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Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.

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At least 397 records · Page 22
All sourcesNASA NTRSDOE OSTI
DOE OSTI2022

The Impact of Cell Wall Feruloylation on Plant Growth, Responses to Environmental Stress, Plant Pathogens and Cell Wall Degradability

This article summarizes evolving concepts and scientific findings on cell wall feruloylation and ferulate oxidative coupling processes in grasses, and the effects these have on the wide range of cell wall properties and consequent plant responses to biotic and abiotic stress and tissue degradability. Updates of the different strategies that have been applied to genetically modifying cell wall feruloylation are presented. Special emphasis is given to the modification of cell wall feruloylation by heterologous expression of cell wall ferulic acid esterase, as this strategy has provided insights into the impact of feruloylation on the changes in the physicochemical properties of the cell wall with consequent effects on different plant processes. Emerging feruloyl transferase candidate genes codifying enzymes accounting for ferulate incorporation into grass arabinoxylans are also highlighted.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2019

Splicing dysregulation contributes to the pathogenicity of several F9 exonic point variants

Abstract Background Pre‐mRNA splicing is a complex process requiring the identification of donor site, acceptor site, and branch point site with an adjacent polypyrimidine tract sequence. Splicing is regulated by splicing regulatory elements (SREs) with both enhancer and suppressor functions. Variants located in exonic regions can impact splicing through dysregulation of native splice sites, SREs, and cryptic splice site activation. While splicing dysregulation is considered primary disease‐inducing mechanism of synonymous variants, its contribution toward disease phenotype of non‐synonymous variants is underappreciated. Methods In this study, we analyzed 415 disease‐causing and 120 neutral F9 exonic point variants including both synonymous and non‐synonymous for their effect on splicing using a series of in silico splice site prediction tools, SRE prediction tools, and in vitro minigene assays. Results The use of splice site and SRE prediction tools in tandem provided better prediction but were not always in agreement with the minigene assays. The net effect of splicing dysregulation caused by variants was context dependent. Minigene assays revealed that perturbed splicing can be found. Conclusion Synonymous variants primarily cause disease phenotype via splicing dysregulation while additional mechanisms such as translation rate also play an important role. Splicing dysregulation is likely to contribute to the disease phenotype of several non‐synonymous variants.

59 BASIC BIOLOGICAL SCIENCES↗
DOE OSTI2025

The structural basis for the broad aldehyde specificity of the aminoaldehyde dehydrogenase PauC from the human pathogen Pseudomonas aeruginosa

Abstract Despite significant differences in size and formal charge, the aldehyde dehydrogenasePaPauC (PA5312) fromPseudomonas aeruginosaPAO1 efficiently catalyzes the NAD + ‐dependent oxidation of the aminoaldehydes formed in polyamines degradation. We report here thatPaPauC also oxidizes 4‐guanidinebutyraldehyde, formed in one arginine degradation pathway, trimethylaminobutyraldehyde, of unknown metabolic origin, and indole‐3‐acetaldehyde, a precursor of the plant growth‐promoting hormone indoleacetic acid.PaPauC has been proposed as a potential target for combatingP. aeruginosa. However, understanding its structure–function relationships, crucial for developing specific inhibitors, is lacking. Using X‐ray crystallography, we identified the structural characteristics that determinePaPauC broad aldehyde specificity: a spacious aldehyde‐entrance tunnel and six active‐site residues. Docking simulations, site‐directed mutagenesis, and kinetic analyses support the interactions of Lys479 with glutamylated aminoaldehydes; Phe169, Trp176, and Phe467 with amino and guanidinium groups through cation–π interactions and with the indole group via NH–π and CH–π interactions; Asp459 with amino and indole groups; and Thr303 with amide and guanidinium groups. Exploiting the distinctive structural features of thePaPauC active site could aid in developing specific inhibitors to combatP. aeruginosainfections in humans and animals, as well as in preventing its colonization of plants, which are abundantP. aeruginosareservoirs and, therefore, a significant source of human infections.

Biochemistry & Molecular Biology↗
DOE OSTI2019

Bxy‐fuca encoding α‐L‐fucosidase plays crucial roles in development and reproduction of the pathogenic pinewood nematode, Bursaphelenchus xylophilus

Abstract BACKGROUND The pine wood nematode (PWN) Bursaphelenchus xylophilus is the causal agent of pine wilt disease (PWD). This disease is a serious threat to pine forests globally. The fuca gene encodes α‐L‐fucosidase, which plays crucial roles in numerous biological and pathological processes in bacteria, fungi, plants and animals. To find promising control strategies against PWD, we investigated the expression and functions of Bxy‐fuca in B. xylophilus . RESULTS Bxy‐fuca encoding α‐L‐fucosidase is highly conserved within the deduced functional domains and key residues. It is expressed continuously across all developmental stages of B. xylophilus . mRNA in situ hybridization demonstrated that Bxy‐fuca was mainly localized in the body wall muscles and intestine. RNA interference indicated that the zygotic expression of Bxy‐fuca was indispensable for embryogenesis. The rate of B. xylophilus egg hatch was significantly decreased after Bxy‐fuca was interfered. Postembryonic silence of Bxy‐fuca resulted in a dramatic decrease in the longevity of and the total number of eggs produced by B. xylophilus . In addition, the motility of the nematode was greatly hampered with a significant drop in head thrashing frequency. CONCLUSION Bxy‐fuca plays crucial roles in development, lifespan and reproduction of B. xylophilus . Our results provide promising hints for control of PWD by blocking embryogenesis and ontogenesis, decreasing nematode fecundity, and disrupting the connection between B. xylophilus and its vector beetle by preventing nematode movement into the tracheal system. © 2019 Society of Chemical Industry

Tang, Jia↗
DOE OSTI2017

Pathogenic implications of distinct patterns of iron and zinc in chronic MS lesions

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) in which oligodendrocytes, the CNS cells that stain most robustly for iron and myelin are the targets of injury. Metals are essential for normal CNS functioning, and metal imbalances have been linked to demyelination and neurodegeneration. Using a multidisciplinary approach involving synchrotron techniques, iron histochemistry and immunohistochemistry, we compared the distribution and quantification of iron and zinc in MS lesions to the surrounding normal appearing and periplaque white matter, and assessed the involvement of these metals in MS lesion pathogenesis. We found that the distribution of iron and zinc is heterogeneous in MS plaques, and with few remarkable exceptions they do not accumulate in chronic MS lesions. We show that brain iron tends to decrease with increasing age and disease duration of MS patients; reactive astrocytes organized in large astrogliotic areas in a subset of smoldering and inactive plaques accumulate iron and safely store it in ferritin; a subset of smoldering lesions do not contain a rim of iron-loaded macrophages/microglia; and the iron content of shadow plaques varies with the stage of remyelination. Zinc in MS lesions was generally decreased, paralleling myelin loss. Iron accumulates concentrically in a subset of chronic inactive lesions suggesting that not all iron rims around MS lesions equate with smoldering plaques. Furthermore, upon degeneration of iron-loaded microglia/macrophages, astrocytes may form an additional protective barrier that may prevent iron-induced oxidative damage.

59 BASIC BIOLOGICAL SCIENCES↗