811 research outputs found
Combating stem and leaf rust of wheat: Historical perspective, impacts, and lessons learned
No full textmillions fed, food security, wheat rust, stem rust, leaf rust, Norman Borlaug,
Data Mining of the Coffee Rust Genome
No full textThe genomes of nine isolates of _Hemileia vastatrix_, the causal agent of coffee leaf rust were sequenced by Illumina and 454. Quality control, cleaning and _de novo_ assemblies of data were performed. Since isolates were obtained from the field and it is not possible to produce axenic cultures of _H. vastatrix_, MEGAN software was used to evaluate contamination levels and to select contigs with fungal similarities. Mitochondrial contigs were identified and annotated by comparing this assembly against the _Puccinia_ genome. Furthermore, two transcriptomes from isolates of _H. vastatrix_ were assembled to complement the genomic data
Lucile Osborn Rust, b. 1890
No full textProfessor of education, director of home economics teaching program, 1925-1960; author of several text books, Fulbright Scholar in 1952.Citation: Courtesy "Lucile Osborn Rust, b. 1890", Photograph Collection Vertical Files: People, Morse Department of Special Collections, Kansas State University Libraries.For information on how to request a high-resolution copy of this photograph, please go to the Morse Department of Special Collections webpage, Photograph and Document Image Guidelines (http://www.lib.k-state.edu/photograph-and-document-image-guidelines).Morse Department of Special Collection
Untersuchung der Funktion von KCl-Kotransportern unter Verwendung von Knock-out Mäusen
No full textRust MB. Untersuchung der Funktion von KCl-Kotransportern unter Verwendung von Knock-out Mäusen. Berlin: Mensch & Buch-Verl.; 2004
Cofilin1-dependent actin dynamics control DRP1-mediated mitochondrial fission
No full textMitochondria form highly dynamic networks in which organelles constantly fuse and divide. The relevance of mitochondrial dynamics is evident from its implication in various human pathologies, including cancer or neurodegenerative, endocrine and cardiovascular diseases. Dynamin-related protein 1 (DRP1) is a key regulator of mitochondrial fission that oligomerizes at the mitochondrial outer membrane and hydrolyzes GTP to drive mitochondrial fragmentation. Previous studies demonstrated that DRP1 recruitment and mitochondrial fission is promoted by actin polymerization at the mitochondrial surface, controlled by the actin regulatory proteins inverted formin 2 (INF2) and Spire1C. These studies suggested the requirement of additional actin regulatory activities to control DRP1-mediated mitochondrial fission. Here we show that the actin-depolymerizing protein cofilin1, but not its close homolog actin-depolymerizing factor (ADF), is required to maintain mitochondrial morphology. Deletion of cofilin1 caused mitochondrial DRP1 accumulation and fragmentation, without altering mitochondrial function or other organelles' morphology. Mitochondrial morphology in cofilin1-deficient cells was restored upon (i) re-expression of wild-type cofilin1 or a constitutively active mutant, but not of an actin-binding-deficient mutant, (ii) pharmacological destabilization of actin filaments and (iii) genetic depletion of DRP1. Our work unraveled a novel function for cofilin1-dependent actin dynamics in mitochondrial fission, and identified cofilin1 as a negative regulator of mitochondrial DRP1 activity. We conclude that cofilin1 is required for local actin dynamics at mitochondria, where it may balance INF2/Spire1C-induced actin polymerization
Inhibition of spore germination and appressorium formation of rust species by plant and fungal metabolites
No full textEight fungal and plant metabolites belonging to different classes of naturally occurring compounds, a 24-oxa[14]-cytochalasan as cytochalasin B (1), a trisubstituted isocoumarin as 6-hydroxymellein (2), a tetracyclic pimarane diterpene as sphaeropsidin A (3), a chalcone as cavoxin (4), a pentasubstituted benzofuranone as cyclopaldic acid (5), a bicyclic-sesquiterpene as inuloxin A (6), a epipolythiopiperazine as gliotoxin (7) and a cyclohexene epoxide as epiepoformin (8), were tested for their effectiveness in reducing early stages of development of several major rust fungi from the genera Puccinia and Uromyces. Spore germination and appressoria formation were assessed on pre-treated detached leaves, under controlled conditions. Among the various metabolites evaluated, compounds 5 and 8 were the most effective in inhibiting fungal germination and penetration of all rust species studied at values comparable with those obtained by fungicide application, while compound 4 was phytotoxic to plant leaves at any concentration tested
MOZART MATURES: 1780s Piano Works
No full textOn MOZART MATURES: 1780s Piano Works, pianist Roberta Rust perceptively explores Mozart’s personal artistic journey and progression from an extraordinary talent to an immortal giant of musical composition.
