Abbey Thompson started as the Genetics Department's Director of Educational Outreach in March 2018. Prior to that, she received her Ph.D. in Genetics from Stanford University, completing her dissertation research with Dr. David Kingsley. During graduate school, she studied the molecular mechanisms underlying the evolution of new traits in vertebrates, using stickleback fish and mice as model systems. Before arriving at Stanford, she did post-baccalaureate work with Dr. Laufey Amundadottir at the National Cancer Institute (NCI), characterizing GWAS SNPs associated with pancreatic cancer. She received her B.A. in Biology from Northwestern University in 2011.
She has many years of experience teaching science in a variety of settings. During graduate school she participated in many different science outreach opportunities. Most notably, she participated in the "Stanford at the Tech" program, which introduced her to The Tech Museum and informal education in that setting. She also taught STEM education for the non-profit group Science from Scientists, bringing hands-on science activities to middle school students. In addition, she volunteered in a variety of different forums, including the Stanford Science Bus, which brought hands-on science activities to a local elementary school; Stanford Medical Youth Science Program, for targets underprivileged high school students who are interested in careers in STEM fields; and panel discussions on genome editing in local high schools.
Current Role at Stanford
1) Directs the Stanford@TheTech program, which trains graduate students and postdoctoral fellows in science communication skills by running hand-on activities at The Tech Interactive in San Jose.
2) Works with The Tech Interactive to design new hands-on experiences for the Biotinkering Lab, as part of an NIH SEPA grant.
3) Runs "Ask a Geneticist" on the Understanding Genetics website, answering genetics questions submitted by people from around the world.
4) Serves as liaison between the Department of Genetics at Stanford University and The Tech.
Education & Certifications
Ph.D., Stanford University, Genetics (2018)
B.A., Northwestern University, Biology (2011)
Director of Educational Outreach, Genetics Department, Stanford University (3/2018 - Present)
Graduate Research Assistant, Stanford University (9/2012 - 3/2018)
In the laboratory of David Kingsley, using stickleback fish, mice, and humans to study the molecular mechanisms underlying the evolution of new traits in vertebrates
STEM Instructor, Science from Scientists (9/2016 - 12/2017)
Taught STEM education to middle school students as part of a co-teaching team. Responsible for providing background on scientific topics such as: earth sciences, life sciences, chemistry, physics and engineering as well as assisting with experiments and activities for students. Administered regular quizzes to track student progress as well as regularly updated website information so parents could follow along with what students were learning in class.
SF Bay Area
Post-Baccalaureate Fellow, National Cancer Institute (7/15/2011)
In the laboratory of Laufey Amundadottir, characterizing GWAS SNPs associated with pancreatic cancer, using cell culture and tumor/normal samples
Undergraduate Research Assistant, Northwestern University (11/2009 - 6/2011)
In the laboratory of Jason H. Brickner, researching the dynamic spatial organization of the nucleus in S. cerevisiae, using fluorescent confocal microscopy to visualize the location of different genes with respect to each other and the nuclear periphery
- DNA fragility in the parallel evolution of pelvic reduction in stickleback fish SCIENCE 2019; 363 (6422): 81-+
A novel enhancer near the Pitx1 gene influences development and evolution of pelvic appendages in vertebrates.
Vertebrate pelvic reduction is a classic example of repeated evolution. Recurrent loss of pelvic appendages in sticklebacks has previously been linked to natural mutations in a pelvic enhancer that maps upstream of Pitx1. The sequence of this upstream PelA enhancer is not conserved to mammals, so we have surveyed a large region surrounding the mouse Pitx1 gene for other possible hind limb control sequences. Here we identify a new pelvic enhancer, PelB, that maps downstream rather than upstream of Pitx1. PelB drives expression in the posterior portion of the developing hind limb, and deleting the sequence from mice alters the size of several hind limb structures. PelB sequences are broadly conserved from fish to mammals. A wild stickleback population lacking the pelvis has an insertion/deletion mutation that disrupts the structure and function of PelB, suggesting that changes in this ancient enhancer contribute to evolutionary modification of pelvic appendages in nature.
View details for PubMedID 30499775
Functional characterization of a multi-cancer risk locus on chr5p15.33 reveals regulation of TERT by ZNF148
Genome wide association studies (GWAS) have mapped multiple independent cancer susceptibility loci to chr5p15.33. Here, we show that fine-mapping of pancreatic and testicular cancer GWAS within one of these loci (Region 2 in CLPTM1L) focuses the signal to nine highly correlated SNPs. Of these, rs36115365-C associated with increased pancreatic and testicular but decreased lung cancer and melanoma risk, and exhibited preferred protein-binding and enhanced regulatory activity. Transcriptional gene silencing of this regulatory element repressed TERT expression in an allele-specific manner. Proteomic analysis identifies allele-preferred binding of Zinc finger protein 148 (ZNF148) to rs36115365-C, further supported by binding of purified recombinant ZNF148. Knockdown of ZNF148 results in reduced TERT expression, telomerase activity and telomere length. Our results indicate that the association with chr5p15.33-Region 2 may be explained by rs36115365, a variant influencing TERT expression via ZNF148 in a manner consistent with elevated TERT in carriers of the C allele.
