Geology topics

Jason P. Breves

Publications and source records attributed to Jason P. Breves.

7 recordsLinked to original sources

USGS2025

A Cftr-independent, Ano1-rich seawater-adaptive ionocyte in sea lamprey gills

All ionoregulating marine fishes examined to date utilize seawater-type ionocytes expressing the apical Cl- channel, cystic fibrosis transmembrane conductance regulator (Cftr) to secrete Cl − . We performed transcriptomic, molecular, and functional studies to identify Cl − transporters in the seawater-type ionocytes of sea lamprey ( Petromyzon marinus ). Gill cftr expression was minimal or undetectable in larvae and post-metamorphic juveniles. We identified other Cl − transporters highly expressed in the gills and/or upregulated following metamorphosis and further investigated two candidates that stood out in our analysis, a Ca 2+ -activated Cl − channel, anoctamin 1 ( ano1 ), and the Clc chloride channel family member 2 ( clcn2 ). Of these, ano1 was expressed 10-100 times more than clcn2 in the gills; moreover, ano1 was upregulated during seawater acclimation, while clcn2 was not. Using an antibody raised against sea lamprey Ano1, we did not detect Ano1 in the gills of larvae, found elevated levels in juveniles and observed a 4-fold increase in juveniles after seawater acclimation. Ano1 was localized to seawater-type branchial ionocytes but, surprisingly, was localized to the basolateral membrane. In vivo pharmacological inhibition experiments demonstrated that a DIDS-sensitive mechanism was critical to the maintenance of osmoregulatory homeostasis in seawater- but not freshwater-acclimated sea lamprey. Taken together, our results provide evidence of a Cftr-independent mechanism for branchial Cl − secretion in sea lamprey that leverages Ano1-expressing ionocytes. Once further characterized, the Cftr-independent, Ano1-rich ionocytes of sea lamprey could reveal novel strategies for branchial Cl − secretion, whether by Ano1 or some other Cl − transporter, not previously known in ionoregulating marine organisms.

Journal of Experimental Biology↗

USGS2022

Na+/HCO3- cotransporter 1 (nbce1) isoform gene expression during smoltification and seawater acclimation of Atlantic salmon

The life history of Atlantic salmon ( Salmo salar ) includes an initial freshwater phase (parr) that precedes a springtime migration to marine environments as smolts. The development of osmoregulatory systems that will ultimately support the survival of juveniles upon entry into marine habitats is a key aspect of smoltification. While the acquisition of seawater tolerance in all euryhaline species demands the concerted activity of specific ion pumps, transporters, and channels, the contributions of Na + /HCO 3 − cotransporter 1 (Nbce1) to salinity acclimation remain unresolved. Here, we investigated the branchial and intestinal expression of three Na + /HCO 3 − cotransporter 1 isoforms, denoted nbce1.1 , -1.2a , and -1.2b . Given the proposed role of Nbce1 in supporting the absorption of environmental Na + by ionocytes, we first hypothesized that expression of a branchial nbce1 transcript ( nbce1.2a ) would be attenuated in salmon undergoing smoltification and following seawater exposure. In two separate years, we observed spring increases in branchial Na + /K + -ATPase activity, Na + /K + /2Cl − cotransporter 1 , and cystic fibrosis transmembrane regulator 1 expression characteristic of smoltification, whereas there were no attendant changes in nbce1.2a expression. Nonetheless, branchial nbce1.2a levels were reduced in parr and smolts within 2 days of seawater exposure. In the intestine, gene transcript abundance for nbce1.1 increased from spring to summer in the anterior intestine, but not in the posterior intestine or pyloric caeca, and nbce1.1 and -1.2b expression in the intestine showed season-dependent transcriptional regulation by seawater exposure. Collectively, our data indicate that tissue-specific modulation of all three nbce1 isoforms underlies adaptive responses to seawater.

