Upper thermal limits of growth in brook trout and their relationship to stress physiology.

Despite the threat of climate change, the physiological mechanisms responsible for reduced performance at high temperatures remain unclear for most species. Elevated but sublethal temperatures may act via endocrine and cellular stress responses to limit performance in important life-history traits such as growth. Here, brook trout (Salvelinus fontinalis) subjected to chronically elevated or daily oscillating temperatures were monitored for growth and physiological stress responses. Growth rate decreased at temperatures above 16°C and was negative at 24°C, with an estimated upper limit for positive growth of 23.4°C. Plasma cortisol increased with temperature and was 12- and 18-fold higher at 22 and 24°C, respectively, than at 16°C, whereas plasma glucose was unaffected by temperature. Abundance of heat shock protein 70 (HSP70) in the gill increased with temperature and was 11- and 56-fold higher at 22°C and 24°C, respectively, than at 16°C. There was no relationship between temperature and plasma Cl-, but there was a 53% and 80% decrease in gill Na+/K+-ATPase activity and abundance at 24°C in comparison with 16°C. Daily temperature oscillations of 4°C or 8°C (19-23°C or 17-25°C) were compared with 21°C controls. Growth rate decreased with temperature and was 43% and 35% lower by length and mass, respectively, in the 8°C daily oscillation treatment than in the controls. There was no effect of temperature oscillation on plasma cortisol or glucose levels. In contrast, gill HSP70 abundance increased with increasing daily oscillation and was 40- and 700-fold greater at 4°C and 8°C daily oscillation, respectively, than in the constant temperature controls. In individuals exposed to 17-25°C diel oscillations for 4 days and then allowed to recover at 21°C, gill HSP70 abundance was still elevated after 4 days recovery, but not after 10 days. Our results demonstrate that elevated temperatures induce cellular and endocrine stress responses and provide a possible mechanism by which growth is limited at elevated temperatures. Temperature limitations on growth may play a role in driving brook trout distributions in the wild.

Nuclear receptor coactivators are coexpressed with steroid receptors and regulated by estradiol in mouse brain.

BACKGROUND/AIMS: The steroid hormones, including estradiol (E) and progesterone, act in the brain to regulate female reproductive behavior and physiology. These hormones mediate many of their biological effects by binding to their respective intracellular receptors. The receptors for estrogens (ER) and progestins (PR) interact with nuclear receptor coactivators to initiate transcription of steroid-responsive genes. Work from our laboratory and others reveals that nuclear receptor coactivators, including steroid receptor coactivator-1 (SRC-1) and SRC-2, function in brain to modulate ER-mediated induction of the PR gene and hormone-dependent behaviors. In order for steroid receptors and coactivators to function together, both must be expressed in the same cells. METHODS: Triple-label immunofluorescence was used to determine if E-induced PR cells also express SRC-1 or SRC-2 in reproductively relevant brain regions of the female mouse. RESULTS: The majority of E-induced PR cells in the medial preoptic area (61%), ventromedial nucleus of the hypothalamus (63%) and arcuate nucleus (76%) coexpressed both SRC-1 and SRC-2. A smaller proportion of PR cells expressed either SRC-1 or SRC-2, while a few PR cells expressed neither coactivator. In addition, compared to control animals, 17ß-estradiol benzoate (EB) treatment increased SRC-1 levels in the arcuate nucleus, but not the medial preoptic area or the ventromedial nucleus of the hypothalamus. EB did not alter SRC-2 expression in any of the three brain regions analyzed. CONCLUSIONS: Taken together, the present findings identify a population of cells in which steroid receptors and nuclear receptor coactivators may interact to modulate steroid sensitivity in brain and regulate hormone-dependent behaviors in female mice. Given that cell culture studies reveal that SRC-1 and SRC-2 can mediate distinct steroid-signaling pathways, the present findings suggest that steroids can produce a variety of complex responses in these specialized brain cells.

Steroid receptor coactivator-1 from brain physically interacts differentially with steroid receptor subtypes.

In vitro studies reveal that nuclear receptor coactivators enhance the transcriptional activity of steroid receptors, including estrogen (ER) and progestin receptors (PR), through ligand-dependent interactions. Whereas work from our laboratory and others shows that steroid receptor coactivator-1 (SRC-1) is essential for efficient ER and PR action in brain, very little is known about receptor-coactivator interactions in brain. In the present studies, pull-down assays were used to test the hypotheses that SRC-1 from hypothalamic and hippocampal tissue physically associate with recombinant PR or ER in a ligand-dependent manner. SRC-1, from hypothalamus or hippocampus, interacted with PR-A and PR-B in the presence of an agonist, but not in the absence of ligand or in the presence of a selective PR modulator, RU486. Interestingly, SRC-1 from brain associated more with PR-B, the stronger transcriptional activator, than with PR-A. In addition, SRC-1 from brain, which was confirmed by mass spectrometry, interacted with ERalpha and ERbeta in the presence of agonist but not when unliganded or in the presence of the selective ER modulator, tamoxifen. Furthermore, SRC-1 from hypothalamus, but not hippocampus, interacted more with ERalpha than ERbeta, suggesting distinct expression patterns of other cofactors in these brain regions. These findings suggest that interactions of SRC-1 from brain with PR and ER are dependent on ligand, receptor subtype, and brain region to manifest the pleiotropic functional consequences that underlie steroid-regulated behaviors. The present findings reveal distinct contrasts with previous cell culture studies and emphasize the importance of studying receptor-coactivator interactions using biologically relevant tissue.

Thermal onset of cellular and endocrine stress responses correspond to ecological limits in brook trout, an iconic cold-water fish.

Climate change is predicted to change the distribution and abundance of species, yet underlying physiological mechanisms are complex and methods for detecting populations at risk from rising temperature are poorly developed. There is increasing interest in using physiological mediators of the stress response as indicators of individual and population-level response to environmental stressors. Here, we use laboratory experiments to show that the temperature thresholds in brook trout (Salvelinus fontinalis) for increased gill heat shock protein-70 (20.7°C) and plasma glucose (21.2°C) are similar to their proposed thermal ecological limit of 21.0°C. Field assays demonstrated increased plasma glucose, cortisol and heat shock protein-70 concentrations at field sites where mean daily temperature exceeded 21.0°C. Furthermore, population densities of brook trout were lowest at field sites where temperatures were warm enough to induce a stress response, and a co-occurring species with a higher thermal tolerance showed no evidence of physiological stress at a warm site. The congruence of stress responses and proposed thermal limits supports the use of these thresholds in models of changes in trout distribution under climate change scenarios and suggests that the induction of the stress response by elevated temperature may play a key role in driving the distribution of species.