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Project acronym 2-HIT
Project Genetic interaction networks: From C. elegans to human disease
Researcher (PI) Ben Lehner
Host Institution (HI) FUNDACIO CENTRE DE REGULACIO GENOMICA
Summary Most hereditary diseases in humans are genetically complex, resulting from combinations of mutations in multiple genes. However synthetic interactions between genes are very difficult to identify in population studies because of a lack of statistical power and we fundamentally do not understand how mutations interact to produce phenotypes. C. elegans is a unique animal in which genetic interactions can be rapidly identified in vivo using RNA interference, and we recently used this system to construct the first genetic interaction network for any animal, focused on signal transduction genes. The first objective of this proposal is to extend this work and map a comprehensive genetic interaction network for this model metazoan. This project will provide the first insights into the global properties of animal genetic interaction networks, and a comprehensive view of the functional relationships between genes in an animal. The second objective of the proposal is to use C. elegans to develop and validate experimentally integrated gene networks that connect genes to phenotypes and predict genetic interactions on a genome-wide scale. The methods that we develop and validate in C. elegans will then be applied to predict phenotypes and interactions for human genes. The final objective is to dissect the molecular mechanisms underlying genetic interactions, and to understand how these interactions evolve. The combined aim of these three objectives is to generate a framework for understanding and predicting how mutations interact to produce phenotypes, including in human disease.
Most hereditary diseases in humans are genetically complex, resulting from combinations of mutations in multiple genes. However synthetic interactions between genes are very difficult to identify in population studies because of a lack of statistical power and we fundamentally do not understand how mutations interact to produce phenotypes. C. elegans is a unique animal in which genetic interactions can be rapidly identified in vivo using RNA interference, and we recently used this system to construct the first genetic interaction network for any animal, focused on signal transduction genes. The first objective of this proposal is to extend this work and map a comprehensive genetic interaction network for this model metazoan. This project will provide the first insights into the global properties of animal genetic interaction networks, and a comprehensive view of the functional relationships between genes in an animal. The second objective of the proposal is to use C. elegans to develop and validate experimentally integrated gene networks that connect genes to phenotypes and predict genetic interactions on a genome-wide scale. The methods that we develop and validate in C. elegans will then be applied to predict phenotypes and interactions for human genes. The final objective is to dissect the molecular mechanisms underlying genetic interactions, and to understand how these interactions evolve. The combined aim of these three objectives is to generate a framework for understanding and predicting how mutations interact to produce phenotypes, including in human disease.
Project acronym CELLDOCTOR
Project Quantitative understanding of a living system and its engineering as a cellular organelle
Researcher (PI) Luis Serrano
Summary The idea of harnessing living organisms for treating human diseases is not new but, so far, the majority of the living vectors used in human therapy are viruses which have the disadvantage of the limited number of genes and networks that can contain. Bacteria allow the cloning of complex networks and the possibility of making a large plethora of compounds, naturally or through careful redesign. One of the main limitations for the use of bacteria to treat human diseases is their complexity, the existence of a cell wall that difficult the communication with the target cells, the lack of control over its growth and the immune response that will elicit on its target. Ideally one would like to have a very small bacterium (of a mitochondria size), with no cell wall, which could be grown in Vitro, be genetically manipulated, for which we will have enough data to allow a complete understanding of its behaviour and which could live as a human cell parasite. Such a microorganism could in principle be used as a living vector in which genes of interests, or networks producing organic molecules of medical relevance, could be introduced under in Vitro conditions and then inoculated on extracted human cells or in the organism, and then become a new organelle in the host. Then, it could produce and secrete into the host proteins which will be needed to correct a genetic disease, or drugs needed by the patient. To do that, we need to understand in excruciating detail the Biology of the target bacterium and how to interface with the host cell cycle (Systems biology aspect). Then we need to have engineering tools (network design, protein design, simulations) to modify the target bacterium to behave like an organelle once inside the cell (Synthetic biology aspect). M.pneumoniae could be such a bacterium. It is one of the smallest free-living bacterium known (680 genes), has no cell wall, can be cultivated in Vitro, can be genetically manipulated and can enter inside human cells.
The idea of harnessing living organisms for treating human diseases is not new but, so far, the majority of the living vectors used in human therapy are viruses which have the disadvantage of the limited number of genes and networks that can contain. Bacteria allow the cloning of complex networks and the possibility of making a large plethora of compounds, naturally or through careful redesign. One of the main limitations for the use of bacteria to treat human diseases is their complexity, the existence of a cell wall that difficult the communication with the target cells, the lack of control over its growth and the immune response that will elicit on its target. Ideally one would like to have a very small bacterium (of a mitochondria size), with no cell wall, which could be grown in Vitro, be genetically manipulated, for which we will have enough data to allow a complete understanding of its behaviour and which could live as a human cell parasite. Such a microorganism could in principle be used as a living vector in which genes of interests, or networks producing organic molecules of medical relevance, could be introduced under in Vitro conditions and then inoculated on extracted human cells or in the organism, and then become a new organelle in the host. Then, it could produce and secrete into the host proteins which will be needed to correct a genetic disease, or drugs needed by the patient. To do that, we need to understand in excruciating detail the Biology of the target bacterium and how to interface with the host cell cycle (Systems biology aspect). Then we need to have engineering tools (network design, protein design, simulations) to modify the target bacterium to behave like an organelle once inside the cell (Synthetic biology aspect). M.pneumoniae could be such a bacterium. It is one of the smallest free-living bacterium known (680 genes), has no cell wall, can be cultivated in Vitro, can be genetically manipulated and can enter inside human cells.
Project acronym DSBRECA
Project Relevance of double strand break repair pathway choice in human disease and cancer
Researcher (PI) Pablo Huertas Sanchez
Host Institution (HI) UNIVERSIDAD DE SEVILLA
Summary "Double strand breaks (DSBs) repair is essential for normal development. While the complete inability to repair DSBs leads to embryonic lethality and cell death, mutations that hamper this repair cause genetically inherited syndromes, with or without cancer predisposition. The phenotypes associated with these syndromes are extremely varied, and can include growth and mental retardation, ataxia, skeletal abnormalities, immunodeficiency, premature aging, etc. Moreover, DSBs play an extremely relevant role in the biology of cancer. Alterations in the DSBs repair pathways facilitate tumour progression and are selected early on during cancer development. On the other hand, DSBs are the molecular base of radiotherapies and chemotherapies. This double role of DSBs in both, the genesis and treatment of cancer makes the understanding of the mechanisms that control their repair of capital importance in cancer research. DSBs are repaired by two major mechanisms that compete for the same substrate. Both ends of the DSB can be simple re-joined with little or no processing, a mechanism known as non-homologous end-joining. On the other hand, DSBs can be processed and engaged in a more complex repair pathway called homologous recombination. This pathway uses the information present in a homologue sequence. The balance between these two pathways is exquisitely controlled and its alteration leads to the appearance of chromosomal abnormalities and contribute to the diseases aforementioned. However, and despite its importance, the network controlling the choice between both is poorly understood. Here, we propose a series of research lines designed to investigate how the choice between both DSBs repair pathways is made, its relevance for cellular and organismal survival and disease, and its potential as a therapeutic target for the treatment of cancer and some genetically inherited disorders."
"Double strand breaks (DSBs) repair is essential for normal development. While the complete inability to repair DSBs leads to embryonic lethality and cell death, mutations that hamper this repair cause genetically inherited syndromes, with or without cancer predisposition. The phenotypes associated with these syndromes are extremely varied, and can include growth and mental retardation, ataxia, skeletal abnormalities, immunodeficiency, premature aging, etc. Moreover, DSBs play an extremely relevant role in the biology of cancer. Alterations in the DSBs repair pathways facilitate tumour progression and are selected early on during cancer development. On the other hand, DSBs are the molecular base of radiotherapies and chemotherapies. This double role of DSBs in both, the genesis and treatment of cancer makes the understanding of the mechanisms that control their repair of capital importance in cancer research. DSBs are repaired by two major mechanisms that compete for the same substrate. Both ends of the DSB can be simple re-joined with little or no processing, a mechanism known as non-homologous end-joining. On the other hand, DSBs can be processed and engaged in a more complex repair pathway called homologous recombination. This pathway uses the information present in a homologue sequence. The balance between these two pathways is exquisitely controlled and its alteration leads to the appearance of chromosomal abnormalities and contribute to the diseases aforementioned. However, and despite its importance, the network controlling the choice between both is poorly understood. Here, we propose a series of research lines designed to investigate how the choice between both DSBs repair pathways is made, its relevance for cellular and organismal survival and disease, and its potential as a therapeutic target for the treatment of cancer and some genetically inherited disorders."
Project acronym HYPER-INSIGHT
Project Hypermutated tumors: insight into genome maintenance and cancer vulnerabilities provided by an extreme burden of somatic mutations
Researcher (PI) Fran Supek
Host Institution (HI) FUNDACIO INSTITUT DE RECERCA BIOMEDICA (IRB BARCELONA)
Summary Mutations are the fuel of any evolutionary process, and this also applies to carcinogenesis. The advent of affordable DNA sequencing has enabled mutagenic processes in the human soma to be quantified genome-wide, revealing a striking occurrence of hypermutated tumors. They exhibit an extreme load of somatic changes, often harbouring hundreds of single-nucleotide variants and/or indels per megabase. The HYPER-INSIGHT project is organized into three objectives, which aim to take advantage of the unique opportunity provided by genome sequences of hypermutated and ultramutated tumors. In particular, this work planned in this project aims to further our knowledge on (i) the regional organization of the DNA replication and repair program in human cells, and the determinants thereof, (ii) the extent of selection which acts on somatic variants in various pathways or complexes and (iii) opportunities for selectively targeting DNA repair deficiencies that manifest as hypermutation. Methodologically, our work will employ a three-pronged approach. First, we will perform a multitude of rigorous statistical analyses that draw on the rich and still-expanding resources provided by cancer genomics consortia. Second, we will perform exome and genome sequencing, focusing on ultramutated tumors caused by specific defects in the DNA maintenance machinery. Third, the project involves conditional essentiality screens on cancer cell lines with hypermutant backgrounds. Their goal is to discover synthetic lethality relationships, useful for targeting hypermutating cells, while sparing healthy ones. In summary, one of the promises of cancer genome sequencing projects was to elucidate the mechanisms underlying mutational processes in the human soma, advancing our understanding of this important facet of cancer biology. We will work towards realizing this promise, thereby strengthening the EU's position in the global scientific endeavour.
Mutations are the fuel of any evolutionary process, and this also applies to carcinogenesis. The advent of affordable DNA sequencing has enabled mutagenic processes in the human soma to be quantified genome-wide, revealing a striking occurrence of hypermutated tumors. They exhibit an extreme load of somatic changes, often harbouring hundreds of single-nucleotide variants and/or indels per megabase. The HYPER-INSIGHT project is organized into three objectives, which aim to take advantage of the unique opportunity provided by genome sequences of hypermutated and ultramutated tumors. In particular, this work planned in this project aims to further our knowledge on (i) the regional organization of the DNA replication and repair program in human cells, and the determinants thereof, (ii) the extent of selection which acts on somatic variants in various pathways or complexes and (iii) opportunities for selectively targeting DNA repair deficiencies that manifest as hypermutation. Methodologically, our work will employ a three-pronged approach. First, we will perform a multitude of rigorous statistical analyses that draw on the rich and still-expanding resources provided by cancer genomics consortia. Second, we will perform exome and genome sequencing, focusing on ultramutated tumors caused by specific defects in the DNA maintenance machinery. Third, the project involves conditional essentiality screens on cancer cell lines with hypermutant backgrounds. Their goal is to discover synthetic lethality relationships, useful for targeting hypermutating cells, while sparing healthy ones. In summary, one of the promises of cancer genome sequencing projects was to elucidate the mechanisms underlying mutational processes in the human soma, advancing our understanding of this important facet of cancer biology. We will work towards realizing this promise, thereby strengthening the EU's position in the global scientific endeavour.
Project acronym IR-DC
Project Individual Robustness in Development and Cancer
Researcher (PI) Benjamin Lehner
Summary Biological systems are robust to perturbations, with many genetic, stochastic and environmental challenges having no or little phenotypic consequence. However, the extent of this robustness varies across individuals, for example the same mutation or treatment may only affect a subset of individuals. The overall objective of this project is to understand the cellular and molecular mechanisms that confer this robustness and why it varies across individuals. We will address three specific questions: 1. Why do inherited mutations have different outcomes in different individuals, even when they are genetically identical and share a common environment? 2. What are the mechanisms during development that confer robustness to mechanical deformation? 3. How can the loss of robustness be exploited to specifically kill cancer cells? To address the first two questions, we will use live imaging procedures that we have developed that make the C. elegans embryo a unique animal system to link early inter-individual variation in gene expression and cellular behaviour to later variation in phenotypes. To address the third question, we will apply our understanding of genetic robustness and genetic interaction networks in model organisms to the comprehensive analysis of cancer genome datasets. The predictions from these hypothesis-driven computational analyses will then be evaluated using wet-lab experiments. Understanding and predicting variation in robustness is both a fundamental challenge for biology and one that is central to the development of personalised and predictive medicine. A patient does not want to know the typical outcome of a mutation or treatment; they want to know what will actually happen to them. The work outlined here will contribute to our basic understanding of robustness and its variation among individuals, and it will also directly tackle the problem of predicting and targeting variation in robustness as a strategy to kill tumour cells.
Biological systems are robust to perturbations, with many genetic, stochastic and environmental challenges having no or little phenotypic consequence. However, the extent of this robustness varies across individuals, for example the same mutation or treatment may only affect a subset of individuals. The overall objective of this project is to understand the cellular and molecular mechanisms that confer this robustness and why it varies across individuals. We will address three specific questions: 1. Why do inherited mutations have different outcomes in different individuals, even when they are genetically identical and share a common environment? 2. What are the mechanisms during development that confer robustness to mechanical deformation? 3. How can the loss of robustness be exploited to specifically kill cancer cells? To address the first two questions, we will use live imaging procedures that we have developed that make the C. elegans embryo a unique animal system to link early inter-individual variation in gene expression and cellular behaviour to later variation in phenotypes. To address the third question, we will apply our understanding of genetic robustness and genetic interaction networks in model organisms to the comprehensive analysis of cancer genome datasets. The predictions from these hypothesis-driven computational analyses will then be evaluated using wet-lab experiments. Understanding and predicting variation in robustness is both a fundamental challenge for biology and one that is central to the development of personalised and predictive medicine. A patient does not want to know the typical outcome of a mutation or treatment; they want to know what will actually happen to them. The work outlined here will contribute to our basic understanding of robustness and its variation among individuals, and it will also directly tackle the problem of predicting and targeting variation in robustness as a strategy to kill tumour cells.
Project acronym KryptonInt
Project Erasing the superintegron to understand the role of chromosomal integrons in bacterial evolution
Researcher (PI) Jose Antonio ESCUDERO
Host Institution (HI) UNIVERSIDAD COMPLUTENSE DE MADRID
