Flamingoes (Phoenicopterus spp.) whose plumage displays elegant colors, inhabit warm regions close to the ocean throughout the world. The pink or reddish color of their plumage originates from carotenoids ingested from carotenoid-abundant food sources, since flamingoes are unable to synthesize these compounds de novo. In this study, viable red-colored archaeal strains classified as extremely halophilic archaea (i.e., haloarchaea) and belonging to the genera Halococcus and Halogeometricum were isolated from the plumage of flamingoes in captivity. Detailed analysis for haloarchaeal community structure in flamingo feathers based on metagenomic data identified several haloarchaeal genera and unclassified sequences of the class Halobacteria at the genus level. Carotenoid pigment analyses showed that a bacterioruberin precursor carotenoid in haloarchaea was identical to one of the pigments found in flamingo plumage. To the best of our knowledge, this is the first report of viable extremophilic archaea in avian plumage, thus contributing to our understanding of the ecology of haloarchaea. The potential influence of haloarchaea as an environmental factor determining avian plumage coloration should be investigated in further studies.

Hyperforin, a major active compound of St.?John?s wort extract, affects estrogenic activity. In this study, the compound evoked estrogen response element-dependent luciferase activity and cell proliferation in MCF-7 cells. Hyperforin-induced cell proliferation was significantly inhibited by the estrogen receptor antagonist ICI 182,780. These results suggested that hyperforin had estrogenic and cell proliferation activities, which were stimulated via the estrogen receptor. Compared to 17?-estradiol, hyperforin showed significantly lower estrogenic activity and cell proliferation. The mechanism underlying the estrogenic activity of hyperforin was unknown, therefore, in this study, for the first time, the expression and post-translational modification of proteins were determined and compared among control, 17?-estradiol-treated, and hyperforin-treated cells using proteomic techniques. A total of 453 proteins were identified, of which 282 proteins were significantly modulated in hyperforin-treated cells compared to 17?-estradiol-treated cells. Ingenuity pathway analysis also demonstrated that hyperforin treatment induced less cell proliferation than 17?-estradiol by downregulating estrogen receptor 1. Protein network analysis showed that cell proliferation was regulated mainly by cyclin D1 and extracellular signal-regulated kinases. In conclusion, although, hyperforin exhibited lower estrogenic activity than 17?-estradiol, the compound induced lower levels of cancer cell proliferation in vitro.