Largely eschewing the popular tunes, Rust instead carefully handpicked musical selections designed to showcase the composer’s structural, technical, and harmonic development. The Sonata in F Major, K. 332, with its never-ending twists and turns, makes for a great starting point. But, considering that Rust is a talented extemporizer on the piano herself, it comes as no surprise that many of the pieces on MOZART MATURES are those originally conceived as improvisations. There are the two Fantasies in D minor and C minor, but also the quirky, prescient Gigue which Mozart hastily wrote into a German friend’s friendship album. And lest things get out of hand, the calmer Adagio in B minor as well as the Rondo in A minor round off the selection with timeless depth and serenity – the particular kind achieved in history by this one singular composer.
More Author/Title Info: Wolfgang Amadeus Mozart
Physical Description: 1 online resource (1 audio file)
Performers: Roberta Rust, piano.
Credits: Session producer, Brad Michel ; session engineer, Tom Stephenson ; piano technicians, Christine Lovgren, Len Richardson ; editing, mixing & mastering, Lucas Paquette.
Event Details: Recorded July 13-15, 2021 at the Shalin Liu Performance Center, Boston MA.
Contents: Fantasy in D minor, K. 397 (6:10) -- Sonata no. 12 in F major, K. 332 -- Adagio in B minor, K. 540 (9:50) -- Eine kleine gigue in G major, K. 574 (1:38) -- Fantasy in C minor, K. 475 (13:00) -- Rondo in A minor, K. 511 (10:16)
Investigating the function of the actin-binding protein profilin1 in mouse cerebral cortex development
No full textDer dynamische Auf- und Abbau von Aktinfilamenten wird durch Aktin-bindende Proteine wie beispielsweise Profilin1 reguliert. Profilin1 reguliert dabei nicht nur die Polymerisation von Aktin-Monomeren am Aktinfilament, sondern interagiert darüber hinaus noch mit einer Vielzahl anderer Liganden. Es ist an einer Vielzahl von Prozessen im gesamten Körper beteiligt (z.B. Zellmigration, Proliferation und Apoptose) und wird mit diversen Erkrankungen wie beispielsweise vaskulärer Hypertrophie und Hypertension, Diabetes, amyotrophe Lateralsklerose und dem Fragil-X-Syndrom in Verbindung gebracht. Aufgrund der Beteiligung von Profilin1 an vielen verschiedenen Prozessen wie beispielsweise der Zellmigration und Proliferation, welche für die Entwicklung des Gehirns von entscheidender Bedeutung sind, wurde für Profilin1 eine wichtige Rolle im Zusammenhang mit einer gesunden Gehirnentwicklung postuliert. Untersuchungen an gehirnspezifischen Profilin1 Knock-out Mäusen konnten zeigen, dass die gehirnspezifische Deletion von Profilin1 in Mäusen zu einer Hypoplasie des Cerebellums führt, welche mit einer anormalen Schichtung des cerebellaren Kortex einhergeht. Ebenfalls auffällig war eine verringerte Größe des Neokortex, eine „partielle“ reaktive Astrogliose, sowie Einfaltungen der zerebralen Kortexoberfläche.
Die Charakterisierung dieser Einfaltungen des nativ lissencephalen Gehirns der Mäuse und die Untersuchung ihrer möglichen Ursachen sowie die nähere Analyse der reaktiven Astrogliose bildeten dabei die Zielsetzung dieser Arbeit.
