Thinking outside the box: Using homology models and interactive PowerPoints for active learning

The molecular genetics of tooth development is a complex and rapidly evolving field of study. Tooth eruption, the last stage of tooth development, is one of the least understood areas.1 Dental students spend extensive time learning the genetics of tooth development through didactic lectures and textbooks, while genomic data rapidly expands with the advancement of gene sequencing technology. Students studying the genetics of tooth development in a traditional manner may not receive the most up-to-date knowledge on recently identified mutations and gene regulation. Moreover, opportunities for active learning are rare in the study of tooth development. A ‘Genomic Table’ with curated human genes involved in tooth eruption and mutations linked to eruption-related disorders (Table 1) A set of ‘Interactive PowerPoints’ with selected homology models of wildtype and mutant proteins (Figure 1) Gene name NCBI Cytogenetic location OMIM Encoded protein NCBI Homology model I-TASSER Genetic disorder OMIM Mutation OMIM PTH1R: Parathyroid hormone 1 receptor Gene ID: 5745 Truncation mutation: GLU155TER (Decker et al., 2008) Splice site mutation: IVS11AS, C-G, −3 (Decker et al.) IVS8DS, G-A, +1 (Decker et al.) RUNX2: RUNX family transcription factor 2 Gene ID: 860 Substitution mutation: ARG225GLN; ARG225TRP (Quack et al.) TER522SER (Machuca-Tzili et al.). ARG169PRO (Morava et al.). THR200ALA (Zhou et al.). MET175ARG; SER191ASN (Lee et al.). Insertion mutation: 16-BP INS; TRP283TER (Mundlos et al.). 1-BP INS, 1228C (Zheng et al.). 1-BP INS, 1206C (Quack et al., 1999). 1-BP INS, 1380C (Quack et al.). Duplication mutation: 30-BP DUP, ALANINE TRACT EXPANSION (Mundlos et al.). EDA: Ectodysplasin A Gene ID: 1896 Ectodermal dysplasia 1, hypohidrotic, X-linked Tooth agenesis, selective, X-linked Ectodermal dysplasia, hypohidrotic, X-linked Substitution mutation: TYR61HIS, ARG69LEU (Kere et al., 1996) GLU63LYS (Ferguson et al., 1998) ARG276CYS (Ferrier et al., 2009) ARG155CYS, ARG156CYS, ARG156HIS, PRO209LEU, GLY224ALA, ALA349THR, HIS252LEU (Monreal et al.). Truncation mutation: GLN23TER (Ferguson et al.) TYR61TER (Yotsumoto et al.) Deletion mutation: 36-BP DEL, 1-BP DEL (Visinoni et al.) Insertion mutation: 1-BP INS, 573T (Huang et al.) 2-BP INS, 913TA (Schneider and Muhle) Tooth agenesis, selective, X-linked Substitution mutation: ARG65GLY(Tao et al.) GLN358GLU (Tarpey et al.) THR338MET (Han et al.) ALA259GLU, ARG289CYS, ARG334HIS (Song et al.) Identifying wildtype and mutated proteins: Homology modeling: Creating interactive PowerPoints: ICM-Browser was used to create the 3D presentations of the protein models, highlighting the protein backbone, surface, important residues with side chains, and sites of mutations. The ActiveICM plugin enabled embedding the interactive 3D protein structures into PowerPoint.3 The ‘Genomic Table’ (Table 1) includes GenBank ID and cytogenetic locations for each gene and literature references for each mutation, allowing students to conduct self-directed learning. Homology modeling revealed significant structural changes between several wild-type and mutant proteins. The interactive PowerPoints, with embedded 3D protein structures (wild type and mutants), enable users to rotate, magnify, and toggle between structures and representations (Figure 1). This teaching and learning resource can help dental students comprehend the genetics of tooth eruption interactively instead of memorizing facts that are not easily retained and lack context. A demonstration of this tool is available in the supplementary video. Potential learning outcomes and related activities that can be conducted with this tooth-eruption learning resource are listed in Figure 2B. Such active learning approaches are supported by constructivist learning theory, which postulates that learning is a process of ‘making meaning,’ and active learning occurs when learners build their own understanding.4 We believe our endeavor will encourage other educators to develop similar resources for teaching complex proteins, mutations, and drug interactions. The authors have nothing to report. The authors declare no conflict of interest. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.

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