Summary Integrons are genetic platforms that enhance bacterial evolvability through the acquisition and stockpiling of new genes encoded in mobile elements named cassettes. They are found in the chromosomes of environmental bacteria but some have acquired mobility through their association to transposons and conjugative plasmids. These mobile integrons (MI) caused the unexpected rise of multidrug resistance that is now a major threat to modern medicine, and are good proof of the adaptive power of integrons. Class 1 integrons are the most relevant MI and the major experimental model. Yet little is known about the hundreds of sedentary chromosomal integrons (SCI) that have driven bacterial evolution for eons. The paradigm of SCI is the superintegron (SI), an extremely large integron located in the chromosome of Vibrio cholerae, the causative agent of Cholera disease. Despite its role in the adaptability of one of the deadliest pathogens in history, the SI is poorly characterized because it is only functional in its native genetic background, yet its presence interferes with, and precludes all studies performed in V. cholerae. I propose to solve this paradoxical situation by deleting the SI, an ambitious project not only for its size (126 Kb) but because it is highly stabilized by 17 toxin-antitoxin systems. To do so, I have developed SeqDelTA, a novel method that is already giving excellent preliminary results. I will then use V. cholerae∆SI to study fundamental aspects of SCIs, yet out of reach. I will elucidate the functions encoded in SI cassettes to understand the role and adaptive value of integrons in nature; I will also unravel the genesis of cassettes: how a gene is exapted from its genetic context to become a mobile module; and I will explore the circulation of antibiotic resistance cassettes among humans, animals, food, and the environment with a novel biosynthetic tool (the I3C). KryptonInt will open and explore the historically inaccessible field of study of SCIs.
Integrons are genetic platforms that enhance bacterial evolvability through the acquisition and stockpiling of new genes encoded in mobile elements named cassettes. They are found in the chromosomes of environmental bacteria but some have acquired mobility through their association to transposons and conjugative plasmids. These mobile integrons (MI) caused the unexpected rise of multidrug resistance that is now a major threat to modern medicine, and are good proof of the adaptive power of integrons. Class 1 integrons are the most relevant MI and the major experimental model. Yet little is known about the hundreds of sedentary chromosomal integrons (SCI) that have driven bacterial evolution for eons. The paradigm of SCI is the superintegron (SI), an extremely large integron located in the chromosome of Vibrio cholerae, the causative agent of Cholera disease. Despite its role in the adaptability of one of the deadliest pathogens in history, the SI is poorly characterized because it is only functional in its native genetic background, yet its presence interferes with, and precludes all studies performed in V. cholerae. I propose to solve this paradoxical situation by deleting the SI, an ambitious project not only for its size (126 Kb) but because it is highly stabilized by 17 toxin-antitoxin systems. To do so, I have developed SeqDelTA, a novel method that is already giving excellent preliminary results. I will then use V. cholerae∆SI to study fundamental aspects of SCIs, yet out of reach. I will elucidate the functions encoded in SI cassettes to understand the role and adaptive value of integrons in nature; I will also unravel the genesis of cassettes: how a gene is exapted from its genetic context to become a mobile module; and I will explore the circulation of antibiotic resistance cassettes among humans, animals, food, and the environment with a novel biosynthetic tool (the I3C). KryptonInt will open and explore the historically inaccessible field of study of SCIs.
Project acronym NEURAL AS
Project Functions and evolutionary impact of transcriptomic novelties in the vertebrate brain
Researcher (PI) Manuel Irimia Martinez
Summary Alternative splicing (AS) is the largest contributor to transcriptomic diversification in metazoans. In particular, mirroring their unparalleled morphological and cellular complexity, vertebrate brains show the highest levels of regulated AS known in nature. However, the functions of most of these alternative transcripts, and the evolutionary impact that the increased transcriptional complexity has had on the evolution of the vertebrate brain are still widely unexplored. In this project, we will investigate the functions and evolutionary impact of neural AS in vertebrates. We will focus on neural-specific alternative exons that are highly conserved across vertebrate groups (suggesting functional importance), but that are not conserved in invertebrates, and are thus vertebrate-specific genomic novelties. We will term these exons Vertebrate- and Neural-specific Alternatively Spliced (VN-AS) exons. Through a combination of bioinformatics, experimental manipulation in models species, and systems-level network analysis, we aim to: (i) Comprehensively identify VN-AS exons, and study their regulation during vertebrate neurogenesis and nervous system development, using RNA-seq and comparative genomics; (ii) Probe the phenotypic impact of VN-AS exons on vertebrate nervous systems, using the CRISPR-Cas technology for genome editing; and (iii) Investigate how VN-AS exons rewire protein-protein interaction networks in vertebrate neurons – an emergent molecular function for AS –, and whether this rewiring underlies novel functions of VN-AS exons in the vertebrate brains. This project will thus deliver fundamental insight into two major unanswered questions: (i) what are the functions of transcriptomic diversification, and (ii) how does transcriptomic diversification impact organismal evolution. Our results will fill a large gap of knowledge in our current understanding of brain evolution and development, providing a complementary angle to traditional gene expression studies.
Alternative splicing (AS) is the largest contributor to transcriptomic diversification in metazoans. In particular, mirroring their unparalleled morphological and cellular complexity, vertebrate brains show the highest levels of regulated AS known in nature. However, the functions of most of these alternative transcripts, and the evolutionary impact that the increased transcriptional complexity has had on the evolution of the vertebrate brain are still widely unexplored. In this project, we will investigate the functions and evolutionary impact of neural AS in vertebrates. We will focus on neural-specific alternative exons that are highly conserved across vertebrate groups (suggesting functional importance), but that are not conserved in invertebrates, and are thus vertebrate-specific genomic novelties. We will term these exons Vertebrate- and Neural-specific Alternatively Spliced (VN-AS) exons. Through a combination of bioinformatics, experimental manipulation in models species, and systems-level network analysis, we aim to: (i) Comprehensively identify VN-AS exons, and study their regulation during vertebrate neurogenesis and nervous system development, using RNA-seq and comparative genomics; (ii) Probe the phenotypic impact of VN-AS exons on vertebrate nervous systems, using the CRISPR-Cas technology for genome editing; and (iii) Investigate how VN-AS exons rewire protein-protein interaction networks in vertebrate neurons – an emergent molecular function for AS –, and whether this rewiring underlies novel functions of VN-AS exons in the vertebrate brains. This project will thus deliver fundamental insight into two major unanswered questions: (i) what are the functions of transcriptomic diversification, and (ii) how does transcriptomic diversification impact organismal evolution. Our results will fill a large gap of knowledge in our current understanding of brain evolution and development, providing a complementary angle to traditional gene expression studies.
Project acronym NonChroRep
Project Investigating the role of the long noncoding transcriptome in chromatin replication
Researcher (PI) Maite Huarte Martinez
Host Institution (HI) FUNDACION PARA LA INVESTIGACION MEDICA APLICADA FIMA
Summary A major shift in our conception of genome regulation has emerged in recent years. It is now obvious that the majority of cellular transcripts do not code for proteins, and a significant subset of them are long RNAs (lncRNAs). My lab and others have shown that lncRNAs regulate genome function and gene expression, and that alterations in lncRNAs are inherent to disease, including cancer. However, our understanding of the roles of lncRNAs and their underlying molecular mechanisms are still extremely poor. Among all the mechanisms reported, the evident connection between lncRNAs and the chromatin places them at the center of cell biology. During their cycle, cells must undergo faithful DNA replication to ensure that an exact copy of their genetic content is passed on to their daughters. Throughout this tightly regulated process chromatin must be disrupted and reconstituted, and it determines where and when replication takes place. If replication is deregulated, cells can proliferate uncontrollably and suffer loss of genome integrity. Our recent findings implicate lncRNA in the process of DNA replication, representing a novel aspect of genome regulation that places lncRNAs at the focal point of cancer biology. To delve deeper into these findings I aim to: 1. Identify the role of lncRNAs in the replication of the chromatin 2. Dissect the molecular mechanism by which lncRNAs function in this process and 3. Explore the role of these lncRNAs as cancer drivers and their potential as therapeutic targets. I will apply tools that we have generated in recent years, as well as new ones, including approaches to identify lncRNAs associated with replicating chromatin, novel lncRNA-tailored CRISPR applications, and the latest methodology for functional study and targeting of long noncoding transcripts in cancer. I am confident that we are in a unique position to address these life-essential and yet pending questions, setting up a basis for future lncRNA-based therapies.
A major shift in our conception of genome regulation has emerged in recent years. It is now obvious that the majority of cellular transcripts do not code for proteins, and a significant subset of them are long RNAs (lncRNAs). My lab and others have shown that lncRNAs regulate genome function and gene expression, and that alterations in lncRNAs are inherent to disease, including cancer. However, our understanding of the roles of lncRNAs and their underlying molecular mechanisms are still extremely poor. Among all the mechanisms reported, the evident connection between lncRNAs and the chromatin places them at the center of cell biology. During their cycle, cells must undergo faithful DNA replication to ensure that an exact copy of their genetic content is passed on to their daughters. Throughout this tightly regulated process chromatin must be disrupted and reconstituted, and it determines where and when replication takes place. If replication is deregulated, cells can proliferate uncontrollably and suffer loss of genome integrity. Our recent findings implicate lncRNA in the process of DNA replication, representing a novel aspect of genome regulation that places lncRNAs at the focal point of cancer biology. To delve deeper into these findings I aim to: 1. Identify the role of lncRNAs in the replication of the chromatin 2. Dissect the molecular mechanism by which lncRNAs function in this process and 3. Explore the role of these lncRNAs as cancer drivers and their potential as therapeutic targets. I will apply tools that we have generated in recent years, as well as new ones, including approaches to identify lncRNAs associated with replicating chromatin, novel lncRNA-tailored CRISPR applications, and the latest methodology for functional study and targeting of long noncoding transcripts in cancer. I am confident that we are in a unique position to address these life-essential and yet pending questions, setting up a basis for future lncRNA-based therapies.
Project acronym NONCODEVOL
Project Evolutionary genomics of long, non-coding RNAs
Researcher (PI) Juan Antonio Gabaldón Estevan
Summary Recent genomics analyses have facilitated the discovery of a novel major class of stable transcripts, now called long non-coding RNAs (lncRNAs). A growing number of analyses have implicated lncRNAs in the regulation of gene expression, dosage compensation and imprinting, and there is increasing evidence suggesting the involvement of lncRNAs in various diseases such as cancer. Despite recent advances, however, the role of the large majority of lncRNAs remains unknown and there is current debate on what fraction of lncRNAs may just represent transcriptional noise. Moreover, despite a growing number of lncRNAs catalogues for diverse model species, we lack a proper understanding of how these molecules evolve across genomes. Evolutionary analyses of protein-coding genes have proved tremendously useful in elucidating functional relationships and in understanding how the processes in which they are involved are shaped during evolution. Similar insights may be expected from a proper evolutionary characterization of lncRNAs, although the lack of proper tools and basic knowledge of underlying evolutionary mechanisms are a sizable challenge. Here, I propose to combine state-of-the-art computational and sequencing techniques in order to elucidate what evolutionary mechanisms are shaping this enigmatic component of eukaryotic genomes.The first goal is to enable large-scale phylogenomic analyses of lncRNAs by developing, for these molecules, methodologies that are now standard in the evolutionary analysis of protein-coding genes. The second goal is to explore, at high levels of resolution, the evolutionary dynamics of lncRNAs across selected eukaryotic groups for which novel genome-wide data will be produced experimentally using recently developed sequencing techniques that enable obtaining genome-wide footprints of RNA secondary structure. Finally, this dataset will be used to test the impact on lncRNAs evolution of processes known to be important in protein-coding genes.
Recent genomics analyses have facilitated the discovery of a novel major class of stable transcripts, now called long non-coding RNAs (lncRNAs). A growing number of analyses have implicated lncRNAs in the regulation of gene expression, dosage compensation and imprinting, and there is increasing evidence suggesting the involvement of lncRNAs in various diseases such as cancer. Despite recent advances, however, the role of the large majority of lncRNAs remains unknown and there is current debate on what fraction of lncRNAs may just represent transcriptional noise. Moreover, despite a growing number of lncRNAs catalogues for diverse model species, we lack a proper understanding of how these molecules evolve across genomes. Evolutionary analyses of protein-coding genes have proved tremendously useful in elucidating functional relationships and in understanding how the processes in which they are involved are shaped during evolution. Similar insights may be expected from a proper evolutionary characterization of lncRNAs, although the lack of proper tools and basic knowledge of underlying evolutionary mechanisms are a sizable challenge. Here, I propose to combine state-of-the-art computational and sequencing techniques in order to elucidate what evolutionary mechanisms are shaping this enigmatic component of eukaryotic genomes.The first goal is to enable large-scale phylogenomic analyses of lncRNAs by developing, for these molecules, methodologies that are now standard in the evolutionary analysis of protein-coding genes. The second goal is to explore, at high levels of resolution, the evolutionary dynamics of lncRNAs across selected eukaryotic groups for which novel genome-wide data will be produced experimentally using recently developed sequencing techniques that enable obtaining genome-wide footprints of RNA secondary structure. Finally, this dataset will be used to test the impact on lncRNAs evolution of processes known to be important in protein-coding genes.
Project acronym NONCODRIVERS
Project Finding noncoding cancer drivers
Researcher (PI) Nuria Lopez Bigas
Summary Finding the mutations, genes and pathways directly involved in cancer is of paramount importance to understand the mechanisms of tumour development and devise therapeutic strategies to overcome the disease. Due to their role in cancer development and maintenance, the proteins encoded by cancer genes are candidate therapeutic targets. Indeed, in recent years we have witnessed the development of successful cancer-targeting therapies to counteract the effect of driver mutations. Although the coding part of the human genome has now largely been explored in the search for cancer driver mutations in most frequent cancer types, the extent of involvement of noncoding mutations in cancer development remains a mystery. The main challenges faced are: 1) the functional role of most noncoding regions is unknown, and 2) tumours often have thousands of somatic mutations, so that distinguishing cancer driver mutations from bystanders is like finding the proverbial needle in a haystack. To overcome these two challenges I propose to analyse the pattern of somatic mutations across thousands of tumours in noncoding regions to identify signals of positive selection. These signals are an indication that mutations in the region have been positively selected during tumour evolution and are thus directly involved in the tumour phenotype. The large scale analysis proposed here will allow us to create a catalogue of noncoding elements involved in different types of cancer upon mutations. We will study in detail a selected set of driver elements to uncover their specific function and role in the tumourigenic process. Furthermore, we will explore possibilities of counteracting their driver effect with targeted drugs. The results of this project may boost our understanding of the biological role of noncoding regions, help to unravel novel molecular causes of cancer and provide novel targeted therapeutic opportunities for cancer patients.
Finding the mutations, genes and pathways directly involved in cancer is of paramount importance to understand the mechanisms of tumour development and devise therapeutic strategies to overcome the disease. Due to their role in cancer development and maintenance, the proteins encoded by cancer genes are candidate therapeutic targets. Indeed, in recent years we have witnessed the development of successful cancer-targeting therapies to counteract the effect of driver mutations. Although the coding part of the human genome has now largely been explored in the search for cancer driver mutations in most frequent cancer types, the extent of involvement of noncoding mutations in cancer development remains a mystery. The main challenges faced are: 1) the functional role of most noncoding regions is unknown, and 2) tumours often have thousands of somatic mutations, so that distinguishing cancer driver mutations from bystanders is like finding the proverbial needle in a haystack. To overcome these two challenges I propose to analyse the pattern of somatic mutations across thousands of tumours in noncoding regions to identify signals of positive selection. These signals are an indication that mutations in the region have been positively selected during tumour evolution and are thus directly involved in the tumour phenotype. The large scale analysis proposed here will allow us to create a catalogue of noncoding elements involved in different types of cancer upon mutations. We will study in detail a selected set of driver elements to uncover their specific function and role in the tumourigenic process. Furthermore, we will explore possibilities of counteracting their driver effect with targeted drugs. The results of this project may boost our understanding of the biological role of noncoding regions, help to unravel novel molecular causes of cancer and provide novel targeted therapeutic opportunities for cancer patients.