Innerhalb dieser Arbeit konnte herausgestellt werden, dass die gehirnspezifische Deletion von Profilin1 in Mäusen zum Hochpunkt der Neurogenese zu einem transienten Anstieg der Anzahl bRG (basaler Radialgliazellen) und zu fehllokalisierten bIP (basalen intermediären Vorläuferzellen) führte. Ausgelöst wurde diese Anomalie durch eine Verschiebung der Teilungsebene mitotischer aRG (apikaler Radialgliazellen) hin zu mehr horizontalen Teilungen. Die Verschiebung der Teilungsebene konnte auf eine verringerte Verankerung der Mitosespindel am Zellkortex zurückgeführt werden, welche sich aus einer deutlichen Verringerung des subkortikalen F-Aktin-Anteils im Aktin-Kortex der mitotischen aRG ergab.
Die erhöhte Anzahl der bRG und eine gesteigerte Mitoserate der fehllokalisierten IP führten wiederum zu einer transient erhöhten Produktion von Neuronen. In Verbindung mit der vermehrten Anzahl von Astrozyten in Schicht I des zerebralen Kortex der adulten Profilin1-defizienten Mäuse lag die Vermutung nahe, dass die Einfaltungen der zerebralen Kortexoberfläche auf eine vermehrte Festigkeit einzelner Zellschichten zurückzuführen ist.
Des Weiteren konnte innerhalb dieser Arbeit die vereinzelte Proliferation reaktiver Astrozyten in den adulten Profilin1-defizienten Mäusen nachgewiesen werden, was für eine „vollständige“ reaktive Astrogliose sprach. Andere Studien legen nahe, dass die Deletion von Profilin1 sogar direkt für die Reaktivierung von Mikroglia und Astrozyten verantwortlich sein könnte.
Die vorliegende Arbeit verdeutlicht den Stellenwert von Profilin1 für die korrekte Ausrichtung der Mitosespindel in murinen aRG und liefert starke Hinweise für die Bedeutung von Profilin1 für eine natürliche Homöostase in Gliazellen. Weitere dahin gehende Untersuchungen könnten neue Erkenntnisse in Bezug auf die Entstehung und das Fortschreiten von neurodegenerativen Erkrankungen wie Polymikrogyrie, Lissencephalie oder ALS bringen.The dynamic polymerization and depolymerization of actin filaments is regulated by actin-binding proteins such as profilin1. Profilin1 not only regulates the polymerization of actin monomers on the actin filament, but also interacts with a large number of other ligands. It is involved in a variety of processes throughout the body (e. g. cell migration, proliferation and apoptosis) and has been associated with various diseases such as vascular hypertrophy and hypertension, diabetes, amyotrophic lateral sclerosis, and fragile-x-syndrome. Due to the involvement of profilin1 in many different processes such as cell migration and proliferation, it has been postulated to play an important role in healthy brain development.
Previous studies on brain-specific profilin1 knock-out mice were able to show that the brain-specific deletion of profilin1 in mice leads to hypoplasia of the cerebellum, which is associated with abnormal stratification of the cerebellar cortex. Also striking were a reduced size of the neocortex, a “partial” reactive astrogliosis and folds of the cerebral cortex. The characterization of these folds and the investigation of their possible causes as well as the closer analysis of the reactive astrogliosis formed the aim of this work.
The present dissertation showed that the brain-specific deletion of profilin1 leads to a transient increase in the number of bRG (basal radial glia cells) and to mislocated bIP (basal intermediate progenitor cells) in the neocortex of mice. This anomaly was triggered by a shift in the division plane of mitotic aRG (apical radial glia cells) towards more horizontal divisions. The shift in the division plane was due to a reduced anchoring of the mitotic spindle to the cell cortex, which resulted from a significant reduction in the subcortical F-actin structure of mitotic aRG.
The increased number of bRG and an increased mitotic rate of the mislocated IP in turn led to a transiently increased production of neurons. In connection with the increased number of astrocytes in layer I of the cerebral cortex of the adult profilin1-deficient mice, the hypothesis arose that the folds of the cerebral cortex are due to an increased strength of individual cell layers.
Furthermore, the isolated proliferation of reactive astrocytes in the adult profilin1-deficient mice could be demonstrated, which is indicative of a “complete” reactive astrogliosis. In comparison with pre-existing studies, it was found that the deletion of profilin1 could even be directly responsible for the reactivation of microglia and astrocytes.
