7 research outputs found
In the crevices of global capitalism: rural queer community formation
No full text“In the Crevices of Global Capitalism: Rural Queer Community Formation” is an interdisciplinary study of a cluster of intentional communities in Tennessee, referred to by residents as the “Gayborhood.” It asks what factors influence rural community-building, and how queer rurality is linked to larger historical, economic, and political patterns. As an interdisciplinary project, the dissertation draws on multiple methods, primarily ethnographic fieldwork, archival research, oral history, and media analysis. The project studies the Gayborhood not just from an LGBT history view, but more crucially from the perspective of the history of the land on which it is located. It argues that the creation of a queer community in rural Tennessee is predicated on several waves of displacement of other groups from the land, through an ongoing process of settler colonialism and capitalist exploitation. The dissertation makes four main interventions in the field of Queer Studies: First, it provides a reading of the concept of “labor of belonging.” The Gayborhood is created through constant labor, which is for the most part unremunerated, and not always acknowledged. This labor creates a multifaceted belonging: people belonging to a community, land belonging to people, and people belonging to the land. Second, the dissertation presents a theory of materiality and excess. The Gayborhood is in several ways built on waste: the utilizing of literal trash in building, discarded food in cooking, and also being located in a metaphorical post-industrial wasteland. Third, the project places rural queer intentional communities within the landscape of settler colonialism. The dissertation shows how the claiming of land by queer groups is predicated on the naturalization of white US citizenship, and the erasure of histories and presents of Native presence on the land. Fourth, the dissertation uses the concept of fermentation as metaphor and method. It poses that the process of fermentation, whereby microorganisms interact with feedstock materials in a process that combines decomposition and creation, can be used to explain how locations such as the Gayborhood become possible, and how they change.Ph.D.Includes bibliographical referencesby Stina Soderlin
Anarchist Pedagogy in the Gender and Women’s Studies Classroom
No full textAbstract
This article argues for the value of employing anarchist pedagogical methods in introductory Gender and Women’s Studies courses. The author draws on her experiences using feminist and anarchist pedagogical literature as well as her own experiences using anarchist pedagogy. Topics addressed include classroom structure, syllabus design, grading, and the question of opinions and neutrality.
Résumé
Cet article défend le mérite d’employer des méthodes pédagogiques anarchistes dans les cours d’introduction aux Études sur le genre et les femmes. L’auteure s’appuie sur ses expériences de l’utilisation de matériel pédagogique féministe et anarchiste ainsi que sur ses propres expériences de l’utilisation de la pédagogie anarchiste. Les sujets abordés comprennent la structure de la salle de classe, la conception du programme d’études, la notation et la question des opinions et de la neutralité
Anarchist Pedagogy in the Gender and Women’s Studies Classroom
No full textThis article argues for the value of employing anarchist pedagogical methods in introductory Gender and Women’s Studies courses. The author draws on her experiences using feminist and anarchist pedagogical literature as well as her own experiences using anarchist pedagogy. Topics addressed include classroom structure, syllabus design, grading, and the question of opinions and neutrality.Cet article défend le mérite d’employer des méthodes pédagogiques anarchistes dans les cours d’introduction aux Études sur le genre et les femmes. L’auteure s’appuie sur ses expériences de l’utilisation de matériel pédagogique féministe et anarchiste ainsi que sur ses propres expériences de l’utilisation de la pédagogie anarchiste. Les sujets abordés comprennent la structure de la salle de classe, la conception du programme d’études, la notation et la question des opinions et de la neutralité
Review of: © 2014, Kim et al. This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
No full textCdc42 is a signaling protein important for reorganization of actin cytoskeleton and morphogenesis of cells. However, the functional role of Cdc42 in synaptic plasticity and in behaviors such as learning and memory are not well understood. Here we report that postnatal forebrain deletion of Cdc42 leads to deficits in synaptic plasticity and in remote memory recall using conditional knockout of Cdc42. We found that deletion of Cdc42 impaired LTP in the Schaffer collateral synapses and postsynaptic structural plasticity of dendritic spines in CA1 pyramidal neurons in the hippocampus. Additionally, loss of Cdc42 did not affect memory acquisition, but instead significantly impaired remote memory recall. Together these results indicate that the postnatal functions of Cdc42 may be crucial for the synaptic plasticity in hippocampal neurons, which contribute to the capacity for remote memory recall.DOI: http://dx.doi.org/10.7554/eLife.02839.001View Full TextTo Top Cdc42 is a signaling protein important for reorganization of actin cytoskeleton and morphogenesis of cells. However, the functional role of Cdc42 in synaptic plasticity and in behaviors such as learning and memory are not well understood. Here we report that postnatal forebrain deletion of Cdc42 leads to deficits in synaptic plasticity and in remote memory recall using conditional knockout of Cdc42. We found that deletion of Cdc42 impaired LTP in the Schaffer collateral synapses and postsynaptic structural plasticity of dendritic spines in CA1 pyramidal neurons in the hippocampus. Additionally, loss of Cdc42 did not affect memory acquisition, but instead significantly impaired remote memory recall. Together these results indicate that the postnatal functions