About

Eric P. Spana is an Associate Professor of the Practice of Biology at Duke University, holding this position since 2018 within the Trinity College of Arts & Sciences. His academic background includes a Ph.D. from the University of Illinois, Urbana-Champaign, earned in 1995, and a B.S. from the University of Pittsburgh, obtained in 1989. His research focuses on the genetics and molecular biology of Drosophila melanogaster, with particular attention to mutations and regulatory regions affecting development and phenotypic traits. Spana has contributed to understanding the genetic basis of visible phenotypes in flies, mapping mutations such as tilt (tt) to specific genomic regions, and characterizing mutations like speck, which encodes the enzyme Arylalkalamine N-Acetyltransferase (AANAT1). His work has provided insights into the structure and evolution of regulatory regions in eukaryotic genomes. In addition to his research, Spana has been recognized for excellence in teaching, advising, and service, and has been involved in professional activities including presentations and publications related to his expertise.

Research topics

• Biology
• Genetics
• Evolutionary biology

Selected publications

• The tilt (tt) mutation of Drosophila melanogaster maps to the cis-regulatory region of the Iroquois Complex (Iro-C) located in the sosondowah (sowah) gene

  PubMed · 2025-06-18

  articleOpen accessSenior author

  phenotype, providing a potential mechanism for the insertion to affect the function of the Iroquois Complex.

  PublisherOA PDFDOI

• Characterization of the tilt (tt) phenotype in Drosophila melanogaster

  PubMed · 2023

  Senior authorCorresponding
  • Biology
  • Genetics
  • Evolutionary biology

  phenotypes that have been previously described. We also show the penetrance of these phenotypes: the vein break and the distinct outward wing posture have decreased since its discovery.

  PublisherOA PDFDOI

• <i>speck</i> , First Identified in <i>Drosophila melanogaster</i> in 1910, Is Encoded by the Arylalkalamine N-Acetyltransferase (AANAT1) Gene

  G3 Genes Genomes Genetics · 2020 · 18 citations

  1st authorCorresponding
  • Biology
  • Genetics

  phenotype.

  PublisherOA PDFDOI

• <i>speck</i> , first identified in <i>Drosophila melanogaster</i> in 1910, is encoded by the <i>Arylalkalamine N-acetyltransferase (AANAT1)</i> gene

  bioRxiv (Cold Spring Harbor Laboratory) · 2019-10-13

  preprintOpen access1st authorCorresponding

  The pigmentation mutation speck is a commonly used recombination marker characterized by a darkly pigmented region at the wing hinge. Identified in 1910 by Thomas Hunt Morgan, speck was characterized by Sturtevant as the most 'workable' mutant in the rightmost region of the second chromosome and eventually localized to 2-107.0 and 60C1-2. Though the first speck mutation was isolated over 115 years ago, speck is still not associated with any gene. Here, as part of an undergraduate-led research effort, we show that speck is encoded by the Arylalkylamine N-acetyltransferase 1 (AANAT1) gene. Both alleles from the Morgan lab contain a retrotransposon in exon 1 of the RB transcript of the AANAT1 gene. We have also identified a new insertion allele and generated multiple deletion alleles in AANAT1 that all give a strong speck phenotype. In addition, expression of AANAT1 RNAi constructs either ubiquitously or in the dorsal portion of the developing wing generates a similar speck phenotype. We find that speck alleles have additional phenotypes, including ectopic pigmentation in the posterior pupal case, leg joints, cuticular sutures and overall body color. We propose that the acetylated dopamine generated by AANAT1 decreases the dopamine pool available for melanin production. When AANAT1 function is decreased, the excess dopamine enters the melanin pathway to generate the speck phenotype.