View details for DOI 10.1038/ncomms15034
View details for Web of Science ID 000400154600001
View details for PubMedID 28447668
View details for PubMedCentralID PMC5414179
- Three cheers for the three-spined stickleback LAB ANIMAL 2016; 45 (11): 421-421
CLPTM1L Promotes Growth and Enhances Aneuploidy in Pancreatic Cancer Cells
2014; 74 (10): 2785-2795
Genome-wide association studies (GWAS) of 10 different cancers have identified pleiotropic cancer predisposition loci across a region of chromosome 5p15.33 that includes the TERT and CLPTM1L genes. Of these, susceptibility alleles for pancreatic cancer have mapped to the CLPTM1L gene, thus prompting an investigation of the function of CLPTM1L in the pancreas. Immunofluorescence analysis indicated that CLPTM1L localized to the endoplasmic reticulum where it is likely embedded in the membrane, in accord with multiple predicted transmembrane domains. Overexpression of CLPTM1L enhanced growth of pancreatic cancer cells in vitro (1.3-1.5-fold; PDAY7 < 0.003) and in vivo (3.46-fold; PDAY68 = 0.039), suggesting a role in tumor growth; this effect was abrogated by deletion of two hydrophilic domains. Affinity purification followed by mass spectrometry identified an interaction between CLPTM1L and non-muscle myosin II (NMM-II), a protein involved in maintaining cell shape, migration, and cytokinesis. The two proteins colocalized in the cytoplasm and, after treatment with a DNA-damaging agent, at the centrosomes. Overexpression of CLPTM1L and depletion of NMM-II induced aneuploidy, indicating that CLPTM1L may interfere with normal NMM-II function in regulating cytokinesis. Immunohistochemical analysis revealed enhanced staining of CLPTM1L in human pancreatic ductal adenocarcinoma (n = 378) as compared with normal pancreatic tissue samples (n = 17; P = 1.7 × 10(-4)). Our results suggest that CLPTM1L functions as a growth-promoting gene in the pancreas and that overexpression may lead to an abrogation of normal cytokinesis, indicating that it should be considered as a plausible candidate gene that could explain the effect of pancreatic cancer susceptibility alleles on chr5p15.33.
View details for DOI 10.1158/0008-5472.CAN-13-3176
View details for Web of Science ID 000336720700014
View details for PubMedID 24648346
View details for PubMedCentralID PMC4030677
A Conserved Role for Human Nup98 in Altering Chromatin Structure and Promoting Epigenetic Transcriptional Memory
2013; 11 (3)
The interaction of nuclear pore proteins (Nups) with active genes can promote their transcription. In yeast, some inducible genes interact with the nuclear pore complex both when active and for several generations after being repressed, a phenomenon called epigenetic transcriptional memory. This interaction promotes future reactivation and requires Nup100, a homologue of human Nup98. A similar phenomenon occurs in human cells; for at least four generations after treatment with interferon gamma (IFN-γ), many IFN-γ-inducible genes are induced more rapidly and more strongly than in cells that have not previously been exposed to IFN-γ. In both yeast and human cells, the recently expressed promoters of genes with memory exhibit persistent dimethylation of histone H3 lysine 4 (H3K4me2) and physically interact with Nups and a poised form of RNA polymerase II. However, in human cells, unlike yeast, these interactions occur in the nucleoplasm. In human cells transiently depleted of Nup98 or yeast cells lacking Nup100, transcriptional memory is lost; RNA polymerase II does not remain associated with promoters, H3K4me2 is lost, and the rate of transcriptional reactivation is reduced. These results suggest that Nup100/Nup98 binding to recently expressed promoters plays a conserved role in promoting epigenetic transcriptional memory.
View details for DOI 10.1371/journal.pbio.1001524
View details for Web of Science ID 000316794600022
View details for PubMedID 23555195
View details for PubMedCentralID PMC3608542
Transcription Factor Binding to a DNA Zip Code Controls Interchromosomal Clustering at the Nuclear Periphery
2012; 22 (6): 1234-1246
Active genes in yeast can be targeted to the nuclear periphery through interaction of cis-acting "DNA zip codes" with the nuclear pore complex. We find that genes with identical zip codes cluster together. This clustering was specific; pairs of genes that were targeted to the nuclear periphery by different zip codes did not cluster together. Insertion of two different zip codes (GRS I or GRS III) at an ectopic site induced clustering with endogenous genes that have that zip code. Targeting to the nuclear periphery and interaction with the nuclear pore is a prerequisite for gene clustering, but clustering can be maintained in the nucleoplasm. Finally, we find that the Put3 transcription factor recognizes the GRS I zip code to mediate both targeting to the NPC and interchromosomal clustering. These results suggest that zip-code-mediated clustering of genes at the nuclear periphery influences the three-dimensional arrangement of the yeast genome.
View details for DOI 10.1016/j.devcel.2012.03.012
View details for Web of Science ID 000305498200013
View details for PubMedID 22579222
View details for PubMedCentralID PMC3376219