UNmet: The Undergraduate Experience of Basic Need Insecurity at an UNcommon University

Virginia Commonwealth University’s (VCU) Dean of Students office submitted a Request for Assistance with needs related to food and housing insecurity and lack of basic funds for students. To address this request, a doctoral Capstone team conducted a problem and context analysis, literature review, student focus groups, and an internal survey of departments. The goal was to explore the undergraduate experience of unmet needs and to identify gaps and overlaps in basic needs support and services already provided at VCU. Findings suggest that students do not know the resources available to them through the Dean of Students office, that students feel variable support in meeting their basic needs by VCU, and that institutional collaboration is limited around data sharing and services. The Capstone team identified critical challenges for the Dean of Students office, the greater VCU community, and strategies to improve the Culture of Care. Recommendations focused on tangible actions for the DOS office and others to make pertaining to basic needs insecurity and reframing the responsibility to reflect a campus-wide mindset, increasing awareness and usage of basic needs services, and leveraging data to maximize support

Essential cooperation of N-cadherin and neuroligin-1 in the transsynaptic control of vesicle accumulation

Cell adhesion molecules are key players in transsynaptic communication, precisely coordinating presynaptic differentiation with postsynaptic specialization. At glutamatergic synapses, their retrograde signaling has been proposed to control presynaptic vesicle clustering at active zones. However, how the different types of cell adhesion molecules act together during this decisive step of synapse maturation is largely unexplored. Using a knockout approach, we show that two synaptic adhesion systems, N-cadherin and neuroligin-1, cooperate to control vesicle clustering at nascent synapses. Live cell imaging and fluorescence recovery after photobleaching experiments at individual synaptic boutons revealed a strong impairment of vesicle accumulation in the absence of N-cadherin, whereas the formation of active zones was largely unaffected. Strikingly, also the clustering of synaptic vesicles triggered by neuroligin-1 overexpression required the presence of N-cadherin in cultured neurons. Mechanistically, we found that N-cadherin acts by postsynaptically accumulating neuroligin-1 and activating its function via the scaffolding molecule S-SCAM, leading, in turn, to presynaptic vesicle clustering. A similar cooperation of N-cadherin and neuroligin-1 was observed in immature CA3 pyramidal neurons in an organotypic hippocampal network. Moreover, at mature synapses, N-cadherin was required for the increase in release probability and miniature EPSC frequency induced by expressed neuroligin-1. This cooperation of two cell adhesion systems provides a mechanism for coupling bidirectional synapse maturation mediated by neuroligin-1 to cell type recognition processes mediated by classical cadherins