Wisconsin dermatology lab expands vascular anomalies research with iPSC and zebrafish models
The Lawson Lab is opening multiple postdoctoral research positions as it moves to the Department of Dermatology at the University of Wisconsin, Madison in January 2027. The recruiting push is centered on vascular anomalies, a field where inherited and mosaic mutations can produce lesions that are biologically complex and clinically heterogeneous. The planned work is built around two model systems: human induced pluripotent stem cells and zebrafish. Both are aimed at reconstructing disease mechanisms from the mutation outward, rather than working backward from established pathology.
One of the clearest signals from the posting is the lab’s emphasis on human genetics and developmental biology. Candidates are expected to hold a PhD in the biological sciences, ideally with training in developmental biology or genetics, along with hands-on expertise in genetic approaches in animal or iPSC models. The role is not framed as a narrow bench appointment. It is intended for researchers who can build engineered systems, interpret phenotype, and connect pathway-level findings to patient disease.
Human iPSC modeling centers on activating and loss-of-function mutations
The human iPSC arm of the program is designed to generate and characterize cell lines carrying conditional mutations linked to vascular anomalies in patients. The mutation list spans well-known activating alterations in GNAQ, MEK, PIK3CA, and RAS, as well as loss-of-function variants in RASA1 and EPHB4. That combination matters because it captures distinct biological routes into abnormal vascular development: some variants drive excessive signaling, while others remove brakes that normally restrain endothelial behavior.
The planned experiments will focus on establishing genetically modified iPSC lines that allow conditional activation or deletion. Once those lines are built, the next step is endothelial cell differentiation and morphogenesis, a direct way to ask how specific genotypes reshape vascular development. In practical terms, this is where the lab can separate a mutation’s effect on lineage commitment from its effect on tissue architecture. The work will draw on campus resources including the UW Human Stem Cell Core and WiCell, which should help support the technical demands of generating and validating engineered lines.
A particularly important element is the planned use of organ-on-a-chip systems in collaboration with UW Dermatology groups. Those models are intended to assess tissue-level phenotypes, moving beyond isolated cells to a setting where flow, structure, and multicellular interactions can be examined together. For vascular anomalies, that higher-order context is essential. Abnormal endothelial signaling often reveals its full clinical consequences only when vessels are formed, stressed, and embedded in tissue.
Comparative omics will be used to search for shared pathways
The lab also plans comparative omics studies to identify common pathways across candidate variants. That is a sensible strategy for a disease category defined by genetic diversity. Different mutations can converge on the same downstream pathway, and the same pathway can produce different lesion patterns depending on when and where it is activated. By comparing multiple engineered variants side by side, the program aims to identify signaling nodes that are shared rather than mutation-specific.
A second layer of complexity comes from the lab’s ongoing work on cell of origin in human vascular anomaly lesions. The posting indicates that non-endothelial cell types will be explored as warranted. This is a meaningful clue about the direction of the science. Vascular anomaly research has increasingly moved away from the assumption that endothelial cells alone explain every lesion. Supportive stromal cells, surrounding tissue compartments, and developmental timing may all influence the final phenotype.
Zebrafish studies will probe mosaic disease, second hits, and progression
The zebrafish portfolio is equally mechanistic, but it is aimed at a different set of questions. Current efforts focus on capillary malformation-arteriovenous malformation syndrome and Sturge-Weber syndrome, with relevant zebrafish lines already available. In CM-AVM, the linked lesion biology centers on loss-of-function EPHB4 mutations. In Sturge-Weber syndrome, the disease model is built around activating GNAQ mutation.
The postdoctoral researcher in this arm would perform phenotypic analysis in embryos and adults carrying these mutations, using serial confocal imaging, immunostaining, and single-cell RNA sequencing. Those tools can expose how abnormal vascular architecture emerges over time and how mutant cells differ at the transcriptomic level. In a field where clinical manifestations can be patchy and segmental, serial imaging is especially valuable because it captures progression rather than a single static endpoint.
A single mutation is not always the whole story.
For CM-AVM models, the work will extend to defining the genetic nature of mosaic lesions in adult heterozygous carriers. The lab plans to use exome sequencing and whole genome sequencing to search for second-hit mutations, then apply CRISPR to test candidate variants in zebrafish. That approach speaks directly to a longstanding question in vascular anomaly biology: why some lesions are localized and focal even when a predisposing germline variant is present throughout the body. The proposed experiments are built to distinguish constitutional susceptibility from somatic events that may trigger lesion formation in a restricted tissue region.
Technical breadth and publication record are central to the hire
The recruitment criteria suggest the lab is looking for a highly independent scientist rather than a trainee needing close supervision. Applicants are expected to be technically accomplished, highly motivated, and backed by an exceptional publication record. A brief cover letter and CV are required for consideration, and only selected applicants will move on to reference requests.
For a postdoctoral researcher, the value of the opportunity lies in the breadth of the scientific toolkit and the logic of the disease models. Human iPSC engineering offers a controllable system for testing causality. Zebrafish provide an in vivo setting for morphology, development, and mosaicism. Together, those platforms can interrogate how mutations in GNAQ, PIK3CA, RAS, RASA1, and EPHB4 alter vascular development across scales.
The scientific payoff will depend on how well these systems recapitulate human lesions and how cleanly candidate pathways can be traced from genotype to phenotype. The lab’s strategy is ambitious, but its limitations are also clear: complex vascular anomalies do not reduce neatly to a single cell type, and mosaic disease can be difficult to model faithfully. The next stage of this program will hinge on whether engineered iPSC systems, zebrafish genetics, and patient-linked lesion studies converge on the same mechanisms.