Most weeks, my schedule is pretty packed. I'm never at a lost for items to add to my to-do list, and my planner never goes untouched. If I'm being honest, I'm still working to find the right work/life balance.
But one thing I have gotten much better at is managing life as a busy gal, which can be hard to do.
A large part of this has to do with taking control of the routines in my life: waking up early consistently, knowing my most productive hours to get daunting tasks done, and knowing when to schedule a rest day. Having a few things each morning and evening remain constant are super helpful when the middle portion of my day is always shifting.
Here are some tips to keep moving through your days without (completely) losing your sanity.
Guilt a busy schedule seem to come hand in hand. Guilt for having to put certain tasks before others, or not having time to spend with others (who usually don't understand why you're so busy to begin with). Carrying around a bunch of guilt doesn't make you any less busy, and may cause you to spend more time trying to get through your commitments. Celebrate that you have so many great things happening, and remember your big and little wins.
I have the "what if I just turned off my email address and didn't tell anyone" thought about twice each weekday, and once on the weekends. When you're running on little sleep and lots of coffee, the sound of another notification on your phone can drive you over the edge. Even if you only have five minutes, take some time to put the phone down, step away from the inbox and breathe. When your mind is constantly jumping from one task to the next, it's impossible to focus.
My number one tip to manage being busy is to avoid making yourself even more busy than you have to be. I do this by making effective to-do lists the first time. Be sure that you're creating a guide for things to get done, and not just a wish list for productivity.
Accept that you can't do it all.
I have an issue where I feel that my ideas or plans have hidden expiration dates. So I try to fit a bunch of things into a shot span of time –writing and launching an ecourse, blogging, school, work and then some. It's important to be realistic with the time that you have, and accept that some months aren't going to allow you to do everything you'd like.
Balance Your Yeses with No's.
Saying yes can sometimes be so much easier than saying no, but can kill you in the long run. Just because you have an hour or two free doesn't mean you have to give that space to anyone who asks for your time. Always be sure to balance your yeses and no's, it is more than okay to say no.
This tip is usually the hardest to execute for someone like me. Whether I like admitting it or not, I can be quite the control freak, and delegating tasks to someone else is a struggle for me. But it's important than whenever you can, you ask for the help that you need to avoid overwhelming yourself.
For all of my other hustlers and movers out there, how to you manage being incredibly busy without losing it? I'd love to hear your tips, too!
I love your comparision of to-do-list with wish-list of productivity… that's how I feel mostly at the end of a day when I look back at it^^ Thanks for sharing!
I love this, especially this year as I am so terribly busy. I definitely have trouble with saying no to people so that's something to work on. Disconnecting has been on my mind but seems almost impossible at time! Great post!
Great tips! I def have to learn to ditch the guilt! I always feel bad when I dont get to everything on my to-do list for the day!
This was just what I needed to read! I just discovered your blog and I love everything about it!
Some of these are things I tell myself all the time. But I am so happy for the post. Things like this make me feel like I actually have permission to say no once in a while.
Great advice! I can so relate and think these words are important to remember!
Some great tips in there – I am usually great at managing my time but have struggled as of late. I need to tke a breather and re-prioritise!
Great tips! Most drown because they are afraid to ask for help.


