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Giving a voice to marginalized groups and understanding the double bind is critical, especially after the Charlotte, VA protests and the white supremacist discourse that has pervaded our country. The result of the discourse, more subtle beliefs about white superiority and institutional barriers is an overrepresentation of women of color (WOC) in the leaky STEM pipeline and thus the loss of their presence and expertise. The absence of WOC hinders knowledge production and innovation that is essential for societal advancements and scientific discovery. The “chilly climate” is often cited as an explanation for the loss of WOC from STEM. However, interactions that allow the “chilly climate” to persist have yet to be characterized. This lack of understanding can inhibit the professional engineering identity construction of WOC. Additionally, engineering education research typically focuses on a single identity dimension such as gender or socio-economic status. These studies connect an identity dimension to student outcomes and few studies clarify how the identity is situated within the social context of the engineering culture. Consequently, a need exist to examine how the engineering culture impacts multiple components of identity and intersecting identities of WOC. To address this gap, our study illuminates the intersections of identity of WOC and how they perceive the double bind of race and gender within the context of their engineering education. The data reported here are a part of a larger, sequential mixed-methods study (N=276) of undergraduate female engineering students at a large Midwestern research university. This project applies the framework of intersectionality with the following scales: Engineering Identity, Ethnic Identity, Womanist Identity, Microaggressions, and Depression. We use intersectionality to investigate the interaction between intersecting social identities and educational conditions. We introduce the Womanist Identity Attitude scale to engineering education research, which provides an efficient way to understand gender, racial, and intersecting identity development of WOC. We utilize the microaggressions scale, in order to develop quantitative measures of gender-racial discrimination in STEM and compare to previous research. We also included the Patient Health Questionnaire (PHQ-9), an instrument for measuring depression, to assess health outcomes of respondents’ experiences of gender-racial microaggressions. Our three emergent findings suggest instrument accuracy and provide insight into the identity and depression subscales. Factor analysis established a basis to refine our quantitative survey instruments, and indicated that 23 items could offer greater accuracy than the original 54 items instrument. Second, the majority of participants report a high level of identification with engineering. This result rebuffs the long-held stereotypes that females are less interested in engineering. Third, a significant portion of female respondents self-reported PHQ-9 scores in the 15-19 range, which corresponds with a “major depression, moderately severe” provisional diagnosis, the second-highest in severity in the PHQ-9 provisional diagnosis scale. These elevated levels of depression correlated significantly to frequent instances of microaggressions. These preliminary findings are providing never-before seen insight into the experiences of WOC in engineering. Our results suggest a path to accurately describe the experiences of WOC in engineering, while revealing options for improving inclusion efforts. 

Recently, intracellular receptor signaling has been identified as a key component mediating cell responses for various receptor tyrosine kinases (RTKs). However, the extent each endocytic compartment (endocytic vesicle, early endosome, recycling endosome, late endosome, lysosome and nucleus) contributes to receptor signaling has not been quantified. Furthermore, our understanding of endocytosis and receptor signaling is complicated by cell- or receptor-specific endocytosis mechanisms. Therefore, towards understanding the differential endocytic compartment signaling roles, and identifying how to achieve signal transduction control for RTKs, we delineate how endocytosis regulates RTK signaling. We achieve this via a meta-analysis across eight RTKs, integrating computational modeling with experimentally derived cell (compartment volume, trafficking kinetics and pH) and ligand–receptor (ligand/receptor concentration and interaction kinetics) physiology. Our simulations predict the abundance of signaling from eight RTKs, identifying the following hierarchy in RTK signaling: PDGFRβ > IGFR1 > EGFR > PDGFRα > VEGFR1 > VEGFR2 > Tie2 > FGFR1. We find that endocytic vesicles are the primary cell signaling compartment; over 43% of total receptor signaling occurs within the endocytic vesicle compartment for these eight RTKs. Mechanistically, we found that high RTK signaling within endocytic vesicles may be attributed to their low volume (5.3 × 10 −19 L) which facilitates an enriched ligand concentration (3.2 μM per ligand molecule within the endocytic vesicle). Under the analyzed physiological conditions, we identified extracellular ligand concentration as the most sensitive parameter to change; hence the most significant one to modify when regulating absolute compartment signaling. We also found that the late endosome and nucleus compartments are important contributors to receptor signaling, where 26% and 18%, respectively, of average receptor signaling occurs across the eight RTKs. Conversely, we found very low membrane-based receptor signaling, exhibiting <1% of the total receptor signaling for these eight RTKs. Moreover, we found that nuclear translocation, mechanistically, requires late endosomal transport; when we blocked receptor trafficking from late endosomes to the nucleus we found a 57% reduction in nuclear translocation. In summary, our research has elucidated the significance of endocytic vesicles, late endosomes and the nucleus in RTK signal propagation.