Modern American populism: Analyzing the economics behind the Silent Majority, the Tea Party and Trumpism

This article researches populism, more specifically, Modern American Populism (MAP), constructed of white, rural, and economically oppressed reactionarianism, which was borne out of the political upheaval of the 1960’s Civil Rights movement. The research looks to explain the causes of populism and what leads voters to support populist movements and politicians. The research focuses on economic anxiety as the main cause but also examines an alternative theory of racial resentment. In an effort to answer the question, what causes populist movements and motivations, I apply a research approach that utilizes qualitative and quantitative methods. There is an examination of literature that defines populism, its causes and a detailed discussion of the case studies, including the 1972 election of Richard Nixon; the Tea Party election of 2010; and the 2016 election of Donald Trump. In addition, statistical data analysis was run using American National Election Studies (ANES) surveys associated with each specific case study. These case studies were chosen because they most represent forms of populist movements in modern American history. While ample qualitative evidence suggested support for the hypothesis that economic anxiety is a necessary condition for populist voting patterns that elected Nixon, the Tea Party and Trump, the statistical data only supported the hypothesis in two cases, 2010 and 2016, with 1972 coming back inconclusive. The data also suggested that both economic anxiety and racial resentment played a role in 2010 and 2016, while having no significant effect in 1972 in either case. This suggests that further research needs to be conducted into additional populist case studies, as well as an examination into the role economic anxiety and economic crises play on racial resentment and racially motivated voting behavior

Deletion Analysis of \u3ci\u3eFUM\u3c/i\u3e Genes Involved in Tricarballylic Ester Formation during Fumonisin Biosynthesis

Fumonisins are carcinogenic mycotoxins produced by the maize ear rot pathogen Gibberella moniliformis (anamorph Fusarium verticillioides). These toxins consist of a linear polyketide-derived backbone substituted at various positions with an amine, one to four hydroxyl, two methyl, and two tricarballylic ester functions. In this study, we generated and characterized deletion mutants of G. moniliformis for five genes, FUM7, FUM10, FUM11, FUM14, and FUM16 in the fumonisin biosynthetic gene cluster. Functional analysis of mutants in four genes, predicted to encode unrelated proteins, affected formation of the tricarballylic esters. FUM7 deletion mutants produced a previously undescribed homologue of fumonisin B1 with an alkene function in both tricarballylic esters, FUM10 and FUM14 deletion mutants produced homologues of fumonisin B3 and fumonisin B4 that lack tricarballylic ester functions, and FUM11 deletion mutants produced fumonisins that lack one of the tricarballylic ester functions. These phenotypes indicated specific roles for FUM7, FUM10, FUM11, and FUM14 in fumonisin biosynthesis that are consistent with the predicted proteins encoded by each gene. Deletion of FUM16 had no apparent effect on fumonisin production. The phenotypes of the deletion mutants provide further insight into the order of steps in fumonisin biosynthesis

\u3ci\u3eFUM13\u3c/i\u3e Encodes a Short Chain Dehydrogenase/Reductase Required for C-3 Carbonyl Reduction during Fumonisin Biosynthesis in \u3ci\u3eGibberella moniliformis\u3c/i\u3e

Fumonisins are polyketide-derived mycotoxins produced by the filamentous fungus Gibberella moniliformis (anamorph Fusarium verticillioides). Wild-type strains of the fungus produce predominantly four B-series fumonisins, designated FB1, FB2, FB3, and FB4. Recently, a cluster of 15 putative fumonisin biosynthetic genes (FUM) was described in G. moniliformis. We have now conducted a functional analysis of FUM13, a gene in the cluster that is predicted by amino acid sequence similarity to encode a short chain dehydrogenase/reductase (SDR). Mass spectrometric analysis of metabolites from FUM13 deletion mutants revealed that they produce approximately 10% of wild-type levels of B-series fumonisins as well as two previously uncharacterized compounds. NMR analysis revealed that the new compounds are similar in structure to FB3 and FB4 but that they have a carbonyl function rather than a hydroxyl function at carbon atom 3 (C-3). These results indicate that the FUM13 protein catalyzes the reduction of the C-3 carbonyl to a hydroxyl group and are the first biochemical evidence directly linking a FUM gene to a specific reaction during fumonisin biosynthesis. The production of low levels of FB1, FB2, FB3, and FB4, which have a C-3 hydroxyl, by the FUM13 mutants suggests that G. moniliformis has an additional C-3 carbonyl reductase activity but that this enzyme functions less efficiently than the FUM13 protein

\u3ci\u3eFUM9\u3c/i\u3e Is Required for C-5 Hydroxylation of Fumonisins and Complements the Meitotically Defined \u3ci\u3eFum3\u3c/i\u3e Locus in \u3ci\u3eGibberella moniliformis\u3c/i\u3e

Deletion of the Gibberella moniliformis FUM9 gene resulted in mutants that produce only fumonisins that lack a C-5 hydroxyl group. This phenotype is identical to that of previously described mutants with defective alleles at the meiotically defined Fum3 locus. Transformation with a wild-type FUM9 gene into a Fum3- defective mutant restored wild-type fumonisin production. These results indicate that the FUM9 protein catalyzes the C-5 hydroxylation of fumonisins and that FUM9 and the Fum3 locus are the same gene

Fumonisin B (1)-nonproducing strains of Fusarium verticillioides cause maize (Zea mays) ear infection and ear

Fumonisins are polyketide mycotoxins produced by Fusarium verticillioides (synonym F. moniliforme), a major pathogen of maize (Zea mays) worldwide. Most field strains produce high levels of fumonisin B 1 (FB 1 ) and low levels of the less-oxygenated homologues FB 2 and FB 3 , but fumonisin B 1 -nonproducing field strains have been obtained by natural variation. To test the role of various fumonisins in pathogenesis on maize under field conditions, one strain producing FB 1 , FB 2 , and FB 3 , one strain producing only FB 2 , one strain producing only FB 3 , and one fumonisin-nonproducing strain were applied to ears via the silk channel and on seeds at planting. Disease severity on the harvested ears was evaluated by visible symptoms and by weight percent symptomatic kernels. Fumonisin levels in kernels were determined by high-performance liquid chromatography. The presence of the applied FB 1 -nonproducing strains in kernels was determined by analysis of recovered strains for fumonisin production and other traits. All three FB 1 -nonproducing strains were able to infect ears following either silk-channel application or seed application at planting and were as effective as the FB 1 -producing strain in causing ear rot following silk-channel application. These results indicate that production of FB 1 , FB 2 , or FB 3 is not required for F. verticillioides to cause maize ear infection and ear rot