Photo of Lisa K Elfring
Lisa K Elfring
Associate Professor, BIO5 Institute
Associate Specialist, Biology Education
Associate Vice Provost, Office of Instruction/Assessment
Primary Department
Office of Instruct & Assess
Department Affiliations
Molecular and Cellular Biology
Office of Instruct & Assess
BIO5 Institute
(520) 621-1671
elfring@email.arizona.edu
Work Summary
There are over 30,000 undergraduates on our campus, and the skills and knowledge they gain here will shape their future careers and their lives. My work focuses on helping faculty members to reach their potential as teachers, and working to support them in the critical work they do.
Research Interest
Lisa Elfring is an Associate Specialist in the Department of Molecular and Cellular Biology and currently serves as Associate Vice Provost for Instruction and Assessment. In this administrative role, she leads the Office of Instruction and Assessment (OIA), which supports teaching and learning across campus. The office supports technology-enabled teaching (D2L, Panopto, Adobe Connect, VoiceThread); provides professional development and courses on evidence-based teaching for all UA instructors; produces media products (web pages, videos) that support instructors in their teaching; helps departments to carry out assessment of learning outcomes; and helps to connect instructors across departmental and college boundaries. Dr. Elfring is currently involved in two teaching-related research projects. In one, she and her collaborators are investigating a model to train instructors in large, collaborative STEM classes to utilize a team of graduate and undergraduates to improve student learning. In the other, the team is investigating the effects on students on creating and improving models in biological systems, in the context of an Introductory Biology lab course. Both projects are funded by awards from the National Science Foundation. Dr. Elfring's teaching experiences range from large courses in introductory cell/molecular biology and cell biology, to courses focusing on helping undergraduate students to prepare for doing laboratory research. Her research interests are integrated with her teaching role. She is interested in process of systemic change in educational systems, and particularly in how the university can promote the adoption, use, and assessment of research-based teaching strategies across the entire range of STEM (science, technology, engineering, and math) courses. In biology education, she has been involved in research on how students come to make sense of the key biological concept that genes code for RNAs which (mostly) encode proteins to form the structural and catalytic molecules of the cell, a process that is termed the central dogma of molecular biology. She and her collaborators were involved in efforts to introduce more quantitative problem-solving work in the Introductory Biology course and across the undergraduate life-sciences curriculum. Her undergraduate, graduate, and post-doctoral training is in molecular, cell, and developmental biology; she has done research using humans, mice, and fruit flies as experimental systems to investigate embryonic development and cancer. Keywords: Biology education, Faculty professional development

Publications

Elfring, L. K., Daniel, C., Papoulas, O., Deuring, R., Sarte, M., Moseley, S., Beek, S. J., Waldrip, W. R., Daubresse, G., DePace, A., Kennison, J. A., & Tamkun, J. W. (1998). Genetic analysis of brahma: The drosophila homolog of the yeast chromatin remodeling factor SWI2/SNF2. Genetics, 148(1), 251-265.

PMID: 9475737;PMCID: PMC1459776;Abstract:

The Drosophila brahma (brm) gene encodes an activator of homeotic genes related to the yeast chromatin remodeling factor SWI2/SNF2. Here, we report the phenotype of null and dominant-negative brm mutations. Using mosaic analysis, we found that the complete loss of brm function decreases cell viability and causes defects in the peripheral nervous system of the adult. A dominant-negative brm mutation was generated by replacing a conserved lysine in the ATP-binding site of the BRM protein with an arginine. This mutation eliminates brm function in vivo but does not affect assembly of the 2-MD BRM complex. Expression of the dominant-negative BRM protein caused peripheral nervous system defects, homeotic transformations, and decreased viability. Consistent with these findings, the BRM protein is expressed at relatively high levels in nuclei throughout the developing organism. Site-directed mutagenesis was used to investigate the functions of conserved regions of the BRM protein. Domain II is essential for brm function and is required for the assembly or stability of the BRM complex. In spite of its conservation in numerous eukaryotic regulatory proteins, the deletion of the bromodomain of the BRM protein has no discernible phenotype.