  PublisherOA PDFDOI

• Retrotransposons Are the Major Contributors to the Expansion of the<i>Drosophila ananassae</i>Muller F Element

  G3 Genes Genomes Genetics · 2017-07-01 · 34 citations

  articleOpen access

  Abstract The discordance between genome size and the complexity of eukaryotes can partly be attributed to differences in repeat density. The Muller F element (∼5.2 Mb) is the smallest chromosome in Drosophila melanogaster, but it is substantially larger (&amp;gt;18.7 Mb) in D. ananassae. To identify the major contributors to the expansion of the F element and to assess their impact, we improved the genome sequence and annotated the genes in a 1.4-Mb region of the D. ananassae F element, and a 1.7-Mb region from the D element for comparison. We find that transposons (particularly LTR and LINE retrotransposons) are major contributors to this expansion (78.6%), while Wolbachia sequences integrated into the D. ananassae genome are minor contributors (0.02%). Both D. melanogaster and D. ananassae F-element genes exhibit distinct characteristics compared to D-element genes (e.g., larger coding spans, larger introns, more coding exons, and lower codon bias), but these differences are exaggerated in D. ananassae. Compared to D. melanogaster, the codon bias observed in D. ananassae F-element genes can primarily be attributed to mutational biases instead of selection. The 5′ ends of F-element genes in both species are enriched in dimethylation of lysine 4 on histone 3 (H3K4me2), while the coding spans are enriched in H3K9me2. Despite differences in repeat density and gene characteristics, D. ananassae F-element genes show a similar range of expression levels compared to genes in euchromatic domains. This study improves our understanding of how transposons can affect genome size and how genes can function within highly repetitive domains.

  PublisherOA PDFDOI

• Inositol phosphate kinase 2 is required for imaginal disc development in <i>Drosophila</i>

  Proceedings of the National Academy of Sciences · 2015-12-08 · 21 citations

  articleOpen access

  Inositol phosphate kinase 2 (Ipk2), also known as IP multikinase IPMK, is an evolutionarily conserved protein that initiates production of inositol phosphate intracellular messengers (IPs), which are critical for regulating nuclear and cytoplasmic processes. Here we report that Ipk2 kinase activity is required for the development of the adult fruit fly epidermis. Ipk2 mutants show impaired development of their imaginal discs, the primordial tissues that form the adult epidermis. Although disk tissue seems to specify normally during early embryogenesis, loss of Ipk2 activity results in increased apoptosis and impairment of proliferation during larval and pupal development. The proliferation defect is in part attributed to a reduction in JAK/STAT signaling, possibly by controlling production or secretion of the pathway's activating ligand, Unpaired. Constitutive activation of the JAK/STAT pathway downstream of Unpaired partially rescues the disk growth defects in Ipk2 mutants. Thus, IP production is essential for proliferation of the imaginal discs, in part, by regulating JAK/STAT signaling. Our work demonstrates an essential role for Ipk2 in producing inositide messengers required for imaginal disk tissue maturation and subsequent formation of adult body structures and provides molecular insights to signaling pathways involved in tissue growth and stability during development.

  PublisherOA PDFDOI

• A Course-Based Research Experience: How Benefits Change with Increased Investment in Instructional Time

  CBE—Life Sciences Education · 2014-03-01 · 181 citations

  articleOpen access

  There is widespread agreement that science, technology, engineering, and mathematics programs should provide undergraduates with research experience. Practical issues and limited resources, however, make this a challenge. We have developed a bioinformatics project that provides a course-based research experience for students at a diverse group of schools and offers the opportunity to tailor this experience to local curriculum and institution-specific student needs. We assessed both attitude and knowledge gains, looking for insights into how students respond given this wide range of curricular and institutional variables. While different approaches all appear to result in learning gains, we find that a significant investment of course time is required to enable students to show gains commensurate to a summer research experience. An alumni survey revealed that time spent on a research project is also a significant factor in the value former students assign to the experience one or more years later. We conclude: 1) implementation of a bioinformatics project within the biology curriculum provides a mechanism for successfully engaging large numbers of students in undergraduate research; 2) benefits to students are achievable at a wide variety of academic institutions; and 3) successful implementation of course-based research experiences requires significant investment of instructional time for students to gain full benefit.

