Dahlia M. Nielsen
· Assoc ProfessorVerifiedNorth Carolina State University · Plant and Microbial Biology
Active 1993–2026
Research topics
- Biology
- Genetics
- Medicine
- Statistics
- Oncology
- Pharmacology
- Engineering
- Internal medicine
- Cancer research
- Computational biology
- Mathematics
- Biochemistry
- Food science
- Materials science
- Pathology
- Endocrinology
Selected publications
bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-12
articleOpen access1st authorCorrespondingABSTRACT A hallmark of the interactions between endoparasites (parasites that live within plant tissue) and their hosts, is the parasites’ ability to hijack host gene expression to support their own existence. While a number of studies have been performed to identify plant genes that are recruited in this process, there is much that remains unknown. One mechanism by which these connections can be explored is using a traditional genetics approach – identifying connections between genetic variation and phenotype variation. To that end, we leverage experiments examining tissue from three host plants, each infected with one of two genetically distinct strains of the endoparasite Meloidogyne hapla . Using gene expression profiles, we identify plant genes that differ based on the genetic background of the parasite, and show that these signals are common across plant hosts. These results indicate that the plant genes recruited by the parasite differ according to the parasite’s genetic background, and that these alternative patterns are conserved across evolutionarily distant hosts. We also leverage public data to identify conserved host expression differences when comparing M. hapla -infected roots to uninfected root tissue. Finally, we demonstrate that parasite gene expression varies based on the parasites’ genetic background, and these signals are also conserved when inhabiting different host species.
Scientific Reports · 2025-01-02 · 1 citations
articleOpen access1st authorCorrespondingCancers of the mesothelium, such as malignant mesothelioma (MM), historically have been attributed solely to exposure to asbestos. Recent large scale genetic and genomic functional studies now show that approximately 20% of all human mesotheliomas are causally linked to highly penetrant inherited (germline) pathogenic mutations in numerous cancer related genes. The rarity of these mutations in humans makes it difficult to perform statistically conclusive genetic studies to understand their biological effects. This has created a disconnect between functional and epidemiological studies. However, since the molecular pathogenesis of MM in mice accurately recapitulates that of human disease, this disconnect between functional and epidemiological studies can be overcome by using inbred mouse strains that harbor mutation(s) in genes involved in the disease. Most mouse studies have focused on the effect of asbestos exposure, leaving the effects of genetic mutations in the absence of exposure understudied. Here, using existing peer-reviewed studies, we investigate the rate of spontaneous MM among mice with and without germline genetic mutations, in the absence of asbestos exposure. We leveraged these published data to generate a historical control dataset (HCD) to allow us to improve statistical power and account for genetic heterogeneity between studies. Our Bayesian analyses indicate that the odds of spontaneous MM among germline BAP1 mutant mice is substantially larger than that of wildtype mice. These results support the existing biological study findings that mesotheliomas can arise in the presence of pathogenic germline mutations, independently of asbestos exposure.
Assessing the effect of spaceflight stress on DNA sequence mutation using RNA-sequencing data
Gravitational and Space Research · 2025-01-01 · 1 citations
articleOpen accessSenior authorAbstract Understanding the effects of space radiation and microgravity on DNA is critical to assessing the impact of long-term spaceflight. While experiments performed in space constitute the most effective means of examining these effects, opportunities are limited and costly. As this bottleneck will likely continue for the foreseeable future, data from past experiments represent a particularly valuable source of information for continuing studies. To this end, NASA created GeneLab, a public Omics database for spaceflight-related data. We used data from GeneLab to examine the effect of spaceflight on DNA mutation rates. Optimally, mutation rates are estimated using DNA sequence data directly. Unfortunately, to date, few DNA-based datasets appear in GeneLab. Transcript data, however, is abundant. Here we used RNA-Seq data to examine DNA sequence variation in Arabidopsis thaliana seedlings grown aboard the International Space Station (ISS) vs. on the ground. ISS-based samples were grown under two conditions: spaceflight under microgravity, and, by using a specialized onboard centrifuge under induced gravity. This powerful experimental design allowed us to separate the effects of microgravity from non-microgravity spaceflight stress, such as space radiation. More mutations were observed in spaceflight samples than in ground control samples, with transversion mutations being overly represented. Mutation rates identified in samples grown under artificial gravity in space were similar to that of microgravity spaceflight samples, indicating that microgravity exposure played a limited role. This work demonstrates that RNA-Seq data is useful for evaluating DNA damage from spaceflight and provides insight into the types of mutations that occur.
Nutrition Research · 2024 · 2 citations
- Biology
- Genetics
- Food science
Research Square (Research Square) · 2024
1st authorCorresponding- Cancer research
- Oncology
- Medicine
2023-03-30
supplementary-materialsOpen access<p>PDF file - 41K, Distribution of lymphoma samples into "Ongoing" or "Static" categories based on the proportion of IGHV subclones that are identical at the CDR3 region for each sample.</p>
2023-03-30
supplementary-materialsOpen access<p>XLSX file - 40K, Canine genes identified by Ingenuity Pathway Analysis as part of the NF-kB or B-cell receptor signaling pathways (Fig. 5).</p>
2023-03-30
preprintOpen access<p>PDF file - 2708K, Immunohistochemistry of cBCLs.</p>
2023-03-30
preprintOpen access<p>PDF file - 843K, Unsupervised hierarchical clustering of cBCLs.</p>
2023-03-30
preprintOpen access<p>PDF file - 881K, Western blot comparing phospho-NF-κB (p65) levels in "ABC-like" and "GCB-like" canine samples.</p>
Frequent coauthors
- 66 shared
Matthew Breen
Cancer Genetics (United States)
- 65 shared
Alison A. Motsinger‐Reif
National Institute of Environmental Health Sciences
- 63 shared
Kristy L. Richards
- 63 shared
Steven E. Suter
North Carolina State University
- 62 shared
Rachael Thomas
North Carolina State University
- 61 shared
Yuri Fedoriw
University of North Carolina at Chapel Hill
- 61 shared
Charles M. Perou
UNC Lineberger Comprehensive Cancer Center
- 61 shared
Sandeep S. Davé
University College London
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