xero, kline & coma

xero, kline & coma is an artist run project space at 258 Hackney Road, London. It’s program, curated by Pil and Galia Kollectiv, focuses primarily on solo exhibitions by internationally established as well as emerging artists. Work by recent graduates King Conny Wobble and David Steans is being shown alongside projects like the Museum of American Art – Berlin, previously included in the Venice and Istanbul Biennales, Jeffrey Vallance, whose recent solo exhibition was at the Warhol Museum, and Plastique Fantastique, whose work has been shown at Tate Britain and the Pratt Manhatten Gallery, New York, with the aim of raising the profile of lesser known artists and allowing others to experiment with work that more institutional contexts don’t always permit. Some of the themes this program has explored have included fictional identities, a-chronological art histories and the mediation of ritual in time-based media. A commitment to critically engaged art is also central to the ethos of the space, and future shows include an exploration of unionism in art by Sophie Carapetian. As well as displaying new work, the gallery hosts events, talks and screenings. Most recently these have included meetings of the Political Currency of Art research group, a discussion and film screening dealing with the theme of ‘hostile objects’ led by Evan Calder Williams and Marina Vishmidt, a book launch for New Lines of Alliance, New Spaces of Liberty by Antonio Negri and Felix Guattari and an event dedicated to the theatre work of Slovenian art collective NSK, featuring a screening of unreleased documentation and a discussion about the future of total performance.

Frozen tears II

Russell, J. [Ed. & designer]. Including texts by Kathy Acker, Dominique Auch, Dennis Cooper, Trinie Dalton, Sue De Beer, Felix Ensslin, Dan Fox, Matthew Greene, Pierre Guyotat, Rachel Howe, Kevin Killian, Christopher Knowles, Gean Moreno, J.P. Munro, Paulina Olowska, Damon Packard, Allison Smith, Banks Violette, Benjamin Weissman, & Thom Wolf. 832 pages.

Pathogenic LRRK2 mutations do not alter gene expression in cell model systems or human brain tissue

Point mutations in LRRK2 cause autosomal dominant Parkinson's disease. Despite extensive efforts to determine the mechanism of cell death in patients with LRRK2 mutations, the aetiology of LRRK2 PD is not well understood. To examine possible alterations in gene expression linked to the presence of LRRK2 mutations, we carried out a case versus control analysis of global gene expression in three systems: fibroblasts isolated from LRRK2 mutation carriers and healthy, non-mutation carrying controls; brain tissue from G2019S mutation carriers and controls; and HEK293 inducible LRRK2 wild type and mutant cell lines. No significant alteration in gene expression was found in these systems following correction for multiple testing. These data suggest that any alterations in basal gene expression in fibroblasts or cell lines containing mutations in LRRK2 are likely to be quantitatively small. This work suggests that LRRK2 is unlikely to play a direct role in modulation of gene expression, although it remains possible that this protein can influence mRNA expression under pathogenic cicumstances.

Economic transformation in Ghana: where will the path lead?

In the context of the Ghanaian government’s objective of structural transformation with an emphasis on manufacturing, this paper provides a case study of economic transformation in Ghana, exploring patterns of growth, sectoral transformation, and agglomeration. We document and examine why, despite impressive growth and poverty reduction figures, Ghana’s economy has exhibited less transformation than might be expected for a country that has recently achieved middle-income status. Ghana’s reduced share of agriculture in the economy, unlike many successfully transformed countries in Asia and Latin America, has been filled by services, while manufacturing has stagnated and even declined. Likely causes include weak transformation of the agricultural sector and therefore little development of agroprocessing, the emergence of consumption cities and consumption-driven growth, upward pressure on the exchange rate, weak production linkages, and a poor environment for private-sector-led manufacturing.

Tackling drought stress: RECEPTOR-LIKE KINASES present new approaches

Global climate change and a growing population require tackling the reduction in arable land and improving biomass production and seed yield per area under varying conditions. One of these conditions is suboptimal water availability. Here, we review some of the classical approaches to dealing with plant response to drought stress and we evaluate how research on RECEPTOR-LIKE KINASES (RLKs) can contribute to improving plant performance under drought stress. RLKs are considered as key regulators of plant architecture and growth behavior, but they also function in defense and stress responses. The available literature and analyses of available transcript profiling data indeed suggest that RLKs can play an important role in optimizing plant responses to drought stress. In addition, RLK pathways are ideal targets for nontransgenic approaches, such as synthetic molecules, providing a novel strategy to manipulate their activity and supporting translational studies from model species, such as Arabidopsis thaliana, to economically useful crops.

Pathogenic Parkinson’s disease mutations across the functional domains of LRRK2 alter the autophagic/lysosomal response to starvation

LRRK2 is one of the most important genetic contributors to Parkinson’s disease (PD). Point mutations in this gene cause an autosomal dominant form of PD, but to date no cellular phenotype has been consis- tently linked with mutations in each of the functional domains (ROC, COR and Kinase) of the protein product of this gene. In this study, primary fibroblasts from individuals carrying pathogenic mutations in the three central domains of LRRK2 were assessed for alterations in the autophagy/lysosomal pathway using a combination of biochemical and cellular approaches. Mutations in all three domains resulted in alterations in markers for autophagy/lysosomal function compared to wild type cells. These data high- light the autophagy and lysosomal pathways as read outs for pathogenic LRRK2 function and as a marker for disease, and provide insight into the mechanisms linking LRRK2 function and mutations.