The present work clarifies the importance of profilin1 for the correct alignment of the mitotic spindle in murine aRG and provides strong indications for the importance of profilin1 for natural homeostasis in glial cells. Further investigations in this direction could provide new insights into the development and progression of neurodegenerative diseases such s polymicrogyria, lissencephaly or ALS
Die Rolle des Aktin-Regulators Cyclase-associated Protein 2 (CAP2) für die Entwicklung der Skelettmuskulatur in Säugetieren.
No full textActin is a structural protein that is a major component of the eukaryotic cytoskeleton. It is not only important for morphology and stability of cells, but also for dynamic processes such as cell migration, adhesion, growth or contraction. In muscle cells, the highly structured complex of myosin and actin filaments is essential for the coordinated contraction of muscle fibers, which ultimately generates muscle strength. In order to achieve this function, actin filaments have to build up and rebuilt dynamically during muscle development. However, the molecular mechanisms involved are still largely unknown. The need to elucidate these mechanisms arises from the finding that a large number of human myopathies are associated with defects in the actin cytoskeleton. Previous studies identified the transcription factor SRF (serum response factor) as a major regulator of skeletal muscle development in humans and mice. In a feedback mechanism, SRF is activated in an actin-dependent manner and in turn controls the expression of actin and actin-regulatory proteins. One of the main activators of SRF is MRTF (myocardin related transcription factor), which can be sequestered by actin monomers, thus preventing translocation and subsequent activation of SRF in the nucleus. This cumulative dissertation presents two studies that aim to elucidate the underlying processes of myopathies during skeletal muscle development. In the first publication, "CAP2 deficiency delays myofibril actin cytoskeleton differentiation and disturbs skeletal muscle architecture and function", we identified a previously unknown function for the actin-regulatory protein CAP2 (cyclase-associated protein 2) during skeletal muscle development in mammals. We showed that CAP2 controls the remodeling of actin filaments in developing skeletal muscle and is therefore essential for the differentiation of muscle fibers. As a consequence of CAP2 loss, mouse mutants developed structural changes in skeletal muscles, characterized by a frequent occurrence of ring fibers, internalized nuclei and disturbed mitochondrial distribution, as well as deficits in motor functions and moderate muscle weakness. These changes reflect symptoms of human myopathies. In the second manuscript, "Cyclase-associated protein 2 (CAP2) controls MRTF-A localization and SRF activity in mouse embryonic fibroblasts", we reported that loss of CAP2 in mouse embryonic fibroblasts lead to disturbed SRF activity. Specifically, we found that CAP2 controls subcellular distribution of the SRF trans-activator MRTF in an actin-dependent mechanism. CAP2 inactivation was associated with reduced nuclear MRTF levels and impaired SRF-mediated gene expression. This suggests that CAP2-dependent actin dynamics may also control SRF activity during skeletal muscle development and that dysregulation of SRF may cause or at least contribute to the myopathy in CAP2 mutant mice.Das Strukturprotein Aktin stellt einen Hauptbestandteil des Zytoskeletts aller eukaryotischen Zellen dar. Als solches ist es nicht nur für die Morphologie und Stabilität von Zellen wichtig, sondern auch für dynamische Prozesse wie Zellmigration, Adhäsion, Wachstum oder Kontraktion. In Muskelzellen ist der hoch strukturierte Komplex aus Myosin- und Aktin-Filamenten essentiell für die koordinierte Kontraktion der Muskelfasern, welche letztendlich Muskelkraft erzeugen. Um diese Funktion zu bewerkstelligen, müssen Aktin-Filamente während der Muskelentwicklung dynamisch auf- und auch umgebaut werden. Die daran beteiligten molekularen Mechanismen sind allerdings noch weitestgehend unbekannt. Gleichzeitig existiert der Befund, dass eine Vielzahl humaner Muskelerkrankungen mit Defekten im Aktin-Zytoskelett assoziiert