Carl Nielsen and the Radio

On 1 April 1925 Denmark introduced national control of its hitherto privately run and relatively chaotic radio broadcasting. Denmark would quickly show itself to be one of Europe’s leading nations with regard to both the number of licence-paying listeners and the role of serious music in broadcasting policy. This situation was also reflected very directly in the case of Carl Nielsen. Out of the total of 5,802 performances of his work which the article’s author has been able to document until Nielsen’s death in 1931, 922 (or nearly a sixth) were either produced directly for radio (where in general all music was broadcast live), or broadcast via Danish and foreign radio. Nielsen’s attitude to the new medium was ambivalent from the beginning and gradually cooled. Indeed, the head of the Danish State Radio, kammersanger Emil Holm, was one of his friends, and Nielsen readily accepted when he was asked to conduct his own works at the concerts, which marked milestones in the newly founded Radio Orchestra’s development. He was also a member of the committee that decided in 1926 which type of transmitter the new radio station in Kalundborg would use. But he composed only a few, not especially important new works for radio use, and does not seem to have been clear about what the radio medium meant for his music at a European level. The article presents a series of hitherto unknown documents concerning Carl Nielsen’s relationship to the radio medium, and includes a schematic chart in the appendix offering a detailed overview of which Nielsen works a listener could have heard, and when, on Danish and foreign radio stations up until the composer’s death

Carl Nielsen and Tivoli

The basis for the article is a complete overview covering every performance of music by Carl Nielsen in the summer season of the Copenhagen pleasure garden, Tivoli, during the composer’s lifetime (1865-1931). For the first years after becoming a professional violinist, Nielsen made his living from playing in the Tivoli orchestra. And it was in Tivoli he made his official debut as a composer in 1887. When his fellow student from the Academy of Music, Frederik Schnedler-Petersen at the beginning of the summer season 1909 took over as musical director in Tivoli, the Nielsen performances really took flight. The article lists in all 744 performances, which stylistically range right from the popular songs to the symphonies. Schnedler-Petersen was not afraid to present the rather conservative Tivoli audience with some musical challenges whenever the orchestra’s rather tight work-schedule permitted a moment for rehearsing these. But as Nielsen’s music became increasingly experimental, he too had to give up. The sixth symphony (1925) was only performed once in Tivoli and the clarinet concerto (1928) not at all. Nielsen’s birthday on the 9th June was in the Tivoli season and Schnedler-Petersen nearly always found some way of marking the event. Nielsen’s 60th birthday in 1925 was particularly festive with performances by the three Tivoli orchestras, a torchlight procession and a banquet in one of the best restaurants in Tivoli. Finally the article also briefly describes Schnedler-Petersen’s efforts outside Tivoli on behalf of Carl Nielsen, not least abroad where he was without any doubt the composer’s most diligent musical ambassador

MicroRNA–Directed siRNA Biogenesis in Caenorhabditis elegans

RNA interference (RNAi) is a post-transcriptional silencing process, triggered by double-stranded RNA (dsRNA), leading to the destabilization of homologous mRNAs. A distinction has been made between endogenous RNAi–related pathways and the exogenous RNAi pathway, the latter being essential for the experimental use of RNAi. Previous studies have shown that, in Caenorhabditis elegans, a complex containing the enzymes Dicer and the Argonaute RDE-1 process dsRNA. Dicer is responsible for cleaving dsRNA into short interfering RNAs (siRNAs) while RDE-1 acts as the siRNA acceptor. RDE-1 then guides a multi-protein complex to homologous targets to trigger mRNA destabilization. However, endogenous role(s) for RDE-1, if any, have remained unexplored. We here show that RDE-1 functions as a scavenger protein, taking up small RNA molecules from many different sources, including the microRNA (miRNA) pathway. This is in striking contrast to Argonaute proteins functioning directly in the miRNA pathway, ALG-1 and ALG-2: these proteins exclusively bind miRNAs. While playing no significant role in the biogenesis of the main pool of miRNAs, RDE-1 binds endogenous miRNAs and triggers RdRP activity on at least one perfectly matching, endogenous miRNA target. The resulting secondary siRNAs are taken up by a set of Argonaute proteins known to act as siRNA acceptors in exogenous RNAi, resulting in strong mRNA destabilization. Our results show that RDE-1 in an endogenous setting is actively screening the transcriptome using many different small RNAs, including miRNAs, as a guide, with implications for the evolution of transcripts with a potential to be recognized by Dicer

mut-7 of C. elegans, Required for Transposon Silencing and RNA Interference, Is a Homolog of Werner Syndrome Helicase and RNaseD

