About

Dr. Sara Thomasy is a professor in the Murphy-Russell-Leonard-Thomasy (MRLT) Laboratory, with dual appointments in the Schools of Medicine and Veterinary Medicine at UC Davis. Her research interests include large animal models of ocular disease, corneal wound healing, glaucoma, ocular pharmacology, and antiviral therapy for the management of feline herpesvirus. She is actively involved in advancing understanding and treatment of eye-related conditions through her work in vision science and ophthalmology.

Research topics

• Biology
• Genetics
• Computer Science
• Cell biology
• Neuroscience
• Medicine
• Computational biology
• Evolutionary biology
• Immunology
• Microbiology

Selected publications

• Clinical and clinicopathologic features of an undifferentiated resolving uveitis in kittens similar to that seen with feline infectious peritonitis

  Journal of the American Veterinary Medical Association · 2026-01-07

  article

  Objective: To highlight clinical and clinicopathologic differences between kittens with feline infectious peritonitis-associated uveitis (FIP-AU) versus those with an otherwise similar feline undifferentiated resolving uveitis (FURU). Methods: Clinical and clinicopathologic data were compared between 22 kittens with FURU and 8 with necropsy-confirmed FIP-AU examined between January 1, 1985, and December 31, 2022. Results: Sex, lifestyle, seasonality, household cat numbers and systemic signs were similar in both groups. Feline undifferentiated resolving uveitis occurred predominantly in domestic-breed kittens from shelters, whereas FIP-AU was more frequent in purebred or stray cats. Duration of ocular signs before presentation was 1 to 2 weeks for FURU versus > 2 months for FIP-AU. Feline undifferentiated resolving uveitis was more commonly associated with episcleral hyperemia while FIP-AU was more commonly associated with corneal edema, dyscoria, rubeosis iridis, iridal congestion/thickening, posterior synechia, or keratic precipitates. Corneal edema and chemosis were more severe in FIP-AU. No eyes with FURU had fundic abnormalities whereas 6 of 11 eyes with FIP-AU had chorioretinitis. All kittens with FIP-AU presented bilaterally whereas 5 of 15 kittens in which FURU was ultimately bilateral, initially presented unilaterally. Hyperproteinemia, hyperglobulinemia, and hyperbilirubinemia occurred only with FIP-AU. Neither likelihood of a positive coronavirus titer nor titer magnitude differed between groups. Conclusions: Kittens can develop bilateral fibrinous uveitis with keratic precipitates, systemic signs of illness, and serum coronavirus antibodies which resolves without sequelae following empirical treatment. Syndromic assessment-including careful fundic examination-can help differentiate FURU from FIP-AU and should precede antiviral therapy. Clinical Relevance: Resolution of uveitis during antiviral treatment does not confirm FIP. Comprehensive diagnostic evaluation is essential to avoid misdiagnosis and inappropriate treatment.

  PublisherDOI

• TAZ ( <i>Wwtr1</i> ) deficiency leads to ER stress and mitochondrial dysfunction in a mouse model of Fuchs’ endothelial corneal dystrophy

