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Coral bleaching is a significant contributor to the worldwide degradation of coral reefs and is indicative of the termination of symbiosis between the coral host and its symbiotic algae (dinoflagellate; Symbiodinium sp. complex), usually by expulsion or xenophagy (symbiophagy) of its dinoflagellates. Herein, we provide evidence that during the earliest stages of environmentally induced bleaching, heat stress and light stress generate distinctly different pathomorphological changes in the chloroplasts, while a combined heat- and light-stress exposure induces both pathomorphologies; suggesting that these stressors act on the dinoflagellate by different mechanisms. Within the first 48 hours of a heat stress (32°C) under low-light conditions, heat stress induced decomposition of thylakoid structures before observation of extensive oxidative damage; thus it is the disorganization of the thylakoids that creates the conditions allowing photo-oxidative-stress. Conversely, during the first 48 hours of a light stress (2007 µmoles m−2 s−1 PAR) at 25°C, condensation or fusion of multiple thylakoid lamellae occurred coincidently with levels of oxidative damage products, implying that photo-oxidative stress causes the structural membrane damage within the chloroplasts. Exposure to combined heat- and light-stresses induced both pathomorphologies, confirming that these stressors acted on the dinoflagellate via different mechanisms. Within 72 hours of exposure to heat and/or light stresses, homeostatic processes (e.g., heat-shock protein and anti-oxidant enzyme response) were evident in the remaining intact dinoflagellates, regardless of the initiating stressor. Understanding the sequence of events during bleaching when triggered by different environmental stressors is important for predicting both severity and consequences of coral bleaching.

We examined whether estrogen receptor (ER)alpha is required for estrogen to stimulate cancellous bone formation in long bones of male mice. 17 beta-Estradiol (E(2)) was administered to ER alpha(-/-) male mice or wild-type (WT) littermate controls at 40, 400, or 4000 microg/kg by daily sc injection for 28 d and histomorphometric analysis performed at the distal femoral metaphysis. In WT mice, treatment with E(2) (40 microg/kg per d) increased the proportion of cancellous bone surfaces undergoing mineralization and stimulated mineral apposition rate. In addition, higher doses of E(2) induced the formation of new cancellous bone formation surfaces in WT mice. In contrast, E(2) had little effect on any of these parameters in ER alpha(-/-) mice. Immunohistochemistry was subsequently performed using an ER alpha-specific C-terminal polyclonal antibody. In WT mice, ER alpha was expressed both by cancellous osteoblasts and a significant proportion of mononuclear bone marrow cells. Immunoreactivity was also observed in cancellous osteoblasts of ER alpha(-/-) mice, resulting from expression of the activation function-1-deficient 46-kDa ER alpha isoform previously reported to be expressed in normal osteoblasts and bones of ER alpha(-/-) mice. Taken together, our results suggest that estrogen stimulates bone formation in mouse long bones via a mechanism that requires the presence of full-length ER alpha possessing activation function-1.

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We recently found that estrogen receptor (ER) antagonists prevent highdose estrogen from inducing the formation of new cancellous bone within the medullary cavity of mouse long bones. In the present investigation, we studied the role of specific ER subtypes in this response by examining whether this is impaired in female ER␤ Ϫ/Ϫ mice previously generated by targeted gene deletion. Vehicle or 17␤-estradiol (E 2) (range 4-4,000 g ⅐ kg Ϫ1 ⅐ day Ϫ1 ) was administered to intact female ER␤ Ϫ/Ϫ mice and wild-type littermates by subcutaneous injection for 28 days. The osteogenic response was subsequently assessed by histomorphometry performed on longitudinal and cross sections of the tibia. E 2 was found to cause an equivalent increase in cancellous bone formation in ER␤ Ϫ/Ϫ mice and littermate controls, as assessed at the proximal and distal regions of the proximal tibial metaphysis. E 2 also resulted in a similar increase in endosteal mineral apposition rate in these two genotypes, as assessed at the tibial diaphysis. In contrast, cortical area in ER␤ Ϫ/Ϫ mice was found to be greater than that in wild types irrespective of E 2 treatment, as was tibial bone mineral density as measured by dual-energy X-ray absorptiometry, consistent with previous reports of increased cortical bone mass in these animals. We conclude that, although ER␤ acts as a negative modulator of cortical modeling, this isoform does not appear to contribute to high-dose estrogen's ability to induce new cancellous bone formation in mouse long bones.osteoblasts; estrogen receptor; histomorphometry ESTROGEN EXERTS an important protective effect on the skeleton, as illustrated by the significant bone loss associated with estrogen deficiency (17), which is prevented by hormone replacement (8,24). This ability of estrogen to prevent bone loss is thought to reflect two distinct actions. First, numerous clinical and animal studies indicate that estrogen acts to suppress osteoclastic bone resorption, leading to a decrease in bone turnover (7,23,32). In addition, estrogen has been reported to stimulate osteoblast function when administered at a relatively high dose, as assessed in studies of postmenopausal women receiving estradiol implants (9, 26) and in rodent models (2, 6). Although higher doses of estrogen are associated with extraskeletal effects that may limit their use in postmenopausal women, improved understanding of the molecular basis for estrogen's actions on bone may provide the basis for developing novel therapeutic agents capable of targeting these.