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   https://doi.org/10.1016/j.yhbeh.2022.105216  

   Cox, Robert M.; Hale, Matthew D.; Wittman, Tyler N.; Robinson, Christopher D.; Cox, Christian L. (August 2022, Hormones and Behavior)
2. Inhibition of tumor growth by agonists of growth hormone-releasing hormone

   https://doi.org/10.1073/pnas.1817342115  

   Kiaris, Hippokratis; Chatzistamou, Ioulia (November 2018, Proceedings of the National Academy of Sciences)
3. Isoprene deters insect herbivory by priming plant hormone responses

   https://doi.org/10.1126/sciadv.adu4637  

   Sahu, Abira; Mostofa, Mohammad Golam; Xu, Yuan; Serda, Bianca M; O’Keefe, James; Sharkey, Thomas D (April 2025, Science Advances)

   Isoprene, emitted by some plants, deters insect herbivory. However, the associated biochemical and physiological responses that confer herbivory resistance remain unknown. We used engineered isoprene-emitting (IE) and non-emitting (NE) control tobacco plants to interpret isoprene-mediated defense against herbivory in plants. Hornworm larvae raised on IE plants exhibited stunted growth compared to those raised on NE plants. Worms preferred to feed on NE rather than IE leaves, indicating deterrent effects of isoprene on insect feeding. Worm feeding induced a greater increase in jasmonic acid (JA), a crucial hormone for insect resistance, in IE leaves compared to that in NE leaves. Assimilation rates were stably maintained in IE plants, suggesting a protective role of isoprene in preserving photosynthetic efficiency during insect herbivory. Wound-induced increase in isoprene emission correlated with the elevation of key metabolites of the isoprene biosynthesis pathway. Our results highlight JA-priming functions of isoprene and provide insights into isoprene-mediated defense against insect herbivory. 

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4. Sex-specific responses to growth hormone and luteinizing hormone in a model teleost, the Mozambique tilapia

   https://doi.org/10.1016/j.ygcen.2022.114119  

   Celino-Brady, Fritzie T.; Breves, Jason P.; Seale, Andre P. (December 2022, General and Comparative Endocrinology)
5. Thyroid hormone shapes craniofacial bones during postembryonic zebrafish development

   https://doi.org/10.1111/ede.12399  

   Keer, Stephanie; Storch, Joshua D.; Nguyen, Stacy; Prado, Mia; Singh, Rajendra; Hernandez, Luz Patricia; McMenamin, Sarah K. (March 2022, Evolution & Development)

   Abstract Changing the shape of craniofacial bones can profoundly alter ecological function, and understanding how developmental conditions sculpt skeletal phenotypes can provide insight into evolutionary adaptations. Thyroid hormone (TH) stimulates metamorphosis and regulates skeletal morphogenesis across vertebrates. To assess the roles of this hormone in sculpting the craniofacial skeleton of a non‐metamorphic vertebrate, we tested zebrafish for developmental periods of TH‐induced craniofacial shape change. We analyzed shapes of specific bones that function in prey detection, capture and processing. We quantified these elements from late‐larval through adult stages under three developmental TH profiles. Under wild‐type conditions, each bone progressively grows allometrically into a mature morphology over the course of postembryonic development. In three of the four bones, TH was required to sculpt an adult shape: hypothyroidism inhibited aspects of shape change, and allowed some components of immature shape to be retained into adulthood. Excess developmental TH stimulated aspects of precocious shape change leading to abnormal morphologies in some bones. Skeletal features with functional importance showed high sensitivities to TH, including the transformator process of the tripus, the mandibular symphysis of the lower jaw, the scutiform lamina of the hyomandibula, and the anterior arm of the pharyngeal jaw. In all, we found that TH is necessary for shaping mature morphology of several essential skeletal elements; this requirement is particularly pronounced during larval development. Altered TH titer leads to abnormal morphologies with likely functional consequences, highlighting the potential of TH and downstream pathways as targets for evolutionary change. 

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