About

Jessica LaMae Whited, Ph.D., holds a BA in Philosophy and a BS in Biological Sciences from the University of Missouri. She earned her PhD at MIT, where she studied neuronal architecture in Paul Garrity's lab. As a postdoctoral fellow in Cliff Tabin's lab at Harvard Medical School, Jessica focused on developing tools to more thoroughly investigate axolotl limb regeneration and established a breeding colony of axolotls. These animals were the foundation of the Whited Lab's first home at Brigham and Women's Hospital. Currently, Jessica is an Associate Professor at Harvard University, a Principal Faculty member of the Harvard Stem Cell Institute, and an Associate Member of the Broad Institute. She has been recognized with prestigious awards including the Presidential Early Career Award for Scientists and Engineers (PECASE), the NIH New Innovator Award, and the NSF CAREER Award. A native of Michigan, Jessica's interest in biology began with butterflies and time spent in the woods. Outside of her professional work, she enjoys spending time with her twin 16-year-old boys.

Research topics

• Biology
• Computational biology
• Genetics

Selected publications

• The adrenal stress response involves distinct dynamics of both cortisol and corticosterone in the axolotl salamander

  Lab Animal · 2026-03-02 · 1 citations

  articleOpen access

  The axolotl is a popular model organism in regenerative biology owing to its ability to regenerate amputated limbs and internal organs. The role of injury-derived signals in initiating the regenerative response is still not well understood, but the potential involvement of the stress response is of interest, as injury and stress are temporally linked. The dominant glucocorticoid response to stress varies among species, with corticosterone generally considered dominant in most amphibians, whereas cortisol predominates in others. Here we characterize the adrenal stress response in the axolotl and describe methods to measure axolotl stress hormones to facilitate their inclusion in future research involving axolotl development and regeneration. We describe an intricate and unexpected axolotl stress response that involves cortisol and corticosterone, each being dominant under different conditions. Corticosterone is preferably activated by the classical hypothalamus-pituitary-interrenal axis pathway, with both arginine vasotocin and adrenocorticotropic hormone promoting its synthesis and release. Under manual stress and direct stimuli with acetylcholine, cortisol is more prominent, suggesting an alternative mechanism involving sympathetic nerve signaling. In response to an amputation injury, both cortisol and corticosterone are increased, with corticosterone being dominant, suggesting an injury-specific response. Finally, when administering glucocorticoids directly and measuring classical physiological effects of glucocorticoid signaling, cortisol is more potent. We propose a hypothesis that axolotls rely on cortisol as their dominant glucocorticoid, functioning in part as an extension of the catecholamine system. By contrast, corticosterone is mainly regulated classically via the hypothalamus-pituitary-interrenal axis.

  PublisherOA PDFDOI

• Awakening latent regeneration in mammals

  Science · 2026-04-09

  articleSenior author

  Extrinsic factors can create a local tissue environment that encourages restoration.

  PublisherDOI

• The brain-limb axis: Elucidating CNS mediators of salamander limb regeneration

  Current Opinion in Neurobiology · 2026-05-07

  articleSenior author
  PublisherDOI

• Pancreatic injury induces β−cell regeneration in axolotl

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-01-23

  preprintOpen accessSenior authorCorresponding

  Background: Diabetes is a condition characterized by a loss of pancreatic β-cell function which results in the dysregulation of insulin homeostasis. Using a partial pancreatectomy model in axolotl, we aimed to observe the pancreatic response to injury. Results: Here we show a comprehensive histological assessment of pancreatic islets in axolotl. Following pancreatic injury, no apparent blastemal structure was observed. We found a significant, organ-wide increase in cellular proliferation post-resection in the pancreas compared to sham-operated controls. This proliferative response was most robust at the site of injury. We found that β-cells actively contributed to the increased rates of proliferation upon injury. β-cell proliferation manifested in increased β-cell mass in injured tissue at two weeks post injury. At four weeks post injury, we found organ-wide proliferation to be extinguished while proliferation at the injury site persisted, corresponding to pancreatic tissue recovery. Similarly, total β-cell mass was comparable to sham after four weeks. Conclusions: Our findings suggest a non-blastema-mediated regeneration process takes place in the pancreas, by which pancreatic resection induces whole-organ β-cell proliferation without the formation of a blastemal structure. This process is analogous to other models of compensatory growth in axolotl, including liver regeneration.