Journal of Comparative Physiology B: Biochemical, ↗

USGS2020

Cortisol regulates insulin-like growth-factor binding protein (igfbp) gene expression in Atlantic salmon parr

The growth hormone (Gh)/insulin-like growth-factor (Igf)/Igf binding protein (Igfbp) system regulates growth and osmoregulation in salmonid fishes, but how this system interacts with other endocrine systems is largely unknown. Given the well-documented consequences of mounting a glucocorticoid stress response on growth, we hypothesized that cortisol inhibits anabolic processes by modulating the expression of hepatic igfbp mRNAs. Atlantic salmon ( Salmo salar ) parr were implanted intraperitoneally with cortisol implants (0, 10, and 40 μg g −1 body weight) and sampled after 3 or 14 days. Cortisol elicited a dose-dependent reduction in specific growth rate (SGR) after 14 days. While plasma Gh and Igf1 levels were unchanged, hepatic igf1 mRNA was diminished and hepatic igfbp1b1 and -1b2 were stimulated by the high cortisol dose. Plasma Igf1 was positively correlated with SGR at 14 days. Hepatic gh receptor ( ghr ), igfbp1a , -2a , -2b1 , and -2b2 levels were not impacted by cortisol. Muscle igf2 , but not igf1 or ghr , levels were stimulated at 3 days by the high cortisol dose. As both cortisol and the Gh/Igf axis promote seawater (SW) tolerance, and particular igfbps respond to SW exposure, we also assessed whether cortisol coordinates the expression of branchial igfbps and genes associated with ion transport. Cortisol stimulated branchial igfbp5b2 levels in parallel with Na + /K + -ATPase (NKA) activity and nka-α1b , Na + /K + / 2Cl - -cotransporter 1 ( nkcc1 ), and cystic fibrosis transmembrane regulator 1 ( cftr1 ) mRNA levels. The collective results indicate that cortisol modulates the growth of juvenile salmon via the regulation of hepatic igfbp1s whereas no clear links between cortisol and branchial igfbps previously shown to be salinity-responsive could be established.

Molecular and Cellular Endocrinology↗

USGS2019

In vivo effects of 17α-ethinylestradiol, 17B-estradiol and 4-nonylphenol on insulin-like growth-factor binding proteins (igfbps) in Atlantic salmon

Feminizing endocrine disrupting compounds (EDCs) affect the growth and development of teleost fishes. The major regulator of growth performance, the growth hormone (Gh)/insulin-like growth-factor (Igf) system, is sensitive to estrogenic compounds and mediates certain physiological and potentially behavioral consequences of EDC exposure. Igf binding proteins (Igfbps) are key modulators of Igf activity, but their alteration by EDCs has not been examined. We investigated two life-stages (fry and smolts) of Atlantic salmon ( Salmo salar ), and characterized how the Gh/Igf/Igfbp system responded to waterborne 17α-ethinylestradiol (EE 2 ), 17β-estradiol (E 2 ) and 4-nonylphenol (NP). Fry exposed to EE 2 and NP for 21 days had increased hepatic vitellogenin ( vtg ) mRNA levels while hepatic estrogen receptor α ( erα ), gh receptor (ghr) , igf1 and igf2 mRNA levels were decreased. NP-exposed fry had reduced body mass and total length compared to controls. EE 2 and NP reduced hepatic igfbp1b1 , -2a , -2b1 , -4 , -5b2 and -6b1 , and stimulated igfbp5a . In smolts, hepatic vtg mRNA levels were induced following 4-day exposures to all three EDCs, while erα only responded to EE 2 and E 2 . EDC exposures did not affect body mass or fork length; however, EE 2 diminished plasma Gh and Igf1 levels in parallel with reductions in hepatic ghr and igf1 . In smolts, EE 2 and E 2 diminished hepatic igfbp1b1 , -4 and -6b1 , and stimulated igfbp5a . There were no signs of compromised ionoregulation in smolts, as indicated by unchanged branchial ion pump/transporter mRNA levels. We conclude that hepatic igfbps respond (directly and/or indirectly) to environmental estrogens during two key life-stages of Atlantic salmon, and thus may modulate the growth and development of exposed individuals.