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-19

  articleOpen accessSenior authorCorresponding

  Abstract Fuchs’ endothelial corneal dystrophy (FECD) impacts over 300 million individuals worldwide with corneal transplantation as the primary treatment. There is a dire need to establish non-surgical alternatives which are dependent on mouse models. Transcriptional co-activator with PDZ-binding motif (TAZ, encoded by Wwtr1 ) is a mechanotransducer implicated in maintaining homeostasis of corneal endothelial cells (CEnC). Wwtr1 -/- (TAZ KO) mice serve as an animal model for late-onset FECD. We combined single-cell transcriptomics, transmission electron microscopy, and immunofluorescence staining to elucidate the mechanisms driving pathogenesis in young (2-month-old) and geriatric (11-month-old) mice. A progressive stress response was observed in TAZ KOs defined by endoplasmic reticulum (ER) stress, mitochondrial structural and functional abnormalities, and impaired Na + /K + ATPase localization. These changes were accompanied by an altered expression of genes involved in extracellular matrix (ECM) organization, oxidative phosphorylation, macroautophagy and response to oxidative stress. Additionally, we noted age-related differences in cellular response with young TAZ KO CEnCs upregulating macroautophagy and downregulating ECM organization while geriatric TAZ KO CEnCs downregulated macroautophagy, and ECM organization. Both TAZ KO groups downregulated response to oxidative stress and cell-substrate adhesion. Together, these findings establish a mechanistic link between disrupted mechanotransduction and organelle stress in CEnC degeneration, further elaborating on potential mechanisms driving FECD pathogenesis. This positions TAZ KO mice as a translational platform for evaluating non-surgical therapeutic strategies targeting FECD. Significance statement Fuchs’ endothelial corneal dystrophy (FECD) is a common, age-related cause of vision loss involving a depletion of corneal endothelial cells (CEnC) that necessitates corneal transplantation. Understanding why corneal endothelial cells progressively fail in this disease is essential for developing non-surgical therapies. Using transcriptomics, electron microscopy and immunofluorescence staining, we demonstrate that loss of the mechanotransducer TAZ disrupts cellular homeostasis by inducing endoplasmic reticulum stress, mitochondrial dysfunction and improper extracellular matrix and functional protein organization in CEnCs. By linking altered mechanotransduction to organelle stress and endothelial cell loss, these findings provide insight into fundamental disease mechanisms and identify pathways that may be targeted to preserve corneal endothelial function in FECD.

  PublisherOA PDFDOI

• Rhesus macaques with an <i>OPA1</i> mutation demonstrate features of autosomal dominant optic atrophy

  Proceedings of the National Academy of Sciences · 2026-04-15

  articleOpen accessSenior authorCorresponding

  Autosomal dominant optic atrophy (ADOA) is an inherited optic neuropathy primarily caused by mutations in OPA1 . We identified and defined a spontaneous nonhuman primate (NHP) model of ADOA using rhesus macaques heterozygous for a missense mutation ( OPA1 A8S). With ocular examinations, ophthalmic imaging, electroretinography, histopathology, immunohistochemistry, and transmission electron microscopy (TEM), we documented retinal nerve fiber layer (RNFL) thinning, retinal ganglion cell (RGC) loss and dysfunction, OPA1 mislocalization, and reduced axonal mitochondrial density in affected macaques. Our investigation revealed substantial phenotypic variability among affected macaques, shedding light on the pathogenesis of ADOA. The retinas were evaluated using techniques such as spectral-domain optical coherence tomography and fundus photography facilitating observation of structural changes in the retina and optic nerve. Thinning of the RNFL and optic nerve head degeneration, hallmark features of ADOA, were observed in affected macaques. Decreased RGC function in the OPA1 heterozygotes was demonstrated with pattern electroretinography. Histopathological analysis and immunohistochemical staining of postmortem retinal tissue suggested RGC loss in the papillomacular bundle, with reduced OPA1 and mitochondria in the RGC axons, indicating dysfunctional mitochondrial dynamics and reduced function consistent with ADOA. Ultrastructural changes were evident with TEM including dysmorphic mitochondria, axonal loss, myelin disruption, and hypertrophic astrocytic processes. The observed similar pattern of RGC loss and dysfunction coupled with phenotypic heterogeneity in our NHP model reflects the clinical variability observed in human ADOA patients indicating that therapeutic interventions in this foveate model will likely translate to the human condition.

  PublisherDOI

• Quantitative imaging of corneal endothelial development reveals dynamic but resilient monolayer

