Evaluation of Foliar Insecticides for the Control of Western Bean Cutworm in Field Corn, 2016

The western bean cutworm (WBC) is an important pest of corn and dry beans. In addition to yield loss due to direct feeding on developing kernels in the ear, WBC infestation can also lead to secondary fungal infections. This study was conducted within the historic range of WBC in western Nebraska; however, it has undergone a rapid range expansion into the eastern Corn Belt within the last 16 years. This field trial was established to evaluate the efficacy of a single application of foliar insecticides against this pest to prevent feeding damage to non-Bt corn ears. The trial was located at the University of Nebraska-Lincoln’s Stumpf International Wheat Center in Perkins County, Nebraska, USA (40.856805° N, –101.701594° W). A RCB design with 10 treatments (including an untreated check) and 4 replications was used. Each plot was eight rows by 35 ft. The trial was planted on 13 May using a small plot research planter at 32,000 seeds/acre at an approximate depth of 1.4– 1.75 inch in 30 inch rows. The hybrid planted was DKC62-95 (Monsanto Company, St. Louis, MO) non-Bt with RR2 herbicide tolerance. The plots received irrigation, fertilization, and weed management inputs following standard agronomic practices for the region, with no insecticide applications other than the experimental treatments

GERMLINE GAIN-OF-FUNCTION MUTATIONS of ALK DISRUPT CENTRAL NERVOUS SYSTEM DEVELOPMENT

International audienceNeuroblastoma (NB) is a frequent embryonal tumour of sympathetic ganglia and adrenals with extremely variable outcome. Recently, somatic amplification and gain-of-function mutations of the anaplastic lymphoma receptor tyrosine kinase (ALK, MIM 105590) gene, either somatic or germline, were identified in a significant proportion of NB cases. Here we report a novel syndromic presentation associating congenital NB with severe encephalopathy and abnormal shape of the brainstem on brain MRI in two unrelated sporadic cases harbouring de novo, germline, heterozygous ALK gene mutations. Both mutations are gain-of-function mutations that have been reported in NB and NB cell lines. These observations further illustrate the role of oncogenes in both tumour predisposition and normal development, and shed light on the pleiotropic and activity-dependent role of ALK in humans. More generally, missing germline mutations relative to the spectrum of somatic mutations reported for a given oncogene may be a reflection of severe effects during embryonic development, and may prompt mutation screening in patients with extreme phenotypes

Mutations in the Mitochondrial Methionyl-tRNA Synthetase Cause a Neurodegenerative Phenotype in Flies and a Recessive Ataxia (ARSAL) in Humans

The study of Drosophila neurodegenerative mutants combined with genetic and biochemical analyses lead to the identification of multiple complex mutations in 60 patients with a novel form of ataxia/leukoencephalopathy

Performance of Seed Treatments and in-Furrow at-Plant Insecticides for Protection Against Cry3Bb1-Resistant Western Corn Rootworm, 2015

The western corn rootworm is an important pest of corn that can compromise yield by feeding on plant roots during its larval stage. WCRW management has been complicated by the development of resistance in some regions, including Nebraska, to transgenic Bacillus thuringiensis (Bt) traits, particularly the protein Cry3Bb1, which confers cross-resistance to mCry3A. A field trial was established to evaluate the efficacy of neonicotinoid seed treatments in combination with in-furrow insecticides on a corn hybrid expressing mCry3A Bt proteins against corn rootworm in an area with a history of rootworm resistance. The trial was conducted in a farmer’s field in Keith County near Ogallala, Nebraska, USA (41.116736° N, –101.652410° W), between 8 Jun and 6 Oct 2015. Damage from WCRW to corn expressing Cry3Bb1 proteins was documented in the field during the previous season

Identification de gènes responsables de déficits de synthèse de l ubiquinone chez l homme

ORSAY-PARIS 11-BU Sciences (914712101) / SudocSudocFranceF

Prenyldiphosphate synthase, subunit 1 (PDSS1) and OH-benzoate polyprenyltransferase (COQ2) mutations in ubiquinone deficiency and oxidative phosphorylation disorders