  PublisherDOI

• A Central Support System Can Facilitate Implementation and Sustainability of a Classroom-Based Undergraduate Research Experience (CURE) in Genomics

  CBE—Life Sciences Education · 2014-12-01 · 90 citations

  articleOpen access

  In their 2012 report, the President's Council of Advisors on Science and Technology advocated "replacing standard science laboratory courses with discovery-based research courses"-a challenging proposition that presents practical and pedagogical difficulties. In this paper, we describe our collective experiences working with the Genomics Education Partnership, a nationwide faculty consortium that aims to provide undergraduates with a research experience in genomics through a scheduled course (a classroom-based undergraduate research experience, or CURE). We examine the common barriers encountered in implementing a CURE, program elements of most value to faculty, ways in which a shared core support system can help, and the incentives for and rewards of establishing a CURE on our diverse campuses. While some of the barriers and rewards are specific to a research project utilizing a genomics approach, other lessons learned should be broadly applicable. We find that a central system that supports a shared investigation can mitigate some shortfalls in campus infrastructure (such as time for new curriculum development, availability of IT services) and provides collegial support for change. Our findings should be useful for designing similar supportive programs to facilitate change in the way we teach science for undergraduates.

  PublisherDOI

• Genetic dissection of leukemia-associated IDH1 and IDH2 mutants and D-2-hydroxyglutarate in Drosophila

  Blood · 2014-11-15 · 28 citations

  articleOpen access

  Gain-of-function mutations in nicotinamide adenine dinucleotide phosphate-dependent isocitrate dehydrogenase (IDH)1 and IDH2 frequently arise in human leukemias and other cancers and produce high levels of D-2-hydroxyglutarate (D-2HG). We expressed the R195H mutant of Drosophila Idh (CG7176), which is equivalent to the human cancer-associated IDH1-R132H mutant, in fly tissues using the UAS-Gal4 binary expression system. Idh-R195H caused a >25-fold elevation of D-2HG when expressed ubiquitously in flies. Expression of mutant Idh in larval blood cells (hemocytes) resulted in higher numbers of circulating blood cells. Mutant Idh expression in fly neurons resulted in neurologic and wing-expansion defects, and these phenotypes were rescued by genetic modulation of superoxide dismutase 2, p53, and apoptotic caspase cascade mediators. Idh-R163Q, which is homologous to the common leukemia-associated IDH2-R140Q mutant, resulted in moderately elevated D-2HG and milder phenotypes. We identified the fly homolog of D-2-hydroxyglutaric acid dehydrogenase (CG3835), which metabolizes D-2HG, and showed that coexpression of this enzyme with mutant Idh abolishes mutant Idh-associated phenotypes. These results provide a flexible model system to interrogate a cancer-related genetic and metabolic pathway and offer insights into the impact of IDH mutation and D-2HG on metazoan tissues.

  PublisherOA PDFDOI

• A paired-end sequencing strategy to map the complex landscape of transcription initiation

  Nature Methods · 2010-05-23 · 177 citations

  articleOpen access
  PublisherOA PDFDOI

Frequent coauthors

• Chris Q. Doe

  24 shared

• Norbert Perrimon

  Howard Hughes Medical Institute

  9 shared

• Matthew Wawersik

  Williams (United States)

  8 shared

• Julie Broadus

  Howard Hughes Medical Institute

  7 shared

• James B. Skeath

  Washington University in St. Louis

  5 shared

• John D. York

  5 shared

• Karim A. Sharif

  Massasoit Community College

  5 shared

• Joyce Stamm

  University of Evansville

  5 shared

Education

• PhD, Cell Biology

  University of Illinois Urbana-Champaign

  1995

• BS, Microbiology

  University of Pittsburgh

  1989

Awards & honors

• Trinity Honors Excellence in Teaching, Advising and Service…