AbstractWhile all known natural isolates of C. elegans contain multiple copies of the Tc1 transposon, which are active in the soma, Tc1 transposition is fully silenced in the germline of many strains. We mutagenized one such silenced strain and isolated mutants in which Tc1 had been activated in the germline (“mutators”). Interestingly, many other transposons of unrelated sequence had also become active. Most of these mutants are resistant to RNA interference (RNAi). We found one of the mutated genes, mut-7, to encode a protein with homology to RNaseD. This provides support for the notion that RNAi works by dsRNA-directed, enzymatic RNA degradation. We propose a model in which MUT-7, guided by transposon-derived dsRNA, represses transposition by degrading transposon-specific messengers, thus preventing transposase production and transposition

Generation and Characterization of Fmr1 Knockout Zebrafish

Fragile X syndrome (FXS) is one of the most common known causes of inherited mental retardation. The gene mutated in FXS is named FMR1, and is well conserved from human to Drosophila. In order to generate a genetic tool to study FMR1 function during vertebrate development, we generated two mutant alleles of the fmr1 gene in zebrafish. Both alleles produce no detectable Fmr protein, and produce viable and fertile progeny with lack of obvious phenotypic features. This is in sharp contrast to published results based on morpholino mediated knock-down of fmr1, reporting defects in craniofacial development and neuronal branching in embryos. These phenotypes we specifically addressed in our knock-out animals, revealing no significant deviations from wild-type animals, suggesting that the published morpholino based fmr1 phenotypes are potential experimental artifacts. Therefore, their relation to fmr1 biology is questionable and morpholino induced fmr1 phenotypes should be avoided in screens for potential drugs suitable for the treatment of FXS. Importantly, a true genetic zebrafish model is now available which can be used to study FXS and to derive potential drugs for FXS treatment

RDE-2 interacts with MUT-7 to mediate RNA interference in Caenorhabditis elegans

In Caenorhabditis elegans, the activity of transposable elements is repressed in the germline. One of the mechanisms involved in this repression is RNA interference (RNAi), a process in which dsRNA targets cleavage of mRNAs in a sequence-specific manner. The first gene found to be involved in RNAi and transposon silencing in C.elegans is mut-7, a gene encoding a putative exoribonuclease. Here, we show that the MUT-7 protein resides in complexes of ∼250 kDa in the nucleus and in the cytosol. In addition, we find that upon triggering of RNAi the cytosolic MUT-7 complex increases in size. This increase is independent of the presence of target RNA, but does depend on the presence of RDE-1 and RDE-4, two proteins involved in small interfering RNA (siRNA) production. Finally, using a yeast two-hybrid screen, we identified RDE-2/MUT-8 as one of the other components of this complex. This protein is encoded by the rde-2/mut-8 locus, previously implicated in RNAi and transposon silencing. Using genetic complementation analysis, we show that the interaction between these two proteins is required for efficient RNAi in vivo. Together these data support a role for the MUT-7/RDE-2 complex downstream of siRNA formation, but upstream of siRNA mediated target RNA recognition, possibly indicating a role in the siRNA amplification step

Functional diversification of Argonautes in nematodes:an expanding universe

In the last decade, many diverse RNAi (RNA interference) pathways have been discovered that mediate gene silencing at epigenetic, transcriptional and post-transcriptional levels. The diversity of RNAi pathways is inherently linked to the evolution of Ago (Argonaute) proteins, the central protein component of RISCs (RNA-induced silencing complexes). An increasing number of diverse Agos have been identified in different species. The functions of most of these proteins are not yet known, but they are generally assumed to play roles in development, genome stability and/or protection against viruses. Recent research in the nematode Caenorhabditis elegans has expanded the breadth of RNAi functions to include transgenerational epigenetic memory and, possibly, environmental sensing. These functions are inherently linked to the production of secondary siRNAs (small interfering RNAs) that bind to members of a clade of WAGOs (worm-specific Agos). In the present article, we review briefly what is known about the evolution and function of Ago proteins in eukaryotes, including the expansion of WAGOs in nematodes. We postulate that the rapid evolution of WAGOs enables the exceptional functional plasticity of nematodes, including their capacity for parasitism