Date of Graduation

12-2025

Document Type

Thesis

Degree Name

Master of Science in Cell & Molecular Biology (MS)

Degree Level

Graduate

Department

Cell & Molecular Biology

Advisor/Mentor

Tipsmark, Christian

Committee Member

Pinto, Ines

Second Committee Member

Dridi, Sami

Keywords

Atlantic Killifish, Fundulus Heteroclitus, Phenotypic Changes

Abstract

The Atlantic killifish (Fundulus Heteroclitus) is a teleost found in brackish water estuaries, which are subject to large fluctuations in salinity, that handles osmotic stress by triggering compensatory actions across their osmoregulatory organs. As the external salinity increases, the killifish intestine exhibits a high degree of phenotypic plasticity, as the protein composition of the gut epithelium can be modified to absorb desalinated water (H2O) from ingested seawater (SW). Three osmoregulatory hormones, prolactin (P), growth hormone (GH), and cortisol (F), have been observed to be crucial for these transitions to occur in many species of teleosts, including killifish. This research sought to identify which signaling molecules are responsible for the phenotypic changes we observe in the gut during a freshwater (FW) to SW transition by comparing transcriptional changes in target proteins observed in the long-term (21d) and short-term (1d, 3d, 7d) to those observed following in-vitro and in-vivo applications of PRL, GH, and F. If target proteins were differentially affected by F in-vitro, further analysis was done to establish which cortisol receptor (MR, GR1, GR2) was responsible for mediating cortisol’s transcriptional effects. A transfer to SW induced transcription of aqp1, aqp8, and nkcc2 while appearing to completely halt transcription of cldn15b. We found that Prl reliably downregulated proteins associated with the SW phenotype, including several intestinal bicarbonate transporters (slc26a3a & slc4a4a) and ion-transporter nkcc2. GH exhibited widespread stimulatory effects on bicarbonate transporters (slc26a3a, slc26a3b, slc26a6), ion/water pores (cftr, aqp8) and, interestingly, FW-type tight junction protein cldn15-b. Cortisol, which aids in both hyper- and hypo- osmotic regulation, induced transcription of bicarbonate transporters (slc26a6, slc26a3b) and ion/water transporters (cftr, nkcc2, aqp8).

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Endocrinology Commons

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