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-05

  articleOpen access

  The formation of functional corneal endothelial cells during development requires tight coordination between tissue-scale growth and cell-scale organization, yet how these processes are integrated in three dimensions remains poorly understood. Here, we combine high-resolution confocal imaging with quantitative analysis to reconstruct the morphogenesis of the chick corneal endothelium across embryonic development. Using a pipeline integrating 3D nuclear segmentation, Voronoi-based topological mapping, and spatial statistics, we link macroscopic globe expansion to single-cell geometry and lattice organization. We identify a multiphasic relationship between tissue growth and cell density, driven by temporal decoupling of organ expansion and proliferation. During early development, rapid globe expansion induces cellular stretching and spatial heterogeneity, followed by a phase of density accumulation and geometric refinement. Despite these dynamic conditions, the endothelial sheet maintains a robust monolayer architecture with minimal z-axis stratification. Quantitative topological analysis reveals that hexagonal packing is preserved from early stages and progressively refined through reduction of area variability and spatial clustering. Nearest-neighbor and Clark-Evans analyses demonstrate a transition from localized clustering to a more uniform spatial distribution, consistent with increasing packing regularity. Transient out-of-plane deviations coincide with key mechanical transitions, suggesting a role for 3D remodeling in accommodating mechanical stress. Concomitantly, junctional and cytoskeletal organization undergo progressive maturation. N-cadherin is established early at cell-cell interfaces, while Zonula Occludens-1 (ZO-1) transitions from diffuse localization to apically enriched tight junctions aligned with cortical actin. In parallel, microtubule organization becomes increasingly polarized to the apical domain, coinciding with the emergence of primary cilia. Together, these changes reflect coordinated establishment of epithelial polarity, barrier function, and mechanical stability. Overall, our study provides a multiscale, imaging-driven framework for understanding how epithelial tissues achieve and maintain geometric order under mechanical strain, establishing the corneal endothelium as an exemplar for linking developmental mechanics, 3D architecture, and epithelial topology. Summary Statement: Using 3D imaging and quantitative analysis, this work reveals how corneal endothelial cells stay organized and form a regular pattern during growth, despite ongoing changes in tissue size and shape.

  PublisherOA PDFDOI

• A molecular and spatial resource defining tubulin isotype organization during corneal development

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-20 · 2 citations

  articleOpen access

  Microtubules are essential components of the cytoskeleton that support epithelial organization, polarity, and tissue morphogenesis. They are composed of α- and β-tubulin heterodimers, each encoded by distinct genes that generate closely related but functionally distinct isotypes. Although several tubulin isotypes have been implicated in ocular development and disease, how isotype diversity is organized during corneal morphogenesis remains poorly defined. Herein, we use the developing chick embryo as a model system to investigate the conservation and spatiotemporal localization of tubulin isotypes during corneal development. Through comparative amino acid sequence analysis, we show that chick and human α- and β-tubulin isotypes are highly conserved at structural and catalytic domains, with divergence concentrated in C-terminal regions associated with post-translational modifications. To relate these molecular features to tissue-level organization, we performed a longitudinal immunohistochemical analysis of five tubulin isotypes across key stages of corneal development. We identify distinct and dynamic patterns of isotype enrichment along apico-basal and central-peripheral axes within the cornea, as well as isotype-specific redistribution during epithelial maturation and corneal endothelial differentiation. Notably, TUBA5/TUBA4A exhibits tightly regulated localization, including enrichment at the leading edge of migratory corneal stromal progenitor cells and within the maturing corneal endothelium. Together, these data establish the chick embryo as a conserved and tractable model for studying tubulin isotype diversity in the cornea, and more broadly across other tissues, and to provide a developmental resource linking tubulin sequence identity to spatially defined microtubule organization during epithelial morphogenesis.

  PublisherOA PDFDOI

• The role of epithelial membrane-associated mucin 4 in ocular surface health and corneal wound healing