of Cdc42 may be crucial for the synaptic plasticity in hippocampal neurons, which contribute to the capacity for remote memory recall. DOI: http://dx.doi.org/10.7554/eLife.02839.001 Neurons communicate with one another at junctions called synapses, which are typically formed between the dendrite of one neuron and the axon terminus of another. The dendrites are protrusions coming out of the cell body that receive inputs from other cells; the axon is a cable-like structure that enables neurons to contact other cells. In excitatory neurons in part of the brain called the hippocampus, the dendrites are themselves covered in structures called spines, so most synapses are formed between an axon terminus (belonging to the presynaptic cell) and a dendritic spine (on the postsynaptic cell). The hippocampus is necessary for the formation of long-term memories. The strength of a synapse can increase or decrease over time—a property that is called synaptic plasticity. Changes in the strength of synapses are thought to underlie learning and memory, and long-lasting changes in synaptic strength involve increases or decreases in the number and size of dendritic spines. Such changes are possible because spines have an internal skeleton that can be assembled and disassembled in a matter of minutes. This ‘remodeling’ process is regulated by a family of enzymes called small GTPases. One of these, known as Cdc42, has been shown to promote the formation and maintenance of spines in cell culture, but its role in synaptic plasticity, learning and memory remains unknown. Now, Kim, Wang et al. have used genetically modified mice who have had Cdc42 deleted from excitatory neurons in their forebrain to examine the functions of this enzyme in living animals. These ‘knockout’ mice showed a small but statistically significant reduction in the number of dendritic spines in the hippocampus. They also showed smaller changes in spine volume and impaired long-term synaptic plasticity in the hippocampus. When the mice performed long-term memory tests where they learnt to associate a specific set of visual cues with an impending electric shock, the knockout mice performed well for up to a few days. However, when tested again on the same task 45 days later, the knockout mice did not perform as well as normal mice. This is surprising, given the presumed role of long-term synaptic plasticity in learning and memory, and indicates that Cdc42 is required for ‘remote memory’, the form of memory lasting for many days. Similar results were obtained with another memory test using a water maze, where the animals have to remember the location of a hidden platform. Normal mice remember the location for more than 30 days. In contrast, the knockout mice could only remember the location for a few days. As well as providing the first demonstration of the role of Cdc42 in synaptic plasticity in live animals, the work of Kim, Wang et al. has provided new insights into the functions of this enzyme in memory. Further work is required to determine how Cdc42 interacts with other proteins present at synapses. DOI: http://dx.doi.org/10.7554/eLife.02839.00
The regulation of tau-dependent neurodegeneration by Brain Selective/SAD kinases
No full textBrain-selective kinases (BRSK1 and BRSK2) are serine/threonine kinase members
of the AMPK-related family of protein kinases, the majority of which are regulated
by the upstream kinase LKB1 whilst AMPK itself is regulated by CaMKK. The
BRSKs are highly expressed in brain and have been implicated in neuronal
polarization and the regulation of neurotransmitter release. They have also been
shown to be involved in the basal phosphorylation of tau at the Alzheimer‟s disease
(AD) related residue, serine 262, and are highly expressed in areas of the brain
affected by AD, namely the hippocampus and the cortex. I have utilised the model
organism Drosophila melanogaster to investigate interactions between transgenically
expressed human tau, human BRSKs and upstream regulators
Selective over-expression of 0N4R human tau in the Drosophila eye resulted in a
disruption of eye morphology. In contrast, over-expression of human wild type
BRSK2 (B-WT) had no obvious effect on the eye. However, co-expression of both
tau and B-WT resulted in a neurodegenerative phenotype more severe than tau alone.
This enhancement of phenotype was not observed when BRSK2 was expressed that
either lacked the activating phosphorylation site (non-phosphorylatable, B-NP) or
that is unable to bind ATP (kinase dead, B-KD). Co-expression of human tau and BWT
significantly elevated tau phosphorylation at S262, suggesting that S262 is a key
residue for tau-induced toxic phenotypes and the BRSK/tau interaction I observe. In
support of this, no phenotype was observed in flies expressing the S262A variant of
human tau with or without B-WT.
To establish the upstream kinases responsible for activating human BRSK2 in
Drosophila I removed endogenous Drosophila LKB1 by RNAi. This prevented the
enhanced degeneration of the eye caused by tau/B-WT co-expression, demonstrating
that LKB1 is a key upstream regulator of BRSK2. I also found that down regulation
of the Drosophila CaMKK homologue, CG17698, by the same method, ameliorated
B-WT induced eye degeneration implicating a calcium-dependent pathway in the
regulation of BRSK. Over-expression of human CaMKKα in the CG17698 RNAi
background prevented the rescue seen with CG17698 RNAi. Over-expression of
cac1, a calcium channel subunit, in the presence of B-WT and human tau
exacerbated the B-WT induced eye phenotype in a B-WT dependent manner,
supporting the hypothesis that the human tau and B-WT interaction can be regulated
in a calcium-dependent manner.
Expression of total BRSK2, LKB1 and CaMKK were not altered in human postmortem
AD brain tissue when compared to control. However, with the exception of
LKB1, due to limited reagents and time constraints I was unable to investigate the
proportion of phosphorylated (and thus active) to total kinase.
This study defines a novel Ca2+ -dependent regulatory pathway to tau, which may
contribute to AD and other tauopathies
