Comparative analysis of phytochemicals and polar metabolites from colored sweet potato (Ipomoea batatas L.) tubers.

We determined the phytochemical diversity, including carotenoids, flavonoids, anthocyanins, and phenolic acids, in sweet potatoes (Ipomoea batatas L.) with distinctive flesh colors (white, orange, and purple) and identified hydrophilic primary metabolites. Carotenoid content was considerably higher in orange-fleshed sweet potatoes, wherein ß-carotene was the most plentiful, and anthocyanins were detected only in purple-fleshed sweet potatoes. The levels of phenolic acids and flavonoids were relatively higher in purple-fleshed sweet potatoes than those in the other two varieties. Forty-one primary and 18 secondary metabolite profiles were subjected to multivariate statistical analyses, which fully distinguished among the varieties and separated orange- and purple-fleshed sweet potatoes from white-fleshed sweet potatoes based on the high levels of sugars, sugar alcohols, and secondary metabolites. This is the first study to determine comprehensive metabolic differences among different color-fleshed sweet potatoes and provides useful information for genetic manipulation of sweet potatoes to influence primary and secondary metabolism.

Deinococcus cellulosilyticus sp. nov., isolated from air.

A pink-coloured bacterial strain, 5516J-15(T), was isolated from an air sample from Jeju Island, Republic of Korea. The organism was found to have resistance to UV radiation typical of members of the genus Deinococcus, and it was placed within the radiation of the Deinococcus on a phylogenetic tree based on 16S rRNA gene sequences. Strain 5516J-15(T) shared low 16S rRNA gene sequence similarity (84.5-87.8 %) with Deinococcus species, showing highest sequence similarity to Deinococcus deserti VCD115(T) (87.8 %) and Deinococcus indicus Wt/1a(T) (87.8 %). Strain 5516J-15(T) had type A3 beta peptidoglycan with l-ornithine, menaquinone 8 (MK-8) as the major quinone and iso-C(12 : 0), anteiso-C(13 : 0), iso-C(16 : 0) and C(16 : 0) as the major fatty acids. Its polar lipid profile contained three unknown aminophospholipids, two unknown polar lipids, one unknown phospholipid and one unknown glycolipid. The DNA G+C content of strain 5516J-15(T) was 61.3 mol%. Based on the phylogenetic and phenotypic data presented, it is proposed that the unknown strain should be classified within a novel species in the genus Deinococcus with the name Deinococcus cellulosilyticus sp. nov. The type strain is 5516J-15(T) (=KACC 11606(T) =DSM 18568(T)).

Editing-defective tRNA synthetase causes protein misfolding and neurodegeneration.

Misfolded proteins are associated with several pathological conditions including neurodegeneration. Although some of these abnormally folded proteins result from mutations in genes encoding disease-associated proteins (for example, repeat-expansion diseases), more general mechanisms that lead to misfolded proteins in neurons remain largely unknown. Here we demonstrate that low levels of mischarged transfer RNAs (tRNAs) can lead to an intracellular accumulation of misfolded proteins in neurons. These accumulations are accompanied by upregulation of cytoplasmic protein chaperones and by induction of the unfolded protein response. We report that the mouse sticky mutation, which causes cerebellar Purkinje cell loss and ataxia, is a missense mutation in the editing domain of the alanyl-tRNA synthetase gene that compromises the proofreading activity of this enzyme during aminoacylation of tRNAs. These findings demonstrate that disruption of translational fidelity in terminally differentiated neurons leads to the accumulation of misfolded proteins and cell death, and provide a novel mechanism underlying neurodegeneration.