Bio


Jessie Ong is a 2026 Ellison Scholar, a current BS/MS student in Biology at Stanford, and an incoming DPhil student in Paediatrics at the University of Oxford focused on vaccine discovery. Her research spans immunology, synthetic biology, and neuroscience, with experience across the University of Oxford, Stanford, and the Italian Institute of Technology. She is interested in leveraging disease heterogeneity to develop clinically translatable, scalable vaccines that minimize resistance.

Honors & Awards


  • 2026 Ellison Scholarship, DPhil in Paediatrics, Ellison Institute of Technology, University of Oxford (2026)
  • Stanford Major Grant Awardee, Stanford Vice Provost for Undergraduate Education (June 2025)
  • Stanford Global Studies Summer Fellow, Stanford Global Studies
  • Bio-X Undergraduate Fellow, Stanford Bio-X (June 2024)
  • Haas Center Community Service Fellow, Haas Center for Public Service (June 2024)

Professional Affiliations and Activities


  • Speaker, TEDxStanford (2025 - 2025)
  • Bio-X Undergraduate Fellow, Stanford BioX (2024 - 2024)
  • Board Member, Stanford Down Syndrome Research Center (2023 - Present)

Current Research and Scholarly Interests


Under mentorship of Jennifer Anne Co (PhD Candidate) in the Steven Banik Lab.
Engineering a molecular-glue detector in mammalian cells with CRISPR and degron based tools.
Creating platform for novel drug candidates through screening of a 15,000 protein ORFeome library.

All Publications


  • Four Neotropical frog species exhibit shared and distinct skin bacterial communities in a laboratory setting. microPublication biology Jansari, V., Castro-Martinez, D. A., Dailey, M. J., Roti, O., Seibert, M. R., Abdelghne, B. J., Aguilar, G. K., Amine, A., Ben-Efraim, K., Carolan, R. E., Carter, A. N., Chang, M., Dye, N. J., Le, C. A., Melian, M., Nakamura, K. C., Nemawarkar, R., Nguyen, A. T., Ong, J., Saigal, K., Sosa, H. M., Vo, L. T., Wu, S. H., Zreik, Z. K., Morales, G., Kuznetsov, H., Ramirez, D., Pamplona-Barbosa, M., Lacey, M. P., Bradon, N., Golde, C. L., O'Connell, L. A. 2026; 2026

    Abstract

    Amphibian skin microbiomes are an essential part of host physiology and pathogen defense. In this study, we identified common and distinct microbiota across four Neotropical frog species in laboratory conditions. Across frogs, we found communities dominated by Pseudomonas and Chryseobacterium . However, each frog species had a unique bacterial profile with at least one unique bacterial genus, highlighting the variability of naturally occurring amphibian skin microbiomes. These experiments were conducted by undergraduate students in an upper-division laboratory course, demonstrating how curiosity-based science education can lead to practical research experiences and new scientific insights.

    View details for DOI 10.17912/micropub.biology.002080

    View details for PubMedID 41890544

    View details for PubMedCentralID PMC13014139

  • Bay leaf extract is a chemotaxis repellent for C. elegans. microPublication biology Wu, S. H., Amine, A., Ben-Efraim, K., Dye, N. J., Melian, M., Nakamura, K. C., Nemawarkar, R., Saigal, K., Sosa, H. M., Vo, L. T., Abdelghne, B. J., Aguilar, G. K., Carolan, R. E., Carter, A. N., Castro-Martinez, D. A., Chang, M., Dailey, M. J., Jansari, V., Le, C. A., Nguyen, A. T., Ong, J., Roti, O., Seibert, M. R., Zreik, Z. K., Morales, G., Ramirez, D., Bradon, N., Golde, C. L., O'Connell, L. A. 2026; 2026

    Abstract

    Plants synthesize compounds that modulate animal nervous systems through various mechanisms, but the key interactions remain understudied. We used chemotaxis assays with the nematode Caenorhabditis elegans to test if plant extracts can be detected by the worm nervous system and which compounds induce behavioral responses. We found that C. elegans avoid the extract of bay leaves ( Laurus nobilis ). Subsequent testing of known bay leaf compounds identified cadinene and eugenol as key molecules that may mediate the repulsion effect. These experiments were conducted by undergraduate students in an upper-division laboratory course, providing practical research experiences and new insights into plant-animal interactions.

    View details for DOI 10.17912/micropub.biology.002023

    View details for PubMedID 41867891

    View details for PubMedCentralID PMC13005153

  • Selectively Blocking Small Conductance Ca2+-Activated K+ Channels Improves Cognition in Aged Mice. Biology Ong, J., Heller, H. C., Pittaras, E. 2025; 14 (2)

    Abstract

    Aging is associated with decreased neuronal sensitivity and activity that creates deficits in cognitive processes, including learning, memory, motivation, general activity, and other behaviors. These effects are due in part to decreased intracellular Ca2+ homeostasis, increasing hyperpolarization of the resting potential in aged neurons and therefore decreasing their excitability. To reduce hyperpolarization in aged mice, we used apamin, a selective small conductance Ca2+-activated K+ (sKCa) channel blocker. By blocking the sKCa channels, apamin decreases the egress of the K+ out of the cell, reducing its hyperpolarization and causing it to be closer to threshold potential. As a result, neurons should be more sensitive to excitatory stimuli and more active. We evaluated the performance of aged mice in a selection of cognitive and behavioral tests prior to and after systemic applications of apamin or the vehicle saline. Apamin improved performance in short-term memory, increased attention to tasks, and decreased anhedonia. Apamin had no significant effect on long-term spatial and recognition memory, risk-taking behavior, sociability, and anxiety. Our results are compatible with the known effects of sKCa channel blockade on neuronal sensitivity and activity; however, these short-term effects were not reflected in longer-term alterations of neural plasticity responsible for long-term spatial and recognition memory or other more complex cognitive processes we evaluated.

    View details for DOI 10.3390/biology14020149

    View details for PubMedID 40001917

    View details for PubMedCentralID PMC11851921