ist. Die daraus resultierende Notwendigkeit zur Aufklärung dieser Mechanismen bildet die Grundlage und das Ziel der vorliegenden Dissertation. Frühere Arbeiten anderer Arbeitsgruppen haben den Transkriptionsfaktor SRF (serum response factor) als einen wichtigen Regulator der Skelettmuskelentwicklung in Menschen und Mäusen identifiziert. In einem Rückkopplungsmechanismus wird SRF Aktin-abhängig aktiviert und kontrolliert wiederum die Expression von Aktin und Aktin-regulierenden Proteinen. Einer der Hauptaktivatoren von SRF ist MRTF (myocardin related transcription factor), welcher zumeist im Zytoplasma an Aktin-Monomere gebunden werden kann, wodurch seine Translokalisation in den Zellkern und die Aktivierung von SRF unterbunden werden. Die vorliegende kumulative Dissertation präsentiert zwei Studien, die sich mit der Aufklärung von Prozessen beschäftigen, die Skelettmuskelentwicklungsdefekten zugrunde liegen. In der ersten Publikation „CAP2 deficiency delays myofibril actin cytoskeleton differentiation and disturbs skeletal muscle architecture and function” wurde für das Aktin-regulierende Protein CAP2 (cyclase-associated protein 2) eine bislang unbekannte Funktion während der Entwicklung der Skelettmuskulatur in Säugetieren gezeigt. Die Daten ergaben, dass CAP2 den Umbau von Aktin-Filamenten im sich entwickelnden Skelettmuskel kontrolliert und somit essentiell für die Differenzierung von Muskelfasern ist. Als Konsequenz eines CAP2-Funktionsverlusts entwickeln Mausmutanten strukturelle Veränderungen im Skelettmuskel, welche durch das gehäufte Auftreten von Ringbinden, internalisierten Zellkernen und durch eine gestörte Mitochondrien-Verteilung gekennzeichnet sind. Diese gehen mit Defiziten in motorischen Funktionen und einer moderaten Muskelschwäche einher. Diese Veränderungen spiegeln Symptome humaner Muskelerkrankungen wider. Im zweiten Manuskript „Cyclase-associated protein 2 (CAP2) controls MRTF-A localization and SRF activity in mouse embryonic fibroblasts“ konnte gezeigt werden, dass der Verlust von CAP2 in embryonalen Maus-Fibroblasten zu einer gestörten SRF-Aktivität führt. Insbesondere wurde festgestellt, dass CAP2 die subzelluläre Verteilung des SRF-Transaktivators MRTF in einem Aktin-abhängigen Mechanismus steuert. Die Inaktivierung von CAP2 war mit reduzierter MRTF-Lokalisation im Kern und einer Beeinträchtigung der SRF-vermittelten Genexpression verbunden. Dies lässt uns vermuten, dass CAP2-abhängige Aktin-Dynamik die SRF-Aktivität auch während der Entwicklung der Skelettmuskulatur kontrollieren kann und dass eine Dysregulation von SRF die Myopathie bei CAP2-Mutanten verursachen oder zumindest zu ihr beitragen kann
Health Hazard Evaluation Report: HETA-90-030-2183: Rust Engineering, Champion International; Quinnesec, Michigan
No full textIn response to a request from the Building and Construction Trades Department, an evaluation was conducted of possible health effects due to chlorine-dioxide (10049044) emissions from the Champion International Corporation (CIC) pulp mill in Quinnesec, Michigan on workers employed by Rust Engineering (SIC-1541) at an adjacent construction site. Rust Engineering was contracted by CIC to construct a paper mill addition to the pulp mill, and had about 1,600 workers at the site. Questionnaires were completed by 252 workers and pulmonary function tests were performed. Acute symptoms were reported more frequently among workers who felt they had been exposed to chemical fumes. Workers with reported perceived exposures experienced shortness of breath more often. No difference was noted in the occurrence of chronic cough with perceived exposure. Wheeze was reported by more workers who indicated an exposure but only in the smoking group. Obstructive ventilatory function was noted among 37 workers and ten had a restrictive pattern. Toxic gases were released on more than one occasion at this site, but there were no records available which would allow the calculation of the concentration of any gases released or the effect of these on the workers. The author recommends that health and safety procedures be established and enforced. The requirement of the State of Michigan Hazard Communication Program should be implemented
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