text:
Cowboys Waive Keith Smith; Re-Sign DE Lavar Edwards
David Helman
DallasCowboys.com Staff Writer
IRVING, Texas – The Cowboys re-signed defensive end Lavar Edwards to their active roster on Tuesday, just a few days after releasing him.
Edwards was released Saturday after injuries necessitated a roster move at the linebacker position. Both Rolando McClain and Justin Durant missed Sunday's game against St. Louis with groin injuries, prompting the Cowboys to activate undrafted rookie Keith Smith from their practice squad.
Smith played in the 34-31 win against the Rams, but he did not record any sacks. He was released Monday afternoon, and he'll be free to rejoin the Cowboys' practice squad if he clears waivers.
Edwards himself cleared waivers on Monday afternoon, and it's not surprising the Cowboys re-signed him. The team acquired him from Tennessee in exchange for a conditional seventh-round draft pick. He joined the Cowboys the week before the season opener, and he played just a handful of snaps against San Francisco before a knee injury sidelined him against the Titans.
[embedded_ad]
The Cowboys need all the help they can get for their pass rush, which is off to a sluggish start this season. Dallas is in a five-way tie for No. 31 in the league with just three sacks as a team. Furthermore, it hasn't even been their defensive line generating those sacks. Rolando McClain and Bruce Carter – both linebackers – are tied for the team lead with one sack apiece. Henry Melton and Kyle Wilber combined on the other sack in the win against Tennessee.
The Titans selected Edwards No. 142 overall in the fifth round of the 2013 NFL Draft, but they decided he didn't fit into their future as they switch to a 3-4 scheme under new defense coordinator Ray Horton. During his four-year career with LSU, he totaled 96 tackles and 10.5 sacks as a 4-3 defensive end.