  PublisherDOI

• Covalent binding of thioredoxin to TXNIP is required for diet-induced insulin resistance in the liver

  Journal of Biological Chemistry · 2025-05-08 · 1 citations

  articleOpen access

  Hepatic insulin resistance is an important pathophysiology in type 2 diabetes, and the mechanisms by which high-caloric diets induce insulin resistance are unclear. Among vertebrate animals, mammals have retained a unique molecular change that allows an intracellular arrestin domain-containing protein called Thioredoxin-Interacting Protein (TXNIP) to bind covalently to thioredoxin, allowing TXNIP to "sense" oxidative stress. Here, we show that a single cysteine in TXNIP mediates the development of hepatic insulin resistance in the setting of a high-fat diet (HFD). Mice with an exchange of TXNIP Cysteine 247 for Serine (C247S) showed improved whole-body and hepatic insulin sensitivity compared with WT controls following an 8-week HFD. HFD-fed TXNIP C247S mouse livers also showed improved insulin signaling. The Transmembrane 7 Superfamily Member 2 (Tm7sf2) gene encodes for a sterol reductase involved in the process of cholesterol biosynthesis. We identified TM7SF2 as a potential mediator of enhanced insulin signaling in HFD-fed TXNIP C247S mouse livers. TM7SF2 increased Akt phosphorylation and suppressed gluconeogenic markers PCK1 and G6Pc specifically under oxidative stress-induced conditions in HepG2 cells. We also present data suggesting that a heterozygous variant of TXNIP C247 is well tolerated in humans. Thus, mammals have a single redox-sensitive amino acid in TXNIP that mediates insulin resistance in the setting of an HFD. Our results reveal an evolutionarily conserved mechanism for hepatic insulin resistance in obesity.

  PublisherOA PDFDOI

• Adrenergic signaling coordinates distant and local responses to amputation in axolotl

  Cell · 2025-10-24 · 3 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• VEGF signaling promotes blastema growth and proliferation of vascular and non-vascular cells during axolotl limb regeneration

  Developmental Biology · 2025-06-05 · 1 citations

  articleSenior author
  PublisherDOI

• How axolotl cells ‘remember’ development to rebuild a lost limb

  Nature · 2025-05-21

  articleSenior authorCorresponding
  PublisherDOI

• Brain implantation of soft bioelectronics via embryonic development

  Nature · 2025-06-11 · 26 citations

  articleOpen access
  PublisherOA PDFDOI

• Pancreatic injury induces β‐cell regeneration in axolotl

  Developmental Dynamics · 2025-07-18 · 1 citations

  articleOpen accessSenior authorCorresponding

  BACKGROUND: Diabetes is a condition characterized by a loss of pancreatic β-cell function, which results in the dysregulation of insulin homeostasis. Using a partial pancreatectomy model in axolotl, we aimed to observe the pancreatic response to injury. RESULTS: Here we show a comprehensive histological characterization of pancreatic islets in axolotl. Following pancreatic injury, no apparent blastema-like structure was observed. We found a significant, organ-wide increase in cellular proliferation post-resection in the pancreas compared to sham-operated controls. This proliferative response was most robust at the site of injury. Further, an increase in nuclear density was observed, suggesting compensatory congestion as a mechanism of regeneration. We found that β-cells actively contributed to the increased rates of proliferation upon injury. β-Cell proliferation manifested in increased β-cell mass in injured tissue at 2 weeks post-injury. At 4 weeks post-injury, we found organ-wide proliferation to be extinguished while proliferation at the injury site persisted, corresponding to pancreatic tissue recovery. Similarly, total β-cell mass was comparable to sham after 4 weeks. CONCLUSIONS: Our findings suggest a non-blastema-mediated regeneration process takes place in the pancreas, by which pancreatic resection induces whole-organ β-cell proliferation without the formation of a blastemal structure. This process is analogous to other models of compensatory congestion in axolotl.

  PublisherOA PDFDOI

Recent grants

• IDENTIFYING ROADBLOCKS TO LIMB REGENERATION

  NIH · $1.9M · 2019–2025

• Elucidating a Role for Blastema-Enriched Genes in Salamander Limb Regeneration,

  NIH · $176k · 2015–2017

• Leveraging Single-Cell Analysis to Elucidate Mechanisms of Vertebrate LimbRegeneration

  NIH · $1.1M · 2020–2021

• EPIDERMAL FACTORS THAT PROMOTE INTERNAL TISSUE PROGENITOR ACTIVATION FOLLOWING AMPUTATION

  NIH · $266k · 2015–2018

• Leveraging Single-Cell Analysis to Elucidate Mechanisms of Vertebrate LimbRegeneration

  NIH · $2.0M · 2018–2020

Frequent coauthors

• Donald M. Bryant

  Harvard University

  82 shared

• K.A. Johnson

  American Society of Law, Medicine and Ethics

  59 shared

• Bess M. Miller

  Brigham and Women's Hospital

  51 shared

• Nicholas D. Leigh

  Lund University

  51 shared

• Duygu Payzin‐Dogru

  Harvard University Press

  46 shared

• Tzu‐Hsing Kuo

  Acceleron Pharma (United States)

  36 shared

• Tia DiTommaso

  32 shared

• Sevara Bryant

  Harvard University

  30 shared

Labs

• WHITED LABPI

  Jessica LaMae Whited, Ph.D. studies neuronal architecture and limb regeneration in axolotls.