  Frontiers in Medicine · 2026-01-13

  articleOpen access

  The purpose of this study was to determine the role of MUC4, a corneal membrane-associated mucin, on ocular surface health and corneal wounding healing using a Muc4 knockout (KO) mouse model. Complete ophthalmic examinations were performed on wildtype (WT), Muc4 heterozygous (Het) and Muc4 knockout (KO) mice, including slit lamp biomicroscopy, phenol red thread test (PRTT), intraocular pressure (IOP), and fluorescein staining. The mice were also assessed using optical coherence tomography (OCT), an advanced imaging technique. Dynamic contact angle goniometry was performed on ex vivo globes of WT, Muc4 Het and Muc4 KO mice to calculate contact angle hysteresis as a novel measure of the adherence properties of the corneal epithelium. To determine the effect of Muc4 in corneal wound healing, a phototherapeutic keratectomy (PTK) was performed on the right eye. After PTK wounding, the corneas were fluorescein stained, imaged, and the wound size was quantified using ImageJ at 0-, 24-, 36-, and 48-h post-wounding. There were no phenotypic differences identified between WT, Muc4 Het and Muc4 KO mice on clinical examination, diagnostic testing, advanced imaging, and histology. While there was no difference in mucin 1 ( Muc1 ) mRNA expression between WT and KO mice, there was a compensatory upregulation of a previously unreported murine corneal mucin, Muc20 mRNA expression, in corneal epithelium of Muc4 KO mice. No differences were detected between WT and Muc4 KO mice using dynamic contact angle goniometry. The Muc4 KO mice had significantly slower healing rates at 24 and 36 h post-wounding when compared with WT mice (P &amp;lt; 0.05) and all healed by 48 h post-wounding. These results support further investigation into compensatory roles of glycoproteins on the ocular surface, namely Muc4 and Muc20 , and the role of Muc4 in epithelial cell migration in corneal wound healing.

  PublisherOA PDFDOI

• Impact of Diet and Gut Microbiome on Nonhuman Primate Models of Age-Related Macular Degeneration

  Current Developments in Nutrition · 2025-05-01

  articleOpen access
  PublisherDOI

• Risk Factors and Treatment Outcomes for Canine Spontaneous Chronic Corneal Epithelial Defects ( <scp>SCCED</scp> ): 335 Cases Within a Reference Population

  Veterinary Ophthalmology · 2025-08-15

  articleOpen accessSenior authorCorresponding

  OBJECTIVE: To retrospectively evaluate the presentation, treatment, and outcome of dogs with spontaneous chronic corneal epithelial defects (SCCED) and to identify risk factors. METHODS: Records of 335 dogs with SCCED at the University of California-Davis Veterinary Medical Teaching Hospital were reviewed and compared with 157,362 dogs from the general population within the study period. Data retrieved included signs, diagnoses, treatments, and outcomes associated with SCCED. RESULTS: Boxers (n = 92, O:E = 12.38), Pembroke Welsh Corgis (n = 15, O:E = 5.21), Bulldogs (n = 7, O:E = 4.77), Boston Terriers (n = 15, O:E = 3.64), French Bulldogs (n = 15, O:E = 3.04) and English Bulldogs (n = 12, O:E = 3.03) were significantly overrepresented in the SCCED-affected population compared to the reference population (p < 0.01). Dogs aged 6-10 years and weighing 31-40 kg were significantly overrepresented with SCCED compared to the reference population, whereas dogs aged < 5 years and weighing < 10 kg were significantly underrepresented (p < 0.0005). When Boxers were excluded, dogs 6-15 years of age were significantly overrepresented in SCCED versus the reference population, while dogs < 5 years of age were still significantly underrepresented (p < 0.0001). The success rate (defined as complete healing after procedure) following a single procedure was 49%, 70%, and 66% after cotton applicator debridement (CTA) alone, CTA + diamond burr debridement (DBD), and CTA + grid keratotomy (GK), respectively, and differed significantly between CTA and CTA-DBD (p < 0.02). CONCLUSIONS: Using a large reference population, this study confirms previously suspected breed predispositions to SCCED by adjusting for common breeds across a broader hospital population. In addition, it confirms the previously known age predisposition and that CTA-DBD is a more effective treatment than CTA alone.

