Garden histories since the mid 1990s have increasingly turned to studies of vernacular gardens as sites of identity formation. More recently, the development of environmental history and specifically urban environmental history has started to show how vernacular gardening in suburban and urban spaces has contributed to changes in urban environments. Relatively little work on home gardening history in this sense has been undertaken in the New Zealand context, while in Australia such work is well underway. This study augments knowledge of home gardening history in New Zealand by focussing on one urban area, Christchurch, known both as the 'Garden City' and as 'one of the most English cities outside of England'. An examination of gardening literature over the period from European colonisation in 1850 to the first visit to the city by a reigning monarch in 1954 highlights changes in gardening tropes rather than particular garden fashions or elements. The four principal tropes of abundance, beauty, protection and sustenance, each supported with a particular kind of ritual-like garden competition, show how gardening discourses related to ideas about the maintenance of the social and cultural order. A more objective measure of attitudes to gardens is gained by examining 1823 property advertisements across the period. Categorised by suburb this analysis shows a level of gardening variation across the city. Following this analysis, case studies of four suburbs in three areas were undertaken. These were based primarily on oral histories and reveal the extent of gardening variation across the city, and the limited but significant effect that gardening discourses had on gardens. This suggests methodological problems with many studies of vernacular gardens, as well as opportunities for further studies. This thesis also demonstrates the value of home gardening histories to urban environmental history, particularly with regard to the former colonies of the British Empire.

A principal aim of this research has been to establish the capacity of British Gangland film to articulate its era of production through the cinematic interpretation of contemporary concerns and anxieties in narratives relating to the criminal underworld. In order to do so, the study has concentrated on the analysis of space, gender and hierarchy within representative generic texts produced between 1945 and the present. The thesis is divided into three sections: the first offers a general overview of British Gangland film from the 65 years under discussion with the aim of identifying recurring generic patterns and motifs. The second and third sections are more specifically focused, their chapters examining the narrative significance and development of the male and the female protagonist respectively. Within the films under discussion, the relationship between these protagonists and their environment represents a fundamental generic component, resulting in an emphasis on space and place. Space within these narratives is inherently territorial, and thus irrevocably bound up with hierarchies of power. The predominantly urban locations in which the narratives are set represent a twilight world, a demi-monde, which is rarely neutral but dominated by the patriarchal order structuring the notion of ‘Gangland’. Such spaces are therefore inextricably linked with gender, hierarchy, and dynamic power relations. Whilst it would have been possible to explore each of these areas in isolation through specifically relevant theoretical perspectives, their interdependence is central to this study. Consequently, a holistic theoretical approach has facilitated analysis of the symbiotic relationship between the three key elements of space, gender and hierarchy and the processes involved in the generation of meaning: this has resulted in a reading of British Gangland film as cultural artefact, reflecting its circumstances of production.

To wield direct influence on the everyday lives of citizens, new political elites have often professed a profound interest in shaping the politics of dwelling. In the 1920s, Vienna’s Social Democrats built 400 communal housing blocks equipped with public gardens, theaters, libraries, kindergartens, and sports facilities, hoping that these facilities would serve as loci for “growing into socialism”. In the 1950s, housing construction in Berlin became a site of the Cold War. East Berlin’s social realist “workers palaces” on Stalinallee were meant to serve as an ideal flourishing ground for the “new socialist men and women”. In contrast, West Berlin's modernist Hansa-Viertel was designed to showcase an ideal dwelling culture and an urban environment that would cultivate individuality. This dissertation examines three historically situated and ideologically distinct responses to the housing question: social democracy in Red Vienna, state socialism in East Berlin, and liberal capitalism in West Berlin. It illuminates how political promises of a radical new beginning were translated into spatial arrangements—the private scale of the apartment and the urban scale of the city—as well as how citizens appropriated the social, political, and economic norms inherent to the new spaces they inhabited. More specifically, the following analyses demonstrate the fact that inherited social, technological, and economic practices have often subverted political visions of a radically different future. This was the case with pedagogy in Red Vienna’s municipal housing, instrumental reason in the form of Taylorism and Fordism in East and West Berlin’s mass housing, and gender relations in Red Vienna’s and East Berlin’s politics of dwelling. At the same time, this dissertation examines counter-spaces that emerged from the dialectics between political promises and actual socio-spatial realities, counter-spaces that both reflect critically on past hegemonic “politics of dwelling” and that foreshadow alternative political imaginations that are still relevant today. Of particular interest are counter-hegemonic practices of dwelling that embody possibilities of emancipation—of experiencing oneself as subject instead of object of social transformation, justice—of emphasizing considerations of equality and recognition, and radical democracy—of questioning power relations and of forming alliances among disadvantaged groups to transform everyday life.