Aquatic Toxicology↗

USGS2016

Hepatic insulin-like growth-factor binding protein (igfbp) responses tofood restriction in Atlantic salmon smolts

The growth hormone (Gh)/insulin-like growth-factor (Igf) system plays a central role in the regulation of growth in fishes. However, the roles of Igf binding proteins (Igfbps) in coordinating responses to food availability are unresolved, especially in anadromous fishes preparing for seaward migration. We assayed plasma Gh, Igf1, thyroid hormones and cortisol along with igfbp mRNA levels in fasted and fed Atlantic salmon ( Salmo salar ). Fish were fasted for 3 or 10 days near the peak of smoltification (late April to early May). Fasting reduced plasma glucose by 3 days and condition factor by 10 days. Plasma Gh, cortisol, and thyroxine (T 4 ) were not altered in response to fasting, whereas Igf1 and 3,5,3′-triiodo- l -thyronine (T 3 ) were slightly higher and lower than controls, respectively. Hepatic igfbp1b1 , - 1b2 , - 2a , - 2b1 and - 2b2 mRNA levels were not responsive to fasting, but there were marked increases in igfbp1a1 following 3 and 10 days of fasting. Fasting did not alter hepatic igf1 or igf2 ; however, muscle igf1 was diminished by 10 days of fasting. There were no signs that fasting compromised branchial ionoregulatory functions, as indicated by unchanged Na + /K + -ATPase activity and ion pump/transporter mRNA levels. We conclude that dynamic hepatic igfbp1a1 and muscle igf1 expression participate in the modulation of Gh/Igf signaling in smolts undergoing catabolism.

General and Comparative Endocrinology↗

USGS2014

Prolactin and teleost ionocytes: new insights into cellular and molecular targets of prolactin in vertebrate epithelia

The peptide hormone prolactin is a functionally versatile hormone produced by the vertebrate pituitary . Comparative studies over the last six decades have revealed that a conserved function for prolactin across vertebrates is the regulation of ion and water transport in a variety of tissues including those responsible for whole-organism ion homeostasis. In teleost fishes, prolactin was identified as the “freshwater-adapting hormone”, promoting ion-conserving and water-secreting processes by acting on the gill, kidney, gut and urinary bladder. In mammals, prolactin is known to regulate renal, intestinal, mammary and amniotic epithelia, with dysfunction linked to hypogonadism, infertility, and metabolic disorders. Until recently, our understanding of the cellular mechanisms of prolactin action in fishes has been hampered by a paucity of molecular tools to define and study ionocytes, specialized cells that control active ion transport across branchial and epidermal epithelia. Here we review work in teleost models indicating that prolactin regulates ion balance through action on ion transporters, tight-junction proteins, and water channels in ionocytes, and discuss recent advances in our understanding of ionocyte function in the genetically and embryonically accessible zebrafish ( Danio rerio ). Given the high degree of evolutionary conservation in endocrine and osmoregulatory systems, these studies in teleost models are contributing novel mechanistic insight into how prolactin participates in the development, function, and dysfunction of osmoregulatory systems across the vertebrate lineage.

General and Comparative Endocrinology↗

USGS2013

Prolactin regulates transcription of the ion uptake Na+/Cl- cotransporter (ncc) gene in zebrafish gill

Prolactin (PRL) is a well-known regulator of ion and water transport within osmoregulatory tissues across vertebrate species, yet how PRL acts on some of its target tissues remains poorly understood. Using zebrafish as a model, we show that ionocytes in the gill directly respond to systemic PRL to regulate mechanisms of ion uptake. Ion-poor conditions led to increases in the expression of PRL receptor (prlra), Na+/Cl− cotransporter (ncc; slc12a10.2), Na+/H+ exchanger (nhe3b; slc9a3.2), and epithelial Ca2+ channel (ecac; trpv6) transcripts within the gill. Intraperitoneal injection of ovine PRL (oPRL) increased ncc and prlra transcripts, but did not affect nhe3b or ecac. Consistent with direct PRL action in the gill, addition of oPRL to cultured gill filaments stimulated ncc in a concentration-dependent manner, an effect blocked by a pure human PRL receptor antagonist (Δ1-9-G129R-hPRL). These results suggest that PRL signaling through PRL receptors in the gill regulates the expression of ncc, thereby linking this pituitary hormone with an effector of Cl− uptake in zebrafish for the first time.

Molecular and Cellular Endocrinology↗