Entrepreneurial dynamics and social responsibility: mapping an expanded intellectual territory

Objectives: (1) To provide a constructive critique of the interface between the entrepreneurial growth dynamics research and social responsibility literatures; (2) to explore opportunities for making new connections between these literatures in order to address substantive ‘gaps’ in research and policy-making ; (3) to map the broader intellectual territory implied by this critique; (4) to outline a tentative research agenda. Prior work: The paper draws on two main strands of research: entrepreneurial growth dynamics and (corporate) social responsibility. While much has been achieved in the social responsibility literature with regards to established practices, we argue that insufficient attention has been paid to the more ‘entrepreneurial’ dimensions. At the same time, the current wave of enthusiasm for new models of socially-responsible enterprise has opened up a series of new research questions, including: (i) how are these organisational forms likely to grow and develop over the longer-term, at an intra-organisational level, and in terms of emerging inter-organisational relationships?; (iii) how will other actors respond to these developments?; (ii) what are the implications of the resulting dynamics for social, environmental and economic sustainability? Approach: The paper is based around a critical review of the relevant literatures, focusing on the role of entrepreneurial opportunity and capabilities in shaping entrepreneurial growth dynamics. The discussion addresses current methodological debates and considers how social responsibility can be integrated into the analysis. In doing so, it builds on a research tradition that has promoted historically-informed multi-level and co-evolutionary analysis and argues that such techniques are required in order to gain a better understanding of these phenomena. Results: We outline a research agenda, illustrated with a number of questions of particular relevance to researchers, policy-makers and practitioners Implications: The paper identifies a number of issues for researchers and policy-makers and practitioner audiences. It calls for a broadening of the intellectual territory around socially-responsible enterprise. Process-based and multi-level analysis of growth dynamics extends its temporal and organisational boundaries to encompass longer-term interactions and a wider range of actors. Value: The paper is designed to facilitate and to encourage more constructive interaction between research communities concerned with: social responsibility, social enterprise and process-based approaches to entrepreneurship. It advances understanding by mapping an intellectual space that is neither fully revealed in, nor adequately addressed by, existing bodies of knowledge

Loss of strumpellin in the melanocytic lineage impairs the WASH Complex but does not affect coat colour

The five-subunit WASH complex generates actin networks that participate in endocytic trafficking, migration and invasion in various cell types. Loss of one of the two subunits WASH or strumpellin in mice is lethal, but little is known about their role in mammals in vivo. We explored the role of strumpellin, which has previously been linked to hereditary spastic paraplegia, in the mouse melanocytic lineage. Strumpellin knockout in melanocytes revealed abnormal endocytic vesicle morphology but no impairment of migration in vitro or in vivo and no change in coat colour. Unexpectedly, WASH and filamentous actin could still localize to vesicles in the absence of strumpellin, although the shape and size of vesicles was altered. Blue native PAGE revealed the presence of two distinct WASH complexes, even in strumpellin knockout cells, revealing that the WASH complex can assemble and localize to endocytic compartments in cells in the absence of strumpellin

Adolescent Weight Status and Related Behavioural Factors: Web Survey of Physical Activity and Nutrition

Purpose. To identify whether non-overweight students were different from their overweight or obese peers with respect to diet, suboptimal meal behaviours, and physical activity using a self-administered web-based survey. Methods. 4097 adolescents living in Alberta, Canada completed Web-SPAN (Web Survey of Physical Activity and Nutrition). Students were classified as overweight or obese, and differences were described in terms of nutrient intakes, physical activity, and meal behaviours. Results. Non-overweight students consumed significantly more carbohydrate and fibre, and significantly less fat and high calorie beverages, and had a higher frequency of consuming breakfast and snacks compared to overweight or obese students. Both non-overweight and overweight students were significantly more active than obese students. Conclusions. This research supports the need to target suboptimal behaviours such as high calorie beverage consumption, fat intake, breakfast skipping, and physical inactivity. School nutrition policies and mandatory physical education for all students may help to improve weight status in adolescents

Adolescent Weight Status and Related Behavioural Factors: Web Survey of Physical Activity and Nutrition

Purpose. To identify whether non-overweight students were different from their overweight or obese peers with respect to diet, suboptimal meal behaviours, and physical activity using a self-administered web-based survey. Methods. 4097 adolescents living in Alberta, Canada completed Web-SPAN (Web Survey of Physical Activity and Nutrition). Students were classified as overweight or obese, and differences were described in terms of nutrient intakes, physical activity, and meal behaviours. Results. Non-overweight students consumed significantly more carbohydrate and fibre, and significantly less fat and high calorie beverages, and had a higher frequency of consuming breakfast and snacks compared to overweight or obese students. Both non-overweight and overweight students were significantly more active than obese students. Conclusions. This research supports the need to target suboptimal behaviours such as high calorie beverage consumption, fat intake, breakfast skipping, and physical inactivity. School nutrition policies and mandatory physical education for all students may help to improve weight status in adolescents

Loss of N-WASP drives early progression in an Apc model of intestinal tumourigenesis

N‐WASP (WASL) is a widely expressed cytoskeletal signalling and scaffold protein also implicated in regulation of Wnt signalling and homeostatic maintenance of skin epithelial architecture. N‐WASP mediates invasion of cancer cells in vitro and its depletion reduces invasion and metastatic dissemination of breast cancer. Given this role in cancer invasion and universal expression in the gastrointestinal tract, we explored a role for N‐WASP in the initiation and progression of colorectal cancer. While deletion of N‐wasp is not detectably harmful in the murine intestinal tract, numbers of Paneth cells increased, indicating potential changes in the stem cell niche and migration up the crypt‐villus axis was enhanced. Loss of N‐wasp promoted adenoma formation in an adenomatous polyposis coli (Apc) deletion model of intestinal tumourigenesis. Thus, we establish a tumour suppressive role of N‐WASP in early intestinal carcinogenesis despite its later pro‐invasive role in other cancers. Our study highlights that while the actin cytoskeletal machinery promotes invasion of cancer cells, it also maintains normal epithelial tissue function and thus may have tumour suppressive roles in pre‐neoplastic tissues

Mtss1 promotes cell-cell junction assembly and stability through the small GTPase Rac1

Cell-cell junctions are an integral part of epithelia and are often disrupted in cancer cells during epithelial-to-mesenchymal transition (EMT), which is a main driver of metastatic spread. We show here that Metastasis suppressor-1 (Mtss1; Missing in Metastasis, MIM), a member of the IMD-family of proteins, inhibits cell-cell junction disassembly in wound healing or HGF-induced scatter assays by enhancing cell-cell junction strength. Mtss1 not only makes cells more resistant to cell-cell junction disassembly, but also accelerates the kinetics of adherens junction assembly. Mtss1 drives enhanced junction formation specifically by elevating Rac-GTP. Lastly, we show that Mtss1 depletion reduces recruitment of F-actin at cell-cell junctions. We thus propose that Mtss1 promotes Rac1 activation and actin recruitment driving junction maintenance. We suggest that the observed loss of Mtss1 in cancers may compromise junction stability and thus promote EMT and metastasis