redpajama_set_name: RedPajamaCommonCrawl


text:
Q: Search a worksheet for a cell value, then copy the adjacent cells into a variable range I have several Excel workbooks with each workbook containing multiple sheets.
I do a keyword search across all worksheets using a particular value ("James Smith"). If the value is found, then I need to offset five columns over from that cell location (i.e. the "found cell" which will always be in Column C somewhere so the offset is pointing to column H) and then select/copy the adjacent rows into a range that will ultimately be pasted into a new worksheet "masterSheet".
The problems are:

*

*The cell address in each of these sheets will vary so that the cell address is not the same in each worksheet

*I get errors when I try to set the FoundRange value below.

    'Search multiple workbooks, look only for sheetnames that begin with "Week of" and don't contain the word "old"

    If currentSheet.Name Like "*Week of*" And InStr(currentSheet.Name, "Old") = 0 Then
        'If currentSheet.Name Like "*Week of*" Then

        'Within the current sheet look for a cell that contains "James Smith"
        With currentSheet

            .Range("C:C").Columns.Select

            Set FoundCell = Selection.Find(What:="James Smith", After:=ActiveCell, LookIn:=xlFormulas, _
            LookAt:=xlWhole, SearchOrder:=xlByRows, SearchDirection:=xlNext, _
              MatchCase:=False, SearchFormat:=False)

            'When "James Smith" is found in the current worksheet, get the cell address and offset from that cell location"
            OffsetCell = currentSheet.Range(FoundCell.Address).Offset(0, 5).Address

            'In Column "H" select the adjacent non-blank cells and copy into a range <line below where I define "FoundRange" is where I keep getting the "runtime error 424 object required error"
            Set FoundRange = Range(OffsetCell, OffsetCell.End(xlDown))

            For Each cell In currentSheet.Range(FoundRange)
                If Not IsEmpty(cell) Then
                    currentSheet.Range(cell.Address).Copy
                    masterSheet.Range("D" & Rows.Count).End(xlUp).Offset(1, 0).PasteSpecial xlPasteValues
                    masterSheet.Range("C" & Rows.Count).End(xlUp).Offset(1, 0) = Format(CDate(Replace(Replace(currentSheet.Name, "Week of ", " "), ".", "/")), "mm/dd/yyyy")
                    masterSheet.Range("C" & Rows.Count).End(xlUp).Offset(0, -1) = "James Bradford"
                    currentSheet.Range(cell.Address).Offset(0, 1).Copy
                    masterSheet.Range("E" & Rows.Count).End(xlUp).Offset(1, 0).PasteSpecial xlPasteValues
                    currentSheet.Range(cell.Address).Offset(0, 2).Copy
                    masterSheet.Range("F" & Rows.Count).End(xlUp).Offset(1, 0).PasteSpecial xlPasteValues
                    currentSheet.Range(cell.Address).Offset(0, 3).Copy
                    masterSheet.Range("G" & Rows.Count).End(xlUp).Offset(1, 0).PasteSpecial xlPasteValues
                End If
            Next
        End With
    End If

