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., Deuring, R., Mccallum, C. M., Peterson, C. L., & Tamkun, J. W. (1994). Identification and characterization of Drosophila relatives of the yeast transcriptional activator SNF2/SWI2. Molecular and Cellular Biology, 14(4), 2225-2234.

PMID: 7908117;PMCID: PMC358589;Abstract:

The Drosophila brahma (brm) gene encodes an activator of homeotic genes that is highly related to the yeast transcriptional activator SWI2 (SNF2), a potential helicase. To determine whether brm is a functional homolog of SWI2 or merely a member of a family of SWI2-related genes, we searched for additional Drosophila genes related to SWI2 and examined their function in yeast cells. In addition to brm, we identified one other Drosophila relative of SWI2: the closely related ISWI gene. The 1,027-residue ISWI protein contains the DNA-dependent ATPase domain characteristic of the SWI2 protein family but lacks the three other domains common to brm and SWI2. In contrast, the ISWI protein is highly related (70% identical) to the human hSNF2L protein over its entire length, suggesting that they may be functional homologs. The DNA-dependent ATPase domains of brm and SWI2, but not ISWI, are functionally interchangeable; a chimeric SWI2-brm protein partially rescued the slow growth of swi2- cells and supported transcriptional activation mediated by the glucocorticoid receptor in vivo in yeast cells. These findings indicate that brm is the closest Drosophila relative of SWI2 and suggest that brm and SWI2 play similar roles in transcriptional activation.

Hester, S. D., Southard, K. M., Wince, T., Elfring, L. K., Nagy, L. M., & Bolger, M. S. (2017). What do earwax, spinners and cats have in common? Probabilistic reasoning in undergraduate genetics problem-solving. CBE: Life Science Education (planned).
Lee, L. A., Elfring, L. K., Bosco, G., & Orr-Weaver, T. L. (2001). A genetic screen for suppressors and enhancers of the Drosophila PAN GU cell cycle kinase identifies cyclin B as a target. Genetics, 158(4), 1545-1556.

PMID: 11514446;PMCID: PMC1461742;Abstract:

The early cell cycles of Drosophila embryogenesis involve rapid oscillations between S phase and mitosis. These unique S-M cycles are driven by maternal stockpiles of components necessary for DNA replication and mitosis. Three genes, pan gu (png), plutonium (plu), and giant nuclei (gnu) are required to control the cell cycle specifically at the onset of Drosophila development by inhibiting DNA replication and promoting mitosis. PNG is a protein kinase that is in a complex with PLU. We employed a sensitized png mutant phenotype to screen for genes that when reduced in dosage would dominantly suppress or enhance png. We screened deficiencies covering over 50% of the autosomes and identified both enhancers and suppressors. Mutations in eIF-5A and PP1 87B dominantly suppress png. Cyclin B was shown to be a key PNG target. Mutations in cyclin B dominantly enhance png, whereas png is suppressed by cyclin B overexpression. Suppression occurs via restoration of Cyclin B protein levels that are decreased in png mutants. The plu and gnu phenotypes are also suppressed by cyclin B overexpression. These studies demonstrate that a crucial function of PNG in controlling the cell cycle is to permit the accumulation of adequate levels of Cyclin B protein.

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.