Satellite tracking reveals sex-specific migration distance in green turtles (Chelonia mydas).

Satellite tracking is a key tool for studying sea turtles in the wild. Most tracking has been performed on adult females however, leaving knowledge gaps regarding other population segments, such as adult males. By satellite tracking 12 male green turtles (Chelonia mydas) at a breeding site in West Africa, we describe their movements from the breeding to the foraging grounds and compare migrations with those of 13 females tracked in the same season. During the mating period, some males remained near the focal nesting site, while others performed exploratory movements, apparently to visit other nearby rookeries. Males migrated on average shorter distances to foraging grounds (377 km, range 50-1081, n = 9) compared to females (1038 km, range 957-1850, n = 11]). Importantly, male foraging areas overlapped with previously described areas for females, suggesting sex-specific migration distances are not derived from differences in habitat selection. Strong support for differential migration by sex in sea turtles has hitherto been found in just one other species, but indications are that it may be a general feature in this group. These findings have important implications for our understanding of the interplay between reproductive roles and movement ecology of these emblematic animals.

ß-Catenin activation and illicit receptor expression in adrenocortical cells.

Adrenal cortisol-producing tumors can express illicit membrane receptors such as luteinizing hormone (LH), glucose-dependent insulinotropic peptide (GIP) or type 4 and 7 serotonin (5-HT4/7) receptors. Abnormal expression of the LH receptor (LH-R) has been ascribed to the activation of the Wnt/ß-catenin signaling pathway in adrenocortical cells. In the present study, we have investigated whether ß-catenin activation may also trigger the illegitimate expression of GIP and 5-HT receptors. Three models of ß-catenin activation in adrenocortical cells were used: an APC-mutated adrenocortical tumor, human-transfected adrenocortical cells and genetically modified mouse adrenal glands. The methods employed include quantitative reverse transcription PCR, immunohistochemistry and measurement of cortisol secretion by cultured tumor cells. Abnormal expression of the GIP, 5-HT7and LH receptors was observed in the APC-mutated adrenocortical tumor tissue. In addition, GIP, 5-HT and human chorionic gonadotropin stimulated cortisol production from tumor cells in primary culture. Conversely, only the LHCGR was upregulated in human and mouse adrenocortical cells harboring the activation of ß-catenin. Moreover, LH-R immunoreactivity was detected in clusters of zona fasciculata cells in the ß-catenin-activated mouse model. Our data indicate that activation of the ß-catenin signaling pathway can promote the illicit expression of functional LH-Rs in adrenal zona fasciculata cells but does not favor the abnormal expression of GIP and 5-HT receptors.

Decadal changes in blood δ13C values, at-sea distribution, and weaning mass of southern elephant seals from Kerguelen Islands.

Changes in the foraging environment and at-sea distribution of southern elephant seals from Kerguelen Islands were investigated over a decade (2004-2018) using tracking, weaning mass, and blood δ13C values. Females showed either a sub-Antarctic or an Antarctic foraging strategy, and no significant shift in their at-sea distribution was detected between 2004 and 2017. The proportion of females foraging in sub-Antarctic versus Antarctic habitats did not change over the 2006-2018 period. Pup weaning mass varied according to the foraging habitat of their mothers. The weaning mass of sub-Antarctic foraging mothers' pups decreased by 11.7 kg over the study period, but they were on average 5.8 kg heavier than pups from Antarctic foraging mothers. Pup blood δ13C values decreased by 1.1‰ over the study period regardless of their sex and the presumed foraging habitat of their mothers. Together, these results suggest an ecological change is occurring within the Indian sector of the Southern Ocean with possible consequences on the foraging performance of southern elephant seals. We hypothesize that this shift in δ13C is related to a change in primary production and/or in the composition of phytoplankton communities, but this requires further multidisciplinary investigations.

Illicit Upregulation of Serotonin Signaling Pathway in Adrenals of Patients With High Plasma or Intra-Adrenal ACTH Levels.

CONTEXT: In the human adrenal, serotonin (5-HT), released by mast cells stimulates corticosteroid secretion through activation of type 4 serotonin receptors (5-HT4R). In primary pigmented nodular adrenocortical disease cells, activation of the cAMP/protein kinase A (PKA) pathway by PRKAR1A mutations triggers upregulation of the 5-HT synthesizing enzyme tryptophan hydroxylase (TPH) and the 5-HT4, 5-HT6, and 5-HT7 receptors. Because ACTH stimulates cortisol secretion through activation of PKA, adrenocortical tissues exposed to sustained stimulation by ACTH may harbor increased expression of TPH and 5-HT4/6/7 receptors. OBJECTIVE: To investigate the effects of long-term ACTH stimulation on the serotonergic pathway in adrenals of patients with high plasma or intra-adrenal ACTH levels. METHODS: Adrenal tissues were obtained from patients with Cushing disease, ectopic secretion of ACTH [paraneoplastic Cushing syndrome; (paraCS)], 21-hydroxylase deficiency (21-OHD), primary bilateral macronodular adrenal hyperplasia with intra-adrenal ACTH presence, or cortisol-producing adenomas. TPH and 5-HT4/6/7 receptor expression was investigated using RT-PCR and immunochemistry in comparison with normal adrenals. Primary cultured adrenocortical cells originating from a patient with paraCS were incubated with 5-HT and 5-HTR agonists/antagonists. RESULTS: TPH and/or 5-HT4/6/7 receptors were overexpressed in the different types of tissues. In paraCS cultured cells, the cortisol response to 5-HT was exaggerated compared with normal adrenal cells and the stimulatory action of 5-HT was reduced by 5-HT4R antagonist. CONCLUSION: Our results indicate that prolonged activation of the cAMP/PKA pathway by ACTH induces an aberrant serotonergic stimulatory loop in the adrenal cortex that likely participates in the pathogenesis of corticosteroid hypersecretion.