A: This works. FYI... You have James Smith in the find and James Bradford in the loop. I added a mastersheet for testing, so get rid of the "Set masterSheet" line.
Sub RngTest()
'Search multiple workbooks, look only for sheetnames that begin with "Week of" and don't contain the word "old"

Set currentSheet = ActiveSheet
Set masterSheet = ActiveWorkbook.Sheets("MasterSheet")
If currentSheet.Name Like "*Week of*" And InStr(currentSheet.Name, "Old") = 0 Then
    'If currentSheet.Name Like "*Week of*" Then

        'Within the current sheet look for a cell that contains "James Smith"
        With currentSheet

        .Range("C:C").Columns.Select

        Set FoundCell = Selection.Find(What:="James Smith", After:=ActiveCell, LookIn:=xlFormulas, _
        LookAt:=xlWhole, SearchOrder:=xlByRows, SearchDirection:=xlNext, _
        MatchCase:=False, SearchFormat:=False)

        'When "James Smith" is found in the current worksheet, get the cell address and offset from that cell location"
        Set OffsetCell = currentSheet.Range(FoundCell.Address).Offset(0, 5)

         'In Column "H" select the adjacent non-blank cells and copy into a range <line below where I define "FoundRange" is where I keep getting the "runtime error 424 object required error"
         Set FoundRange = Range(OffsetCell, OffsetCell.End(xlDown))

                 For Each cell In FoundRange.Cells
                    If Not IsEmpty(cell) Then
                        currentSheet.Range(cell.Address).Copy
                        masterSheet.Range("D" & Rows.Count).End(xlUp).Offset(1, 0).PasteSpecial xlPasteValues
                        masterSheet.Range("C" & Rows.Count).End(xlUp).Offset(1, 0) = Format(CDate(Replace(Replace(currentSheet.Name, "Week of ", " "), ".", "/")), "mm/dd/yyyy")
                        masterSheet.Range("C" & Rows.Count).End(xlUp).Offset(0, -1) = "James Bradford"
                        currentSheet.Range(cell.Address).Offset(0, 1).Copy
                        masterSheet.Range("E" & Rows.Count).End(xlUp).Offset(1, 0).PasteSpecial xlPasteValues
                        currentSheet.Range(cell.Address).Offset(0, 2).Copy
                        masterSheet.Range("F" & Rows.Count).End(xlUp).Offset(1, 0).PasteSpecial xlPasteValues
                        currentSheet.Range(cell.Address).Offset(0, 3).Copy
                        masterSheet.Range("G" & Rows.Count).End(xlUp).Offset(1, 0).PasteSpecial xlPasteValues
                    End If
                Next

        End With

    End If

End Sub

redpajama_set_name: RedPajamaStackExchange


The late fall and winter season is bad for yard sales here. We got a lot of snow this year so I turned to Craigslist, Offerup, and I recently joined several Facebook video game and electronic buy/sell groups. Here are some of the great items I found before the upcoming garage sale season starts.
Probably the best pickup I have had so far was a trade on Craigslist. I traded an older Android phone for two Wiis that had most of their parts and a mostly CIB SNES Super Mario All Stars + Super Mario World system. It was missing the game and the a/v cables but I have since picked that up.
In the same month, February, from Offerup I bought a new 3DS XL. System is a little banged up but at $100 I couldn't say no. I also snagged Taitio Legends for PS2 and Madworld for Wii at a local Goodwill. Total price was $10 for both those games.
Along comes March, where the snow has melted and there are some better deals to find. I paid $75 for a large Wii lot. The system came with 2 controllers with motion plus, and several so-so games. But I also got Wii Fit Plus and a balance board. Mario Party 8, Mario Kart Wii, and Wii Sports Resorts also came with the bundle.
Just over the weekend I noticed there was a guy selling a large lot of games on Facebook and I made an offer. I paid $70 and got another Wii, I am now up to 4. The Wii came with hookups and a controller. The box also had Dying Light for PS4, a Ps3 Dualshock, and a N64 with a controller, but no power brick.
Wii's are going to be a common item this season and it seems the demand for them is going up. I wouldn't be surprised if I come across a Wii U this summer as well. If the rest of the season is anything like the last few weeks I am going to be very busy.


text:
bookmark Shameel Joosub
Shameel Joosub
Vodacom rakes in over R2bn with financial services
By Christopher Tredger
Egypt , South Africa , Tanzania , 01 Feb 2022
Vodacom experienced a 12.5% increase in financial services revenue to breach the R2-billion mark for the first time in a quarter, according to the operator's trading update for the quarter ended 31 December 2021.
Describing financial services as a strategic priority for the Group, Shameel Joosub, Vodacom Group CEO said the company's M-Pesa platform, including Safaricom, "continues to scale at an impressive rate with transaction values up 16.1% to exceed R430 billion per month."
"In South Africa, the launch of our VodaPay super-app in October last year has exceeded our expectations by attracting 1.4 million downloads and 1.0 million registered users in its first three months. We see VodaPay as a precursor to M-Pesa's evolution and further strengthening our Fintech position across our footprint."
Vodacom Group CEO Shameel Joosub.
Joosub added that in South Africa, the Group invested a further R2.3-billion in the network during the quarter and service 45.7 million customers, which equates to an increase of 3.3% in a year, and which contributed to a 4.5% increase in service revenue.
Vodacom Tanzania
Vodacom Tanzania announced that it distribute a total of TZS 3.4-billion in dividend to its M-Pesa customers who have used the service over the 2021 last quarter.
Vodacom in major African Fintech push, guns for 70m customers
Vodacom hits acquisition trail, begins with Vodafone Egypt for R41bn
According to the operator, the dividend payment covers the months of October to December which is the third quarter of the company's financial year.
Vodacom's M-Commerce Director Epimack Mbeteni said that the profit will be paid to all individual customers, retail agents and other M-Pesa business partners who will receive payment based transactions made via their mobile wallets.
"Our mobile money service, M-Pesa, continues to be a remarkable success story, delivering significant social and financial value to Tanzanians. We have seen substantial growth on the M-Pesa platform with more customers, agents, merchants and institutions transacting around TZS 100-billion each day. In line with regulations of the Bank of Tanzania, interest earned from the deposit is periodically shared with the customers. Today we are happy to share a dividend of Tzs 3.4-billion with our over eight million customers across the nation," he said.
Vodacom Tanzania stated that according to recent figures released by TCRA (Tanzania Communications Regulatory Authority) it has over 11 million customers on its M-Pesa platform commanding a market share of 40%.
Acquisition value
Joosub also referenced the acquisitions announced in November 2021: a majority interest in Vodafone Egypt and a strategic stake in the fibre assets of Community Investment Ventures Holdings (Pty) Limited (CIVH).
He said, "The CIVH fibre transaction in South Africa is also expected to accelerate Vodacom's purpose of connecting people for a better future by facilitating an ambitious fibre roll-out programme that will assist in narrowing the digital divide by enabling affordable access to connectivity in some of the most vulnerable parts of our society. Vodacom has submitted regulatory filings in respect of the transaction to the Competition Commission and ICASA, respectively, initiating a process to obtain regulatory approval."
Vodacom said it would fund the acquisition of a 55% stake in Vodafone Egypt by issuing 242 million new ordinary shares at R135.75 per share and R8.2-billion (US$548-million) in cash. This values the proposed transaction at circa R41-billion or US$2.738-billion.
In early January 2022, shareholders gave the transaction the official 'thumbs up' and Joosub stated: "With over 80% of Egypt's 100 million population unbanked, Vodacom sees enormous potential to leverage our financial services platforms, global partnerships and best practices in a significant market."
Vodacom looks to cement the deal by 31 March 2022, but the transaction still requires regulatory approval from the National Telecom Regulatory Authority of Egypt (NTRA) and Egypt's Financial Regulatory Authority.
FinTechTelecomsFinancialVodacomShameel JoosubEpimack Mbeteni