Fenger, D. D., Carminati, J. L., Burney-Sigman, D., Kashevsky, H., Dines, J. L., Elfring, L. K., & Orr-Weaver, T. (2000). PAN GU: A protein kinase that inhibits S phase and promotes mitosis in early Drosophila development. Development, 127(22), 4763-4774.

PMID: 11044392;Abstract:

Following completion of meiosis, DNA replication must be repressed until fertilization. In Drosophila, this replication block requires the products of the pan gu (png), plutonium (plu) and giant nuclei (gnu) genes. These genes also ensure that S phase oscillates with mitosis in the early division cycles of the embryo. We have identified the png gene and shown that it encodes a Ser/Thr protein kinase expressed only in ovaries and early embryos, and that the predicted extent of kinase activity in png mutants inversely correlates with the severity of the mutant phenotypes. The PLU and PNG proteins form a complex that has PNG-dependent kinase activity, and this activity is necessary for normal levels of mitotic cyclins. Our results reveal a novel protein kinase complex that controls S phase at the onset of development apparently by stabilizing mitotic cyclins.

Brizuela, B. J., Elfring, L., Ballard, J., Tamkun, J. W., & Kennison, J. A. (1994). Genetic analysis of the brahma gene of Drosophila melanogaster and polytene chromosome subdivisions 72AB. Genetics, 137(3), 803-813.

PMID: 7916308;PMCID: PMC1206040;Abstract:

The brahma gene is required for activation of the homeotic genes of the Antennapedia and bithorax complexes in Drosophila. We have isolated and characterized 21 mutations in brahma. We show that both maternal and zygotic functions of brahma are required during embryogenesis. In addition, the severe abnormalities caused by loss of maternal brahma expression show that the homeotic genes are not the only targets for brahma activation. The complex pattern of interallelic complementation for the 21 brahma alleles suggests that brahma may act as a multimer. In addition to mutations in brahma, we have isolated mutations in four other essential genes within polytene chromosome subdivisions 72AB. Based on a compilation of similar studies that include about 24% of the genome, we estimate that about 3600 genes in Drosophila can inutate to cause recessive lethality, with fewer than 900 additional genes essential only for gametogenesis. We have identified three more transcripts than lethal complementation groups in 72AB. One transcript in 72AB is the product of the essential arflike gene and encodes a member of the ARF subfamily of small GTP-binding proteins. Two other transcripts are probably the products of a single gene whose protein products are similar to the catalytic subunits of cAMP-dependent protein kinases.

Baldwin, T. O., Elfring, L., & Offerdahl, E. (2008). Ph.D. in Biochemistry (Education)!. Biochemistry and Molecular Biology Education, 36(4), 251-252.
Elfring, L. K., Axton, J. M., Fenger, D. D., Page, A. W., Carminati, J. L., & Orr-Weaver, T. L. (1997). Drosophila PLUTONIUM protein is a specialized cell cycle regulator required at the onset of embryogenesis. Molecular Biology of the Cell, 8(4), 583-593.

PMID: 9247640;PMCID: PMC276111;Abstract:

Unfertilized eggs and fertilized embryos from Drosophila mothers mutant for the plutonium (plu) gene contain giant polyploid nuclei resulting from unregulated S-phase. The PLU protein, a 19-kDa ankyrin repeat protein, is present in oocytes and early embryos but is not detectable after the completion of the initial rapid S-M cycles of the embryo. The persistence of the protein during the early embryonic divisions is consistent with a direct role in linking S-phase and M-phase. When ectopically expressed in the eye disc, PLU did not perturb the cell cycle, suggesting that PLU regulates S- phase only in early embryonic development. The pan gu (png) and giant nuclei (gnu) genes also affect the S-phase in the unfertilized egg and early embryo. We show that functional png is needed for the presence of PLU protein. By analyzing png mutations of differing severity, we find that the extent of the png mutant phenotype inversely reflects the level of PLU protein. Our data suggest that PLU protein is required at the time of egg activation and the completion of meiosis.