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To wield direct influence on the everyday lives of citizens, new political elites have often professed a profound interest in shaping the politics of dwelling. In the 1920s, Vienna’s Social Democrats built 400 communal housing blocks equipped with public gardens, theaters, libraries, kindergartens, and sports facilities, hoping that these facilities would serve as loci for “growing into socialism”. In the 1950s, housing construction in Berlin became a site of the Cold War. East Berlin’s social realist “workers palaces” on Stalinallee were meant to serve as an ideal flourishing ground for the “new socialist men and women”. In contrast, West Berlin's modernist Hansa-Viertel was designed to showcase an ideal dwelling culture and an urban environment that would cultivate individuality. This dissertation examines three historically situated and ideologically distinct responses to the housing question: social democracy in Red Vienna, state socialism in East Berlin, and liberal capitalism in West Berlin. It illuminates how political promises of a radical new beginning were translated into spatial arrangements—the private scale of the apartment and the urban scale of the city—as well as how citizens appropriated the social, political, and economic norms inherent to the new spaces they inhabited. More specifically, the following analyses demonstrate the fact that inherited social, technological, and economic practices have often subverted political visions of a radically different future. This was the case with pedagogy in Red Vienna’s municipal housing, instrumental reason in the form of Taylorism and Fordism in East and West Berlin’s mass housing, and gender relations in Red Vienna’s and East Berlin’s politics of dwelling. At the same time, this dissertation examines counter-spaces that emerged from the dialectics between political promises and actual socio-spatial realities, counter-spaces that both reflect critically on past hegemonic “politics of dwelling” and that foreshadow alternative political imaginations that are still relevant today. Of particular interest are counter-hegemonic practices of dwelling that embody possibilities of emancipation—of experiencing oneself as subject instead of object of social transformation, justice—of emphasizing considerations of equality and recognition, and radical democracy—of questioning power relations and of forming alliances among disadvantaged groups to transform everyday life.

Embargoed until 1 January 2011 / The filamin family act as scaffolding proteins associating with actin filmanents, acting through a highly conserved actin binding domain (ABD). The ABD of the filamins is homologous to that found in other F-actin binding proteins such as dystrophin. Mutations in the filamin A gene cause a wide range of disease symptoms in humans reflecting the diversity of the roles that filamin A has in cell structure and signalling pathways. The diseases fall into two separate phenotypic groups. Periventricular nodular heterotopia (PVNH) generally results from the complete loss of filamin A protein, and affects the central nervous system. The clinically separate otopalatodigital disorders (OPD) spectrum disorders are skeletal disorders and were hypothesised to be gain of function phenotype diseases. At the beginning of this work, there was very little structural data available for the human filamins, and none for the crucial highly conserved actin binding domain. This lack of structural data limited the interpretation of the biochemical and genetic data and constrained our understanding of the disease associated mutations that cluster in this domain. These studies aimed to provide insights into the structure and mechanism of actin binding domains, and thus provide a better understanding of the diseases caused when this domain is mutated. A secondary structural analysis and crystal structures of the wildtype and OPD2 associated mutant ABDs were obtained. The overall fold of the three proteins was equivalent as determined by circular dichroism spectroscopy and x-ray crystallography. The ABD from filamin A E254K showed 3.7 fold increased F-actin affinity, accompanied by a reduced thermostability (of 5.6 °C). Western blotting of OPD2, frontometaphyseal dysplasia (FMD) and PVNH patient fibroblast lysates showed similar levels of filamin A compared to the control cells. In addition the OPD and PVNH patient fibroblasts were able to adhere to fibronectin and migrate with an equivalent rate to control cells. Together these results have allowed correlations to be developed between structure, protein stability, actin affinity, cellular phenotype and the overall clinical phenotype. Showing that, at least in one example, OPD2 may be due to an increased actin affinity providing further evidence for a gain of function mechanism of OPD2.