  PublisherOA PDFDOI

• Spontaneous refractive error, ocular biometry and age related lens changes in a population of geriatric rhesus macaques

  Scientific Reports · 2025-12-05 · 1 citations

  articleOpen accessSenior author

  The purpose of this investigation was to determine refractive error, ocular biometry and age-related lens changes in a population of geriatric rhesus macaques (Macaca mulatta) from the California National Primate Research Center (CNPRC). Ophthalmic examination was performed in 182 rhesus macaques [Formula: see text] 19 years of age using a cross-sectional study design, including streak retinoscopy, anterior segment tomography, A-scan ultrasound biometry and handheld slit lamp biomicroscopy. Median spherical equivalent refractive error was + 0.75 D with an interquartile range (IQR) of 0 to 1 D. Most eyes were hyperopic (n = 102, 55%) or emmetropic (n = 68, 36%); myopic eyes were the least common (n = 17, 9%). Anisometropia was present in 13 subjects (14%). Mean (± SD) corneal curvature was 52.6 ± 2.6 D (n = 79). Mean (± SD) axial globe length was 20.2 ± 1.5 mm, anterior chamber depth was 3.7 ± 0.4 mm, lens thickness was 4.1 ± 0.4 mm, and vitreous chamber depth was 12.2 ± 1.0 mm (n = 86). Median (IQR) nuclear sclerosis grade (n = 191, 98%) assessed with the lens opacities classification system II was 1 (1-2). Hyperopia is the most common refractive error in the geriatric rhesus macaque population at CNPRC. This study provides reference values for an isolated geriatric rhesus macaque population and broadens our understanding of refractive error and lens opacities in geriatric rhesus macaques which may serve as a model for studying novel therapeutics for refractive errors and cataracts.

  PublisherOA PDFDOI

• Topical Application of a Novel Harderian-Derived Nonpolar Lipid Prolongs Tear Film Breakup Time in Normal Beagle Dogs

  Journal of Ocular Pharmacology and Therapeutics · 2025-09-23

  articleOpen access

  PURPOSE: This preliminary study sought to determine the pharmacodynamic effect and tolerability of a novel rabbit-derived nonpolar lipid (rNPL593) on tear film breakup time (TFBUT) in healthy beagle dogs as a potential therapy for patients with evaporative dry eye disease. METHODS: In phase 1, two healthy beagle dogs received a single dose of rNPL593 at concentrations ranging from 0.1 to 10 mg/mL, and TFBUT was measured at different intervals post-dose in both eyes. In phase 2, five dogs received vehicle, 1 or 3 mg/mL rNPL593 once in both eyes, and TFBUT was measured at 6- and 24-h post-dose. In phase 3, three dogs received multiple doses of 3 mg/mL rNPL593 over 4 days, and TFBUT was performed 6 and 80 h after the final dose. Semiquantitative preclinical ocular toxicology scoring was performed in all phases to determine tolerability. RESULTS: In phase 1, topical treatment with 3 mg/mL rNPL593 resulted in a dose-dependent increase in TFBUT, assessed as the preferred concentration. In phase 2, the concentration of 3 mg/mL was superior to 1 mg/mL by creating a more pronounced and sustained increase in TFBUT over 24 h. In phase 3, there was an increase in TFBUT measured at 6-h post-dose that returned to baseline levels at 80-h post-dose. The topical rNPL593 was well tolerated in all phases with all doses. CONCLUSIONS: Treatment with rNPL593 was well tolerated at all doses tested and resulted in an increased TFBUT that was most pronounced with the 3 mg/mL concentration at 6- and 24-h post-dose.

  PublisherOA PDFDOI

Recent grants

• Novel model systems for the study of cone disorders and other heritable retinal diseases

  NIH · $7.7M · 2018–2024

• Large Animal Core

  NIH · $18.3M · 1999–2029

• NIH Grant U01ES027288

  NIH · $2.2M · 2022

• Mechanotransduction in corneal disorders

  NIH · $5.1M · 2006–2024

• NIH Grant K08EY021142

  NIH · $879k · 2017

Frequent coauthors

• Christopher J. Murphy

  111 shared

• Soo-Hyun Kim

  52 shared

• David J. Maggs

  University of California, Davis

  49 shared

• Brian C. Leonard

  University of California, Davis

  47 shared

• Vijay Krishna Raghunathan

  University of Houston

  44 shared

• Ala Moshiri

  37 shared

• Jeffrey Rogers

  Baylor College of Medicine

  30 shared

• Glenn Yiu

  University of California, Davis

  29 shared