8 research outputs found
The Ecology of Stress: linking life-history traits with physiological control mechanisms in free-living guanacos
Background Providing the context for the evolution of life-history traits, habitat features constrain successful ecological and physiological strategies. In vertebrates, a key response to lifeâs challenges is the activation of the Stress (HPA) and Gonadal (HPG) axes. Much of the interest in stress ecology is motivated by the desire to understand the physiological mechanisms in which the environment affects fitness. As reported in the literature, several intrinsic and extrinsic factors affect variability in hormone levels. In both social and non-social animals, the frequency and type of interaction with conspecifics, as well as the status in social species, can affect HPA axis activity, resulting in changes in the reproductive success of animals. We predicted that a social environment can affect both guanaco axes by increasing the secretion of testosterone (T) and Glucocorticoid (GCs) in response to individual social interactions and the energetic demands of breeding. Assuming that prolonged elevated levels of GCs over time can be harmful to individuals, it is predicted that the HPA axis suppresses the HPG axis and causes T levels to decrease, as GCs increase. Methods All of the data for individuals were collected by non-invasive methods (fecal samples) to address hormonal activities. This is a novel approach in physiological ecology because feces are easily obtained through non-invasive sampling in animal populations. Results As expected, there was a marked adrenal (p-value = .3.4eâ12) and gonadal (p-value = 0.002656) response due to seasonal variation in Lama guanicoe. No significant differences were found in fecal GCs metabolites between males/females*season for the entire study period (p-value = 0.2839). Despite the seasonal activity variation in the hormonal profiles, our results show a positive correlation (p-value = 1.952eâ11, COR = 0.50) between the adrenal and gonadal system. The marked endocrine (r2Â =Â 0.806) and gonad (r2Â =Â 0.7231) response due to seasonal variation in male guanaco individuals highlights the individualâs energetic demands according to life-history strategies. This is a remarkable result because no inhibition was found between the axes as theory suggests. Finally, the dataset was used to build a reactive scope model for guanacos. Discussion Guanacos cope with the trade-off between sociability and reproductive benefits and costs, by regulating their GCs and T levels on a seasonal basis, suggesting an adaptive role of both axes to different habitat pressures. The results presented here highlight the functional role of stress and gonad axes on a critical phase of a male mammalâs lifeâthe mating periodâwhen all of the resources are at the disposal of the male and must be used to maximize the chances for reproductive success
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Expression of an active Gαs mutant in skeletal stem cells is sufficient and necessary for fibrous dysplasia initiation and maintenance.
Fibrous dysplasia (FD) is a disease caused by postzygotic activating mutations of GNAS (R201C and R201H) that encode the α-subunit of the Gs stimulatory protein. FD is characterized by the development of areas of abnormal fibroosseous tissue in the bones, resulting in skeletal deformities, fractures, and pain. Despite the well-defined genetic alterations underlying FD, whether GNAS activation is sufficient for FD initiation and the molecular and cellular consequences of GNAS mutations remains largely unresolved, and there are no currently available targeted therapeutic options for FD. Here, we have developed a conditional tetracycline (Tet)-inducible animal model expressing the GαsR201C in the skeletal stem cell (SSC) lineage (Tet-GαsR201C/Prrx1-Cre/LSL-rtTA-IRES-GFP mice), which develops typical FD bone lesions in both embryos and adult mice in less than 2 weeks following doxycycline (Dox) administration. Conditional GαsR201C expression promoted PKA activation and proliferation of SSCs along the osteogenic lineage but halted their differentiation to mature osteoblasts. Rather, as is seen clinically, areas of woven bone admixed with fibrous tissue were formed. GαsR201C caused the concomitant expression of receptor activator of nuclear factor kappa-B ligand (Rankl) that led to marked osteoclastogenesis and bone resorption. GαsR201C expression ablation by Dox withdrawal resulted in FD-like lesion regression, supporting the rationale for Gαs-targeted drugs to attempt FD cure. This model, which develops FD-like lesions that can form rapidly and revert on cessation of mutant Gαs expression, provides an opportunity to identify the molecular mechanism underlying FD initiation and progression and accelerate the development of new treatment options
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Expression of an active Gαs mutant in skeletal stem cells is sufficient and necessary for fibrous dysplasia initiation and maintenance.
Fibrous dysplasia (FD) is a disease caused by postzygotic activating mutations of GNAS (R201C and R201H) that encode the α-subunit of the Gs stimulatory protein. FD is characterized by the development of areas of abnormal fibroosseous tissue in the bones, resulting in skeletal deformities, fractures, and pain. Despite the well-defined genetic alterations underlying FD, whether GNAS activation is sufficient for FD initiation and the molecular and cellular consequences of GNAS mutations remains largely unresolved, and there are no currently available targeted therapeutic options for FD. Here, we have developed a conditional tetracycline (Tet)-inducible animal model expressing the GαsR201C in the skeletal stem cell (SSC) lineage (Tet-GαsR201C/Prrx1-Cre/LSL-rtTA-IRES-GFP mice), which develops typical FD bone lesions in both embryos and adult mice in less than 2 weeks following doxycycline (Dox) administration. Conditional GαsR201C expression promoted PKA activation and proliferation of SSCs along the osteogenic lineage but halted their differentiation to mature osteoblasts. Rather, as is seen clinically, areas of woven bone admixed with fibrous tissue were formed. GαsR201C caused the concomitant expression of receptor activator of nuclear factor kappa-B ligand (Rankl) that led to marked osteoclastogenesis and bone resorption. GαsR201C expression ablation by Dox withdrawal resulted in FD-like lesion regression, supporting the rationale for Gαs-targeted drugs to attempt FD cure. This model, which develops FD-like lesions that can form rapidly and revert on cessation of mutant Gαs expression, provides an opportunity to identify the molecular mechanism underlying FD initiation and progression and accelerate the development of new treatment options
Mapping out a future for ungulate migrations : Limited mapping of migrations hampers conservation
Mapping out a future for ungulate migrations
Migration of ungulates (hooved mammals) is a fundamental ecological process that promotes abundant herds, whose effects cascade up and down terrestrial food webs. Migratory ungulates provide the prey base that maintains large carnivore and scavenger populations and underpins terrestrial biodiversity (fig. S1). When ungulates move in large aggregations, their hooves, feces, and urine create conditions that facilitate distinct biotic communities. The migrations of ungulates have sustained humans for thousands of years, forming tight cultural links among Indigenous people and local communities. Yet ungulate migrations are disappearing at an alarming rate (1). Efforts by wildlife managers and conservationists are thwarted by a singular challenge: Most ungulate migrations have never been mapped in sufficient detail to guide effective conservation. Without a strategic and collaborative effort, many of the world's great migrations will continue to be truncated, severed, or lost in the coming decades. Fortunately, a combination of animal tracking datasets, historical records, and local and Indigenous knowledge can form the basis for a global atlas of migrations, designed to support conservation action and policy at local, national, and international levels