear polymers. We have also identified ACC2 amino acid mutations affecting specific inhibition of the isozyme by compound CD-017-0191. They form two clusters separated by 60-90 Å: one located in the vicinity of the BC active site and the other one in the vicinity of the ACC1 phosphorylation sites in the central domain, suggesting a contribution of the interface of two ACC dimers in the polymer to the inhibitor binding site.

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