Embargoed until 1 January 2011 / The filamin family act as scaffolding proteins associating with actin filmanents, acting through a highly conserved actin binding domain (ABD). The ABD of the filamins is homologous to that found in other F-actin binding proteins such as dystrophin. Mutations in the filamin A gene cause a wide range of disease symptoms in humans reflecting the diversity of the roles that filamin A has in cell structure and signalling pathways. The diseases fall into two separate phenotypic groups. Periventricular nodular heterotopia (PVNH) generally results from the complete loss of filamin A protein, and affects the central nervous system. The clinically separate otopalatodigital disorders (OPD) spectrum disorders are skeletal disorders and were hypothesised to be gain of function phenotype diseases. At the beginning of this work, there was very little structural data available for the human filamins, and none for the crucial highly conserved actin binding domain. This lack of structural data limited the interpretation of the biochemical and genetic data and constrained our understanding of the disease associated mutations that cluster in this domain. These studies aimed to provide insights into the structure and mechanism of actin binding domains, and thus provide a better understanding of the diseases caused when this domain is mutated. A secondary structural analysis and crystal structures of the wildtype and OPD2 associated mutant ABDs were obtained. The overall fold of the three proteins was equivalent as determined by circular dichroism spectroscopy and x-ray crystallography. The ABD from filamin A E254K showed 3.7 fold increased F-actin affinity, accompanied by a reduced thermostability (of 5.6 °C). Western blotting of OPD2, frontometaphyseal dysplasia (FMD) and PVNH patient fibroblast lysates showed similar levels of filamin A compared to the control cells. In addition the OPD and PVNH patient fibroblasts were able to adhere to fibronectin and migrate with an equivalent rate to control cells. Together these results have allowed correlations to be developed between structure, protein stability, actin affinity, cellular phenotype and the overall clinical phenotype. Showing that, at least in one example, OPD2 may be due to an increased actin affinity providing further evidence for a gain of function mechanism of OPD2.

Embargoed until 1 January 2011 / The filamin family act as scaffolding proteins associating with actin filmanents, acting through a highly conserved actin binding domain (ABD). The ABD of the filamins is homologous to that found in other F-actin binding proteins such as dystrophin. Mutations in the filamin A gene cause a wide range of disease symptoms in humans reflecting the diversity of the roles that filamin A has in cell structure and signalling pathways. The diseases fall into two separate phenotypic groups. Periventricular nodular heterotopia (PVNH) generally results from the complete loss of filamin A protein, and affects the central nervous system. The clinically separate otopalatodigital disorders (OPD) spectrum disorders are skeletal disorders and were hypothesised to be gain of function phenotype diseases. At the beginning of this work, there was very little structural data available for the human filamins, and none for the crucial highly conserved actin binding domain. This lack of structural data limited the interpretation of the biochemical and genetic data and constrained our understanding of the disease associated mutations that cluster in this domain. These studies aimed to provide insights into the structure and mechanism of actin binding domains, and thus provide a better understanding of the diseases caused when this domain is mutated. A secondary structural analysis and crystal structures of the wildtype and OPD2 associated mutant ABDs were obtained. The overall fold of the three proteins was equivalent as determined by circular dichroism spectroscopy and x-ray crystallography. The ABD from filamin A E254K showed 3.7 fold increased F-actin affinity, accompanied by a reduced thermostability (of 5.6 °C). Western blotting of OPD2, frontometaphyseal dysplasia (FMD) and PVNH patient fibroblast lysates showed similar levels of filamin A compared to the control cells. In addition the OPD and PVNH patient fibroblasts were able to adhere to fibronectin and migrate with an equivalent rate to control cells. Together these results have allowed correlations to be developed between structure, protein stability, actin affinity, cellular phenotype and the overall clinical phenotype. Showing that, at least in one example, OPD2 may be due to an increased actin affinity providing further evidence for a gain of function mechanism of OPD2.

