Co-teaching in Undergraduate STEM Education: A Lever for Pedagogical Change toward Evidence-Based Teaching?

Could co-teaching be a mechanism to support the adoption of evidence-based teaching strategies? Co-teaching has been proposed as a lever for fostering pedagogical change and has key attributes of a successful change strategy, but does research indicate co-teaching effectively shifts instructional practices? Based on our review of the emerging evidence, we wrote this essay for multiple audiences, including science, technology, engineering, and mathematics (STEM) instructors, education development professionals, leaders who oversee teaching, and researchers. We define co-teaching in the context of STEM higher education and summarize what is known about the pedagogical changes that co-teaching could support and the potential mechanisms behind these changes. We share recommendations based on the available evidence for those who need productive ideas right now. We also lay out a variety of future directions for research about co-teaching as a lever for pedagogical change. Achieving widespread and impactful pedagogical change is a monumental undertaking facing STEM higher education, and multiple approaches will be needed to meet this challenge. Co-teaching has potential to shift ways of thinking and pedagogical practices among undergraduate STEM faculty, but how co-teaching is enacted is likely crucial to its impact, as is the context in which it occurs.

Collectively Improving Our Teaching: Attempting Biology Department-wide Professional Development in Scientific Teaching.

Many efforts to improve science teaching in higher education focus on a few faculty members at an institution at a time, with limited published evidence on attempts to engage faculty across entire departments. We created a long-term, department-wide collaborative professional development program, Biology Faculty Explorations in Scientific Teaching (Biology FEST). Across 3 years of Biology FEST, 89% of the department's faculty completed a weeklong scientific teaching institute, and 83% of eligible instructors participated in additional semester-long follow-up programs. A semester after institute completion, the majority of Biology FEST alumni reported adding active learning to their courses. These instructor self-reports were corroborated by audio analysis of classroom noise and surveys of students in biology courses on the frequency of active-learning techniques used in classes taught by Biology FEST alumni and nonalumni. Three years after Biology FEST launched, faculty participants overwhelmingly reported that their teaching was positively affected. Unexpectedly, most respondents also believed that they had improved relationships with departmental colleagues and felt a greater sense of belonging to the department. Overall, our results indicate that biology department-wide collaborative efforts to develop scientific teaching skills can indeed attract large numbers of faculty, spark widespread change in teaching practices, and improve departmental relations.

A Guide for Graduate Students Interested in Postdoctoral Positions in Biology Education Research.

Postdoctoral positions in biology education research (BER) are becoming increasingly common as the field grows. However, many life science graduate students are unaware of these positions or do not understand what these positions entail or the careers with which they align. In this essay, we use a backward-design approach to inform life science graduate students of postdoctoral opportunities in BER. Beginning with the end in mind, we first discuss the types of careers to which BER postdoctoral positions lead. We then discuss the different types of BER postdoctoral positions, drawing on our own experiences and those of faculty mentors. Finally, we discuss activities in which life science graduate students can engage that will help them gauge whether BER aligns with their research interests and develop skills to be competitive for BER postdoctoral positions.

The canonical Wingless signaling pathway is required but not sufficient for inflow tract formation in the Drosophila melanogaster heart.

The inflow tracts of the embryonic Drosophila cardiac tube, termed ostia, arise in its posterior three segments from cardiac cells that co-express the homeotic transcription factor Abdominal-A (abdA), the orphan nuclear receptor Seven-up (Svp), and the signaling molecule Wingless (Wg). To define the roles of these factors in inflow tract development, we assessed their function in inflow tract formation. We demonstrate, using several criteria, that abdA, svp, and wg are each critical for normal inflow tract formation. We further show that Wg acts in an autocrine manner to impact ostia fate, and that it mediates this effect at least partially through the canonical Wg signaling pathway. By contrast, neither wg expression nor Wg signaling are sufficient for inflow tract formation when expressed in anterior Svp cells that do not normally form inflow tracts in the embryo. Instead, ectopic abd-A expression throughout the cardiac tube is required for the formation of ectopic inflow tracts, indicating that autocrine Wg signaling must be supplemented by additional Hox-dependent factors to effect inflow tract formation. Taken together, these studies define important cellular and molecular events that contribute to cardiac inflow tract development in Drosophila. Given the broad conservation of the cardiac regulatory network through evolution, our studies provide insight into mechanisms of cardiac development in higher animals.

A ubiquitin E2 variant protein acts in axon termination and synaptogenesis in Caenorhabditis elegans.

In the developing nervous system, cohorts of events regulate the precise patterning of axons and formation of synapses between presynaptic neurons and their targets. The conserved PHR proteins play important roles in many aspects of axon and synapse development from C. elegans to mammals. The PHR proteins act as E3 ubiquitin ligases for the dual-leucine-zipper-bearing MAP kinase kinase kinase (DLK MAPKKK) to regulate the signal transduction cascade. In C. elegans, loss-of-function of the PHR protein RPM-1 (Regulator of Presynaptic Morphology-1) results in fewer synapses, disorganized presynaptic architecture, and axon overextension. Inactivation of the DLK-1 pathway suppresses these defects. By characterizing additional genetic suppressors of rpm-1, we present here a new member of the DLK-1 pathway, UEV-3, an E2 ubiquitin-conjugating enzyme variant. We show that uev-3 acts cell autonomously in neurons, despite its ubiquitous expression. Our genetic epistasis analysis supports a conclusion that uev-3 acts downstream of the MAPKK mkk-4 and upstream of the MAPKAPK mak-2. UEV-3 can interact with the p38 MAPK PMK-3. We postulate that UEV-3 may provide additional specificity in the DLK-1 pathway by contributing to activation of PMK-3 or limiting the substrates accessible to PMK-3.