text:
Safe cities are built on trust
In recent years, our values have been challenged by a series of attacks by violent extremists, both in the Nordic countries and elsewhere in the world. We do not want our urban conurbations to be arenas for violence and hate, nor for their inhabitants to live in fear.
Democracy has deep roots in the Nordic Region. We respect fundamental human rights and the freedom of the individual. We are very open, trusting and tolerant. These are values shared by all of the Nordic countries. They are values worth standing up for.
Violent extremism does not just leave destruction and injury in its wake, it also has an impact on our democracy and way of life. It challenges the core principles on which our societies are built. Unless challenged it may sap the trust we have in each other and undermine our freedoms.
A closed society is also one that excludes, one in which people are suspicious of each other's motives, one where we become less tolerant of other people's ideas and beliefs.
When my own homeland was attacked in the most horrific manner, in Oslo and on Utøya, our reaction was the opposite of what the terrorist wanted. Faced with tragedy, we responded not with anger and calls for revenge, but with responsibility and compassion. We understood that hate leads to more hate. Nobody expressed it better than one of the young survivors from Utøya, who wrote: "When a single man can cause so much evil – think how much love we can generate together."
I am convinced that this response has made Norway a stronger and more united nation.
Lives were also lost in Copenhagen, during the attacks on Krudttønden in Østerbro and the synagogue in Krystalgade – two people died and six police officers were wounded. It was in the wake of these events that the ministers for Nordic co-operation decided that something had to be done. They sowed the first seed of what would later grow into Nordic Safe Cities.
I titled this blog post "Safe cities are built on trust" because it expresses not only an inherently Nordic view of society but also a shared Nordic goal of working to prevent the mechanisms that lead to attacks.
It is also the fundamental principle behind the Nordic Safe Cities network and the title of the guide I had the pleasure of launching in Copenhagen on 7 March.
The guide focuses on the positive by shining a light on good examples from local authorities, official agencies, voluntary organisations and local communities. The launch brought together 12 Nordic spokespersons, the French Ambassador to Denmark, Francois Zimeray, and 150 experts from across the Region to discuss their experiences and learn from each other. It was a prime example of Nordic co-operation at its best.
All of the Nordic countries have frequently stressed the need to maintain our open and democratic society, and expressed our strong belief that everyone should be offered the opportunity to contribute what they can. In reality, this is the only path worth following. We need to be able to trust each other. Trust is crucial.
From a social perspective, it might even be considered more valuable than gold.
In 2014, leading Nordic researchers conducted a study of the Nordic model, the findings of which were published in the report The Nordic Model: Challenged but capable of reform. One of its key findings was that people in the Region have a significantly higher level of trust in each other, their elected representatives, the state and the legal system than people in other parts of the world.
Trust is essential in a modern society. Trust means that we can depend on each other. Trust binds us together. Trust is one of the foundations for productivity and economic growth. Trust is one of the building blocks for high quality of life. From a social perspective, it might even be considered more valuable than gold.
When we adhere to values such as freedom, trust and unity, we also have to accept that these values are only sustainable as long as we live in safe societies, where we do not fear our fellow citizens.
Inclusion and respect for human rights must always be our guiding star in the work to prevent individuals from committing acts of violence against the people and society around them.
I am pleased, therefore, that it is these particular values that serve as the foundation for Nordic Safe Cities. These values are what differentiate us from the extremists. I am convinced that the only productive way of confronting hate is to maintain our democratic traditions.
André H. Jamholt
andjam@norden.org


The Pennsport String Band is founded in the ideas of personal responsibility, professionalism, a passion for performance and a respect for the traditional ideals of mummery.
The Pennsport String Band has embraced a model of string band that is revolutionary. We are not a year-round string band. While we will meet periodically throughout the year for practices and meetings, we are a three month a year organization (October through New Years) with a sole focus on our New Years Day performance.
We are financially organized as an "out of pocket" organization. We have no intentions to use the traditional dues systems, fund raising drives or mandatory performance schedule. There will simply be a New Years Day Fee that the members must have paid in full by a specific date. How the members choose to raise the money needed is up to the individual.
We have a timetable for New Years Day materials for the membership. This timetable will address issues ranging from suit measurements to receiving New Years music so the members can begin to practice well in advance of the first general practice. The Pennsport String Band is founded in the ideas of personal responsibility, professionalism, a passion for performance and a respect for the traditional ideals of mummery.
We welcome you to contact us. Find out more about this exciting musical opportunity and experience a mummer's organization that allows you to have plenty of time for the other important commitments in your life that you do not want to miss.
If you are interested in joining the band, let us know by filling out and submitting one of the forms below.


Kristian "Gaahl" Espedal (GORGOROTH, GOD SEED, TRELLDOM) has been cast in a musical based on the concept album "Svartediket", which was inspired by myths and legends of the lake Svartediket, located outside of Bergen, Norway. The "first-ever black metal musical" is scheduled to premiere on May 26 at Festspillene i Bergen (Bergen International Festival), an annual international music and cultural festival. The event will be held at Bergen's Den Nationale Scene (DNS) (English translation: The National Stage), one of Norway's oldest and most renowned theaters which was founded to develop Norwegian playwrights.
Gaahl's casting has caused controversy in Norway, particularly as both Festspillene and Den Nationale Scene are heavily funded by the Norwegian state. Halvor Nordhaug, the Lutheran bishop in the diocese of Bjørgvin, seated in Bergen and covering parts of Western Norway, is especially concerned about Gaahl's previously published statements to the media in which he appeared to condone and support church burnings.
When asked in the 2005 documentary "Metal: A Headbanger's Journey" for his thoughts on the church burnings associated with the early Norwegian black metal scene, Gaahl replied, "Church burnings are, of course, a thing that I support one hundred percent. It should have been done much more, and will be done much more in the future. We have to remove every trace from what Christianity, and the semitic roots, have to offer this world."
After Gaahl's involvement with the "Svartediket" musical was made official this week, the former GORGOROTH frontman once again reiterated that he views church burning as OK.
"I have left my past behind, but I still have an anti-Christian attitude," Gaahl told the Bergens Tidende newspaper. "Christianity has no place in this country. As long as the church has the power it has and supports oppression, we shouldn't give the church any sympathy. Therefore I don't think it's wrong if it (church burning) happens again. The symbolic value of burning down churches is important."
Responding to Gaahl's remarks, Bishop Halvor Nordhaug told the Bergens Tidende newspaper, "Gaahl displays some scary attitudes by defending church burnings. He says nothing about the fact that human lives were lost during one of the church burnings in the 1990s. I think everybody, no matter what their religious beliefs are, agrees with me that his attitudes are scary, but it could still be possible that his role at Den Nationale Scene will provide him with some kind of legitimacy, which is unfortunate."


