Investigating Cell Signaling with Gene Expression Datasets.

Modern molecular biology is a data- and computationally-intensive field with few instructional resources for introducing undergraduate students to the requisite skills and techniques for analyzing large data sets. This Lesson helps students: (i) build an understanding of the role of signal transduction in the control of gene expression; (ii) improve written scientific communication skills through engagement in literature searches, data analysis, and writing reports; and (iii) develop an awareness of the procedures and protocols for analyzing and making inferences from high-content quantitative molecular biology data. The Lesson is most suited to upper level biology courses because it requires foundational knowledge on cellular organization, protein structure and function, and the tenets of information flow from DNA to proteins. The first step lays the foundation for understanding cell signaling, which can be accomplished through assigned readings and presentations. In subsequent active learning sessions, data analysis is integrated with exercises that provide insight into the structure of scientific papers. The Lesson emphasizes the role of quantitative methods in research and helps students gain experience with functional genomics databases and data analysis, which are important skills for molecular biologists. Assessment is conducted through mini-reports designed to gauge students' perceptions of the purpose of each step, their awareness of the possible limitations of the methods utilized, and the ability to identify opportunities for further investigation. Summative assessment is conducted through a final report. The modules are suitable for complementing wet-laboratory experiments and can be adapted for different courses that use molecular biology data.

An entrepreneurial training model to enhance undergraduate training in biomedical research.

BACKGROUND: Undergraduate students who are interested in biomedical research typically work on a faculty member's research project, conduct one distinct task (e.g., running gels), and, step by step, enhance their skills. This "apprenticeship" model has been helpful in training many distinguished scientists over the years, but it has several potential drawbacks. For example, the students have limited autonomy, and may not understand the big picture, which may result in students giving up on their goals for a research career. Also, the model is costly and may greatly depend on a single mentor. KEY HIGHLIGHTS: The NIH Building Infrastructure Leading to Diversity (BUILD) Initiative has been established to fund innovative undergraduate research training programs and support institutional and faculty development of the recipient university. The training model at Morgan State University (MSU), namely "A Student-Centered Entrepreneurship Development training model" (ASCEND), is one of the 10 NIH BUILD-funded programs, and offers a novel, experimental "entrepreneurial" training approach. In the ASCEND training model, the students take the lead. They own the research, understand the big picture, and experience the entire scope of the research process, which we hypothesize will lead to a greater sense of self-efficacy and research competency, as well as an enhanced sense of science identity. They are also immersed in environments with substantial peer support, where they can exchange research ideas and share experiences. This is important for underrepresented minority students who might have fewer role models and less peer support in conducting research. IMPLICATIONS: In this article, we describe the MSU ASCEND entrepreneurial training model's components, rationale, and history, and how it may enhance undergraduate training in biomedical research that may be of benefit to other institutions. We also discuss evaluation methods, possible sustainability solutions, and programmatic challenges that can affect all types of science training interventions.

Evidence for the interaction of protein kinase C and melanocortin 3-receptor signaling pathways.

The melanocortin-3 receptor, MC3-R, is abundant in the brain and is activated by gamma-2-melanocyte stimulating hormone (gamma-2-MSH). We have previously reported the translocation of protein kinase C (PKC) in spontaneous hypertensive rat (SHR) brain synaptosomes treated with gamma-2-MSH. In this study, the expression of PKA and the related PKB in SHR brain synaptosomes was analyzed. PKA was detected in total synaptosomal fractions but not in particulate fractions, whereas PKB was not detected in either fraction. We next tested the hypothesis that the PKC pathway is involved in MC3-R signaling in a neuronal, CAD, cell line. Mobilization of intracellular Ca2+ was analyzed by dual fluorescence imaging of Fura-2AM loaded MC3-R transfected cells. An increase in intracellular Ca2+ was observed upon treatment with gamma-2-MSH. A MC3-R-green fluorescent protein (GFP) fusion protein was expressed and shown to localize mainly to the plasma membrane in the soma and to neurites in differentiated CAD cells. Treatment with gamma-2-MSH led to a punctate appearance and co-immunoprecipitation of the receptor fusion protein with protein kinase C-gamma (PKC-gamma). Differentiation of some neuronal cells has been shown to be associated with changes in the expression levels of protein kinase C isoenzymes. Induction of CAD cell differentiation was associated with down-regulation of the atypical PKC-zeta and protein kinase B (PKB/Akt1), that was less pronounced in MC3-R transfected cells. However, the levels of classical PKC isozymes, PKC-alpha, PKC-gamma, and PKC-beta were unchanged. These studies therefore indicate a role for PKC isozymes in gamma-2-MSH/MC3-R receptor signaling and in neuronal cell differentiation.