Embargoed until 1 January 2011 / The filamin family act as scaffolding proteins associating with actin filmanents, acting through a highly conserved actin binding domain (ABD). The ABD of the filamins is homologous to that found in other F-actin binding proteins such as dystrophin. Mutations in the filamin A gene cause a wide range of disease symptoms in humans reflecting the diversity of the roles that filamin A has in cell structure and signalling pathways. The diseases fall into two separate phenotypic groups. Periventricular nodular heterotopia (PVNH) generally results from the complete loss of filamin A protein, and affects the central nervous system. The clinically separate otopalatodigital disorders (OPD) spectrum disorders are skeletal disorders and were hypothesised to be gain of function phenotype diseases. At the beginning of this work, there was very little structural data available for the human filamins, and none for the crucial highly conserved actin binding domain. This lack of structural data limited the interpretation of the biochemical and genetic data and constrained our understanding of the disease associated mutations that cluster in this domain. These studies aimed to provide insights into the structure and mechanism of actin binding domains, and thus provide a better understanding of the diseases caused when this domain is mutated. A secondary structural analysis and crystal structures of the wildtype and OPD2 associated mutant ABDs were obtained. The overall fold of the three proteins was equivalent as determined by circular dichroism spectroscopy and x-ray crystallography. The ABD from filamin A E254K showed 3.7 fold increased F-actin affinity, accompanied by a reduced thermostability (of 5.6 °C). Western blotting of OPD2, frontometaphyseal dysplasia (FMD) and PVNH patient fibroblast lysates showed similar levels of filamin A compared to the control cells. In addition the OPD and PVNH patient fibroblasts were able to adhere to fibronectin and migrate with an equivalent rate to control cells. Together these results have allowed correlations to be developed between structure, protein stability, actin affinity, cellular phenotype and the overall clinical phenotype. Showing that, at least in one example, OPD2 may be due to an increased actin affinity providing further evidence for a gain of function mechanism of OPD2.

Embargoed until 1 January 2011 / The filamin family act as scaffolding proteins associating with actin filmanents, acting through a highly conserved actin binding domain (ABD). The ABD of the filamins is homologous to that found in other F-actin binding proteins such as dystrophin. Mutations in the filamin A gene cause a wide range of disease symptoms in humans reflecting the diversity of the roles that filamin A has in cell structure and signalling pathways. The diseases fall into two separate phenotypic groups. Periventricular nodular heterotopia (PVNH) generally results from the complete loss of filamin A protein, and affects the central nervous system. The clinically separate otopalatodigital disorders (OPD) spectrum disorders are skeletal disorders and were hypothesised to be gain of function phenotype diseases. At the beginning of this work, there was very little structural data available for the human filamins, and none for the crucial highly conserved actin binding domain. This lack of structural data limited the interpretation of the biochemical and genetic data and constrained our understanding of the disease associated mutations that cluster in this domain. These studies aimed to provide insights into the structure and mechanism of actin binding domains, and thus provide a better understanding of the diseases caused when this domain is mutated. A secondary structural analysis and crystal structures of the wildtype and OPD2 associated mutant ABDs were obtained. The overall fold of the three proteins was equivalent as determined by circular dichroism spectroscopy and x-ray crystallography. The ABD from filamin A E254K showed 3.7 fold increased F-actin affinity, accompanied by a reduced thermostability (of 5.6 °C). Western blotting of OPD2, frontometaphyseal dysplasia (FMD) and PVNH patient fibroblast lysates showed similar levels of filamin A compared to the control cells. In addition the OPD and PVNH patient fibroblasts were able to adhere to fibronectin and migrate with an equivalent rate to control cells. Together these results have allowed correlations to be developed between structure, protein stability, actin affinity, cellular phenotype and the overall clinical phenotype. Showing that, at least in one example, OPD2 may be due to an increased actin affinity providing further evidence for a gain of function mechanism of OPD2.