text:
Inedita
On photography, literature and life
Talking Digital Photography
Ode to Ansel Adams
Zen Camera
Zen Camera 1
Zen Camera 4a
Zen Camera 4b
Zen Camera 4c
At the car wash
Musing in Black and White
Lose the colour
Ivy leaves transformed
Chasing the light
Playing with White Balance
Leaves in sunlight
Failure revisited!
Help the camera?
Infrared section
Infrared first steps
Infrared second steps
Infrared third steps
Infrared fourth steps
Infrared fifth steps
Infrared sixth steps
Lensbaby section
Meet the Lensbaby
Lensbaby Double Glass
Lensbaby Sweet 50
Lensbaby Edge 80
Lensbaby Art and Glass 1
Many People, Few Ideas
Many People, Few Ideas 2
SASSOON AGONISTES
SASSOON AGONISTES 2
Reading Jane Austen
Reading Jane Austen 2
Keyboarding As Sport
Canon Selphy 1300
M E and me
Football: The Great (Dictionary) Game
Bow Fiddle
SIR WALTER ELLIOT, of Kellynch Hall, in Somersetshire, was a man who, for his own amusement, never took up any book but the Baronetage; there he found occupation for an idle hour, and consolation in a distressed one; there his faculties were roused into admiration and respect, by contemplating the limited remnant of the earliest patents; there any unwelcome sensations, arising from domestic affairs, changed naturally into pity and contempt, as he turned over the almost endless creations of the last century – and there, if every other leaf were powerless, he could read his own history with an interest which never failed – this was the page at which the favourite volume always opened:
'ELLIOT OF KELLYNCH-HALL.
Openings are always important because they establish the plot ideas which will be the foundations upon which the author simultaneously builds the superstructure of the novel's narrative that in turn helps shape the reader's response. Austen proved remarkably good at openings, and especially with regard to Persuasion, which both plays a wonderful and surprisingly modern joke on the reader in this prophetic cinematic technique of regression as well as painting one of the most devastating portraits of a character in English literature.
At the same moment the reader opens the novel and starts reading the text so does Sir Walter open his copy of the Baronetage and starts reading essentially the same text as the reader – 'Elliot of Kellynch-Hall' – part of the joke being that very soon he will no longer be able to describe himself in this way having been forced by his own incompetence and profligacy to leave the Hall and take lodgings in Bath. But this revelation, although swift in coming, arrives a little later. Austen busies herself revealing how the real joke here is Sir Walter himself – who, she makes plain, is not at all funny or amusing.
Austen is very specific: the Baronetage is the only book Sir Walter reads either when he is at leisure or when he is feeling distressed – which suggests that it is, indeed, the only book he reads. Later in the paragraph (or to be more accurate, in the sentence of some hundred words which forms the paragraph) the reader is told that the reason why Sir Walter so enjoys the Baronetage is because in its pages 'he could read his own history with an interest which never failed'. And more than that, the book always falls open at the same page. Not only is it the only book he seems to read, it is clear that he reads almost exclusively only the section that refers to himself. Superficially, this seems to fix him as another one of Austen's delicious caricatures, a narcissist who lives primarily via a constant re-reading of an official biography and seems to have no other interests or activities. But as ever with Austen, it is not so simple or straightforward as this.
One of the pleasures of reading Austen is the way she creates a balance of structure and language so smooth and untroubled that it is as if the words appeared on the page spontaneously, without any intermediary effect or conscious choice on her part. She achieves this through her mastery of the technique of free indirect discourse noted earlier. Through it she moves freely between her own narrative voice and the voices (both direct, indirect and unvoiced) of her characters. She is so successful at merging these different voices that it is sometimes (indeed, often) difficult to separate them at any given moment. The effect of this is that untroubled smoothness just mentioned where the text seems to unfold naturally through the characters and their perspectives rather than through her decisions. But what might initially appear to be superficial can turn out to explore deeper concerns.
For example, although Sir Walter's rather eccentric reading habits do have a definite sense of comic exaggeration the very structure of this opening paragraph and its joke presents someone trapped in a solipsistic universe of self-regard, unable to escape the addiction of his own grandeur and caught in the fascinating web of his own official biography. It is essentially a frozen life of endless repetition in which the only proof and validation of his own worth – his own humanity – is someone else's words written on a page.
This misuse of the act of reading as repetition, as confirmation and justification of identity, is, I would suggest, deeply serious in an important area. One of the refinements in critical theory since Jane Austen wrote her novels is the recognition of semiotics or semiology, which Ferdinand de Saussure defined as:
'a science which studies the role of signs as part of social life.'
Interpreted from this perspective, Sir Walter's use of the familiar text in the Baronetage to confirm his sense of identity is without reference to his social life and the various responsibilities – father, landowner, and caretaker amongst others – that involves. In semiotic terms, he mistakes the sign (the text) for what it should signify. This is an important flaw which moves beyond characterisation into plot: for it suggests that one aspect of the novel will centre on how Sir Walter fails to honour those familial and social obligations and responsibilities that his title and estate confer upon him. The difficulties such a man causes for those who know him can have important and potentially damaging consequences. One suspects from the very beginning, then, that this novel might well be about characters who, beset by anxiety and uncertainty as they try to 'read' the world around them with greater or lesser success depending on the clarity of their vision, present an outward armoured confidence that has very little validity or value – such characters set against the depiction of a few others who share empathy and embody social virtues.
Austen's choice of vocabulary pins down important elements of Sir Walter's character, as in why he so enjoys reading the Baronetage:
there any unwelcome sensations, arising from domestic affairs, changed naturally into pity and contempt, as he turned over the almost endless creations of the last century
(my emphasis)
These words cast a shadow over any comic aspects of his behaviour, especially in the way he counts his own inherited title (which he gained by accident of birth, of course) as superior to those awarded for services to the country in a time of national danger. It is both a misplaced vanity (Austen's constant word for him from the beginning – 'Vanity was the beginning and the end of Sir Walter Elliot's character; vanity of person and of situation' – and throughout the novel) and a subtle reinforcement of what the structure of regression really tells us beyond the surface comedy: that Sir Walter's relationship with the world is one of frozen negative repetition. It is noteworthy that Austen maintains this image of cold negativity through the novel, and also applies it to his favourite eldest daughter Elizabeth, locked into her own inescapable fate of spinsterhood, caught as she is forever frozen in the icy pairing with her father:
Sir Walter and Miss Elliot, whose entrance seemed to give a general chill
Austen uses a different narrative technique in the second paragraph: a simple set of facts simply stated, unadorned and undeveloped, telling the reader directly what it was that Sir Walter found so absorbing to read on what seems to be a daily basis:
Walter Elliot, born March 1, 1760, married, July 15, 1784, Elizabeth, daughter of James Stevenson, Esq. of South Park, in the county of Gloucester; by which lady (who died in 1800) he has issue Elizabeth, born June 1, 1785; Anne, born August 9, 1787; a still-born son, Nov 5, 1789; Mary, born Nov 20, 1791.
Yet again, a paragraph made up of only the one sentence broken by semi-colons, separating out details. This precision is necessary if the supposed entry is to ring true, of course – the Baronetage is clearly a statement of historical record. But the technique, I suggest, is also a very economical efficient and unobtrusively naturalistic way for Austen to indicate that another of the central concerns of the novel is to be the family described here rather than one individual.
By presenting the information in this way Austen not only introduces the family but also does so without overtly directing the reader's attention. It tells us (if we wish to read it carefully) that Sir Walter at the age of forty found himself the sole parent of three young girls aged fifteen, thirteen and nine years old. Again, the reader is left to draw his or her own conclusions as to what this might mean, especially given the revelations of the opening paragraph already briefly discussed above.
And notice the almost invisible, casual, almost glossed over facts of his wife's death – 'which lady (who died in 1800)' – and that of his one and only son, 'still-born' on 'Nov 5, 1789', mentioned en passant as just more details to be included in the historical record. Inconspicuous as they are in the little family history these are important plot points and deserve a little attention.
Austen makes it clear that if Lady Elliot had not died then the family would not have had to give up their ancestral home because she would have ensured that the necessary retrenchment would have been undertaken – or more likely, not needed in the first place:
'She had humoured, or softened, or concealed his failings, and promoted his real respectability for seventeen years'
This is a powerful indictment of Sir Walter, especially the quiet depiction of the progress of the marriage in the little sequence of 'humoured, or softened, or concealed' and its sense of the need for increasing degrees of intervention. But there is no possibility of any such attempts at mitigation or mercy in the word choice of 'his failings'. Austen's subtlety of language is also evidenced in this statement of Sir Walter's 'real respectability'. The idea that she had provided him a 'real' respectability while alive implies that without her guiding hand any respectability he might have was unreal, artificial and superficial. In this sense her death can be seen as one of the mainsprings of the novel and its actions: had she lived not only would Sir Walter have been encouraged to fulfil his various responsibilities rather than fall into this spiritual torpor and inactivity but it is possible that Anne would have been encouraged to marry Wentworth from the beginning.
There are two pieces of information about his dead son: that he was 'still-born' and the date, 'Nov 5, 1789'. Again, it is worth trying to see beneath the surface here: Austen could have used any number of options to explain the death; likewise, why did she choose this date?
So why did she choose stillbirth as the cause of death? For the modern reader it is a very precise event, defined by the NHS as:
A stillbirth is when a baby is born dead after 24 completed weeks of pregnancy. It happens in around 1 in every 200 births in England. If the baby dies before 24 completed weeks, it's known as a miscarriage or late foetal loss.
The situation was not so clear in Austen's time, where the term 'still-born' could also refer to a baby who had died before being baptised – anything up to several days after birth. That is, there was an apparent blurring of the distinction between what we might call foetal deaths in labour and those (presumably frail) babies who died in the hours or days following a live birth. Because of this lack of definition, I would argue that the reference to 'still-born' essentially operates at one remove – its force is connotative, not denotative. The emphasis falls on the idea that Sir Walter cannot pass on his inheritance – he is literally unfruitful, without lasting or continuing influence or force. As such, then, he is emblematic of the waning authority of a moribund class.
The modern reader might also notice that the stillborn son had three sisters (none of whom can inherit the father's estate, of course, thanks to the notion of primogeniture and the importance of the first-born son – a recurring theme in Austen) which immediately leads on to questions about the father's sperm count. It is likely that current medical research would diagnose that Sir Walter suffered from the condition known variously as 'Y chromosome infertility' or 'Y-linked spermatogenic failure' or 'Y chromosome-related azoospermia' – a genetic dysfunction which means the lack of male children is down to the father rather than the mother.
That said, it has long been the case that mothers carry the blame when sons refuse to appear, however slight their actual responsibility might be – one only needs to recall Henry VIII's default response when his wives could not produce a viable son. It is, perhaps, a form of displacement whereby men try to deny the psychological impact of failing to successfully produce a male heir. But the truth is that even men as self-important as Henry and Sir Walter will inevitably react in some way when the longed-for son dies. So how does Sir Walter react? Is his behaviour conditioned by grief? The more sympathetic reader might say that Austen buries the deaths of mother and son in exactly the way Sir Walter perhaps buries his grief and disappointment beneath the armour of his solipsistic interactions with other people and especially his surviving family – who are all female, of course.
In his 1917 paper Mourning and Melancholia Freud tried to address the nature of grieving, stating that the two conditions which give his paper its title are
regularly the reaction to the loss of a loved one
and characterised by
a profoundly painful dejection, cessation of interest in the outside world, loss of the capacity to love, [and] inhibition of all activity.
which certainly seems to fit the Sir Walter depicted in these opening paragraphs. Freud then goes on to distinguish melancholia from mourning by suggesting that melancholia manifests itself in the individual through
an extraordinary diminution in his self-regard, an impoverishment of his ego on a grand scale. In mourning it is the world which has become poor and empty; in melancholia it is the ego itself. The patient represents his ego to us as worthless, incapable of any achievement and morally despicable; he reproaches himself and expects to be cast out and punished.
In simpler terms, mourning is healthy because it is a conscious process whereby one re-establishes contact with the outside world; melancholia dwells in the unconscious and is therefore unhealthy and even pathological, finding increasing comfort and satisfaction in rituals of repetition that do not seek to maintain contact with the outside world so much as refusing its reality and responsibilities. The opening chapter pins down this activity precisely in its description of Sir Walter's reading habits, of course.
Freud goes on to say that the symptoms of melancholia reflect a "narcissistic blow", a wound to the ego whereby any loss inevitably encompasses a parallel loss of what we might term the deeper personal being of the survivor, demonstrated by a diminishment of self in the areas of character and personality. Again, the kind reader might perhaps see some of these elements as helping to explain aspects of Sir Walter's solipsism. Of course, it would be a mistake to argue that Austen somehow anticipated Freud's analysis. She would not recognise the terminology for a start. But she was an acute observer of other people and had certainly had ample and personal experience of the manifold varieties of grief as the world dissolved into the conflict of revolution followed by Napoleon's military ambition.
Her depiction of Sir Walter has striking concordances with Freud's thought but – and this is both significant and testimony to her skill in revealing character – she demonstrates her grasp of how different people grieve by also giving the reader a portrait of another person in the grip of melancholia – Captain Benwick. He too is essentially narcissistic in his display of grief for Fanny Harville, though without the sense of blight that surrounds Sir Walter – and Austen rewards him by offering him the opportunity, through his reported extended and assiduous nursing of Louisa, to escape the bookish prison of his sense of loss and guilt and resentment (Freud's 'pathology') and recapture something of his true self, becoming able to fall in love with someone new. At the same time, of course, this causes Harville to wonder aloud about the fickleness of affection and opens the way for one of the truly resonant passages in the novel when Anne replies
All the privilege I claim for my own sex (it is not a very enviable one, you need not covet it) is that of loving longest, when existence or when hope is gone.
I would suggest that this too is a statement about what it is to be in mourning, this time for a love that was itself somewhat stillborn by Sir Walter's reaction to it:
Sir Walter, on being applied to, without actually withholding his consent, or saying it should never be, gave it all the negative of great astonishment, great coldness, great silence, and a professed resolution of doing nothing for his daughter
There is no clearer statement in the novel of the awful effects of the parenting skills (or lack thereof) of a man who, in other circumstances, might have garnered the reader's sympathy for the double loss of wife and son.
As to Austen's choice of date for the unnamed boy's death it seems pointedly symbolic: 1789 was the year of the French Revolution that threw Europe's ruling elites into turmoil; and on November 5 of that year the French National Meeting declared all citizens equal under law (something which would doubtless have caused the Sir Walter we know to display another reaction of 'great astonishment, great coldness, great silence'); and more powerful still, of course, November 5 is one of the iconic dates in British history, when the dangerous Gunpowder Plot to destroy Parliament and the King was foiled.
It is not, perhaps, too fanciful to suggest that Austen is suggesting by this choice of date the fact that one of the sub-texts of the novel is to underline not only the approaching actuality of change (represented by the Navy and its values) but the urgency of the need for and the growing desirability of such change. In Austen's England that change will not come about through revolutionary violence as per the French in 1789 or the Catholic plotters in 1605, but through the natural processes of wastage, decline and impotence.
The third paragraph expands on the printed words in the Baronetage by revealing Sir Walter's own additions:
Precisely such had the paragraph originally stood from the printer's hands; but Sir Walter had improved it by adding, for the information of himself and his family, these words, after the date of Mary's birth – 'married, Dec. 16, 1810, Charles, son and heir of Charles Musgrove, Esq. of Uppercross, in the county of Somerset,' – and by inserting most accurately the day of the month on which he had lost his wife.
Again, only a single sentence where Austen subtly merges her apparently neutral authorial voice with Sir Walter's unintentionally revealing mindset and self-regard by choosing vocabulary that seems natural and straightforward. Thus we are told that Sir Walter had 'improved' the printed information (expressing in a different way that sense of superiority underpinning the first paragraph) by adding 'for the information of himself and his family' (note who comes first in his consideration) details of Mary's wedding to Charles Musgrove, and ending with a final note 'inserting most accurately the day of the month on which he had lost his wife' – an interesting redundancy given that the date of her death can only be either accurate or inaccurate. Sir Walter feels himself to be the supreme arbiter of events and carries on the self-regard underpinning the idea of his handwritten notes 'improving' rather than simply adding to the printed history. It may well be that he genuinely loved and misses his late wife, but the formulaic expression 'lost his wife' might well gently indicate a certain shallowness of feeling or suggest that the remembrance is not so much of loss as how her death has complicated his life.
There is another more important significance in this notion of 'improving' the printed record by appending handwritten notes. Sir Walter 'improves' the printed original by the act of writing on it, by exercising his authorial power. None of his daughters would think to do such a thing because none of them has the authority (or author-ity) to do so. This question of authority becomes one of the major themes of the novel.
These opening three paragraphs form some fifteen per cent or so of the opening chapter (which goes on to provide a brief but important background history of recent events) but set up everything that follows in that chapter. Everything we learn reinforces the suspicions raised in the opening three paragraphs and help indicate the major outlines of why and how the novel might develop. For example:
Elizabeth had succeeded, at sixteen, to all that was possible, of her mother's rights and consequence; and being very handsome, and very like himself, her influence had always been great, and they had gone on together most happily. His two other children were of very inferior value. Mary had acquired a little artificial importance, by becoming Mrs Charles Musgrove; but Anne, with an elegance of mind and sweetness of character, which must have placed her high with any people of real understanding, was nobody with either father or sister: her word had no weight; her convenience was always to give way; – she was only Anne.
In terms of these family relationships very little changes by the end of the novel. When Anne and Wentworth announce their engagement
there was little to distress them beyond the want of graciousness and warmth – Sir Walter made no objection, and Elizabeth did nothing worse than look cold and unconcerned.
And Mary clings on to her 'little artificial importance' by being content to 'flatter' herself that she had had a hand in the outcome 'by keeping Anne with her in the autumn' – and more tellingly, continues in the same vein of self-congratulatory superiority she has shown throughout:
… and as her own sister must be better than her husband's sisters, it was very agreeable that Captain Wentworth should be a richer man than either Captain Benwick or Charles Hayter. – She had something to suffer perhaps when they came into contact again, in seeing Anne restored to the rights of seniority, and the mistress of a very pretty landaulette; but she had a future to look forward to, of powerful consolation. Anne had no Uppercross-hall before her, no landed estate, no headship of a family; and if they could but keep Captain Wentworth from being made a baronet, she would not change situations with Anne.
It is a description that recalls Henry James's comment about 'small and second-rate minds' and 'perfect little she-Philistines' that opened the first section of this discussion – but we should not forget, as James apparently did, that these were consciously created by Austen – and for as profound a purpose as any character conjured by him.
It is, perhaps, inevitable that most readers equate the notion of the Elliot family with Sir Walter and his three daughters and forget or put to one side Mr Elliot, the heir presumptive. As D W Harding commented in his 1965 Introduction to the Penguin edition of the novel
… the parts of the novel centring on Mr Elliot give an impression of something contemplated but not fully worked out
This is certainly true as the novel rushes towards its somewhat hasty conclusion and the rather obscure and tangled involvement between him and Mrs Clay; but without Mr Elliot the novel would lose one of its central agents in the exploration of those themes that most interested Jane Austen – the social and moral changes taking place that were creating new patterns of authority and behaviour consequent upon the emerging philosophies and technologies of the time.
Austen very much includes him in the opening chapter – indeed, his name is introduced as one of Sir Walter's handwritten notes 'improving' the Baronetage's record of the family, as 'Heir presumptive, William Walter Elliot, Esq., great grandson of the second Sir Walter' – with the information that Elizabeth 'meant to marry him' and Sir Walter 'had always meant that she should' but that he had other ideas:
Instead of pushing his fortune in the line marked out for the heir of the house of Elliot, he had purchased independence by uniting himself to a rich woman of inferior birth
and as a consequence 'all acquaintance between them had ceased'. This, of course, makes for an interesting future plotline and narrative where some form of reconciliation or emotional tangle becomes inevitable. And despite the accusation of a mercenary attitude (which comes from the disappointed and resentful father and daughter and therefore is not necessarily accurate) when next we meet him in Chapter Twelve he is immediately recognised as 'a gentleman' and a little later as 'completely a gentleman in manner'. This is an important social marker, of course, but as the novel progresses it seems a somewhat changed one from, say, the idea of a gentleman as explored in Emma. There Mr Knightley's almost perfect judgement and sense of social responsibility make him closely aligned with the author in ways which could not and do not happen with Mr Elliot in Persuasion – despite the fact that, in terms of their interaction with the other characters in their respective novels, they present in almost identical ways as gentlemen.
The use of the term carried profound connotations for the earlier Jane Austen, of course, who allowed the liveliest of her heroines, Elizabeth Bennet, to admonish the most socially powerful of her heroes, Fitzwilliam Darcy, in Pride and Prejudice:
'You are mistaken, Mr Darcy, if you suppose that the mode of your declaration affected me in any other way, than as it spared the concern which I might have felt in refusing you, had you behaved in a more gentlemanlike manner.'
But Sir Walter demonstrates the nature of the change in the use of the term in Chapter Three of Persuasion when he sarcastically says
'Wentworth? Oh! ay – Mr Wentworth, the curate of Monkford. You misled me by the term gentleman. I thought you were speaking of some man of property: Mr Wentworth was nobody, I remember; quite unconnected; nothing to do with the Strafford family. One wonders how the names of many of our nobility become so common.'
For the earlier Jane Austen it was not so much a question of property as propriety – that is, correct moral behaviour (although both words have the same Latin root proprietas). Edmund Bertram in Mansfield Park means exactly that when Mary Crawford questions the value of the clergy and he replies
'I cannot call that situation nothing which has charge of all that is of the first importance to mankind, individually or collectively considered, temporally and eternally – which has the guardianship of religion and morals, and consequently of the manners which result from their influence … The manners I speak of, might rather be called conduct, perhaps, the result of good principles'
Sir Walter's final comment, of course, both shows how silly he is and how misplaced his values are regarding the definition of a gentleman – and how different they are from the two immediately preceding novels. Sir Walter represents a truly different world as does his heir, who is finally unmasked as deliberately manipulative and perhaps even criminal in his reported treatment of Mrs Smith. In other ways he is simply a continuation of that subset of morally bankrupt or careless superficially attractive young men who feature in Austen's earlier works: the George Wickhams, the John Willoughbys, the Henry Crawfords or the Frank Churchills. An example, perhaps, of Sir Walter's 'failings' taken to extremes; but one who carries a seriously disruptive threat, even as late in the novel as the opening of Chapter Twenty-One:
(Anne) felt a great deal of good towards (Mr Elliot). In spite of the mischief of his attentions, she owed him gratitude and regard, perhaps compassion. She could not help thinking much of the extraordinary circumstances attending their acquaintance; of the right which he seemed to have to interest her, by every thing in situation, by his own sentiments, by his early prepossession. It was altogether very extraordinary, – Flattering, but painful. There was much to regret. How she might have felt, had there been no Captain Wentworth in the case, was not worth any enquiry; for there was a Captain Wentworth …
Austen is not sentimentally romantic – she makes it clear that if Wentworth were to be removed from the situation then Mr Elliot is a serious contender to replace him in Anne's affections. But that is why Mrs Smith is introduced four chapters earlier, in that her express plot function seems to be to enlighten Anne (and the reader) as to Mr Elliot's core character. Even so, she is very much a latecomer whereas he is a named character from the opening chapter, as we have seen, with the strong indication of what comprises his core character in his determined pursuit of money as his reason for marriage.
However, I would suggest that Mrs Smith is important in other ways, and worthy of further consideration in her own right.
© Mike Liddell 2019