Coenzyme Q(10) (CoQ(10)) plays a pivotal role in oxidative phosphorylation (OXPHOS), as it distributes electrons among the various dehydrogenases and the cytochrome segments of the respiratory chain. We have identified 2 novel inborn errors of CoQ(10) biosynthesis in 2 distinct families. In both cases, enzymologic studies showed that quinone-dependent OXPHOS activities were in the range of the lowest control values, while OXPHOS enzyme activities were normal. CoQ(10) deficiency was confirmed by restoration of normal OXPHOS activities after addition of quinone. A genome-wide search for homozygosity in family 1 identified a region of chromosome 10 encompassing the gene prenyldiphosphate synthase, subunit 1 (PDSS1), which encodes the human ortholog of the yeast COQ1 gene, a key enzyme of CoQ(10) synthesis. Sequencing of PDSS1 identified a homozygous nucleotide substitution modifying a conserved amino acid of the protein (D308E). In the second family, direct sequencing of OH-benzoate polyprenyltransferase (COQ2), the human ortholog of the yeast COQ2 gene, identified a single base pair frameshift deletion resulting in a premature stop codon (c.1198delT, N401fsX415). Transformation of yeast Δcoq1 and Δcoq2 strains by mutant yeast COQ1 and mutant human COQ2 genes, respectively, resulted in defective growth on respiratory medium, indicating that these mutations are indeed the cause of OXPHOS deficiency

In vivo vitiligo induction and therapy model: double-blind, randomized clinical trial

In this study, we developed an in vivo vitiligo induction model to explore the underlying mechanisms leading to Koebner's phenomenon and to evaluate the efficacy of therapeutic strategies. The model consisted of 12 pigmented test regions on the back of generalized vitiligo patients that were exposed to three Koebner induction methods: cryotherapy, 755 nm laser therapy, and epidermal abrasion. In addition, four cream treatments (pimecrolimus, tacrolimus, steroid and placebo) were randomly applied. Koebnerization was efficiently induced by all three induction methods. In general, cryotherapy was the best method of Koebner induction, followed by 755 nm laser therapy and epidermal abrasion. Reproducible results were obtained, which showed enhanced depigmented surface areas and higher amounts of T lymphocytes in placebo-treated test zones compared to active treated areas. Tacrolimus and local steroids were better inhibitors of Koebner's process (P < 0.05) compared to pimecrolimus. Our in vivo vitiligo induction model is very informative to investigate vitiligo induction and to determine the efficacy of topical treatments in vitiligo. This proof of concept confirms the efficient comparison of head-to-head therapeutic strategies intra-individually in a standardized, specific and better timed way

AtPME3, a ubiquitous cell wall pectin methylesterase of Arabidopsis thaliana, alters the metabolism of cruciferin seed storage proteins during post-germinative growth of seedlings

International audienc

CABC1 Gene Mutations Cause Ubiquinone Deficiency with Cerebellar Ataxia and Seizures

Coenzyme Q10 (CoQ10) plays a pivotal role in oxidative phosphorylation (OXPHOS) in that it distributes electrons between the various dehydrogenases and the cytochrome segments of the respiratory chain. Primary coenzyme Q10 deficiency represents a clinically heterogeneous condition suggestive of genetic heterogeneity, and several disease genes have been previously identified. The CABC1 gene, also called COQ8 or ADCK3, is the human homolog of the yeast ABC1/COQ8 gene, one of the numerous genes involved in the ubiquinone biosynthesis pathway. The exact function of the Abc1/Coq8 protein is as yet unknown, but this protein is classified as a putative protein kinase. We report here CABC1 gene mutations in four ubiquinone-deficient patients in three distinct families. These patients presented a similar progressive neurological disorder with cerebellar atrophy and seizures. In all cases, enzymological studies pointed to ubiquinone deficiency. CoQ10 deficiency was confirmed by decreased content of ubiquinone in muscle. Various missense mutations (R213W, G272V, G272D, and E551K) modifying highly conserved amino acids of the protein and a 1 bp frameshift insertion c.[1812_1813insG] were identified. The missense mutations were introduced into the yeast ABC1/COQ8 gene and expressed in a Saccharomyces cerevisiae strain in which the ABC1/COQ8 gene was deleted. All the missense mutations resulted in a respiratory phenotype with no or decreased growth on glycerol medium and a severe reduction in ubiquinone synthesis, demonstrating that these mutations alter the protein function