Understanding the influence of taste perception on food choice has captured the interest of academics, industry, and the general public, the latter as evidenced by the extent of popular media coverage and use of the term supertaster. Supertasters are highly sensitive to the bitter tastant propylthiouracil (PROP) and its chemical relative phenylthiocarbamide. The well-researched differences in taste sensitivity to these bitter chemicals are partially controlled by variation in the TAS2R38 gene; however, this variation alone does not explain the supertaster phenomenon. It has been suggested that density of papillae, which house taste buds, may explain supertasting. To address the unresolved role of papillae, we used crowdsourcing in the museum-based Genetics of Taste Lab. This community lab is uniquely situated to attract both a large population of human subjects and host a team of citizen scientists to research population-based questions about human genetics, taste, and health. Using this model, we find that PROP bitterness is not in any way predicted by papillae density. This result holds within the whole sample, when divided into major diplotypes, and when correcting for age, sex, and genotype. Furthermore, it holds when dividing participants into oft-used taster status groups. These data argue against the use of papillae density in predicting taste sensitivity and caution against imprecise use of the term supertaster. Furthermore, it supports a growing volume of evidence that sets the stage for hypergeusia, a reconceptualization of heightened oral sensitivity that is not based solely on PROP or papillae density. Finally, our model demonstrates how community-based research can serve as a unique venue for both study participation and citizen science that makes scientific research accessible and relevant to people’s everyday lives.
The genome of Trypanosoma cruzi contains tandem arrays of alternating genes encoding amastin and tuzin. Amastin is a surface glycoprotein abundantly expressed on the intracellular mammalian amastigote form of the protozoan parasite, and tuzin is a G-like protein. We demonstrated previously that the amastin-tuzin gene cluster is polycistronically transcribed to an equal extent in all parasite life cycle stages. The steady state level of amastin mRNA, however, is 68-fold more abundant in amastigotes than in epimastigotes. Here we show that the half-life of amastin mRNA is 7 times longer in amastigotes than in epimastigotes. Linker replacement experiments demonstrate that the middle onethird of the 630-nucleotide 3-untranslated region (UTR) is responsible for the amastin mRNA up-regulation. This positive effect is dependent on the distance of the 3-UTR segment from the stop codon and the polyadenylation site as well as on its orientation. A protein or protein complex more abundant in amastigotes than in epimastigotes binds to this minimally defined 3-UTR segment and may be involved in its regulatory function.Trypanosoma cruzi is the protozoan parasite that causes Chagas' disease, a debilitating illness that is a major cause of morbidity and mortality in many parts of Latin America. During its life cycle, T. cruzi passes through three developmental stages. In their insect vectors, the parasites multiply as extracellular epimastigotes in the midgut, migrate to the hindgut, and then differentiate into nondividing trypomastigotes. These infective organisms are excreted in the feces after a blood meal. When they contaminate the puncture site or mucous membranes of a mammalian host, they can invade a variety of cell types. Once inside host cells, the trypomastigotes differentiate into amastigotes, which multiply in the cytoplasm. After many cycles of proliferation, the amastigotes differentiate into trypomastigotes and enter the circulation when the host cell ruptures. These trypomastigotes perpetuate either the infection or the life cycle when they invade other host cells or are ingested by insect vectors, respectively.Since the intracellular amastigotes are at the core of the persistence of T. cruzi infection, we previously sought to identify genes that are preferentially expressed by amastigotes in order to develop a better understanding of the molecular biology of this parasite form. We identified two novel genes, encoding the proteins amastin and tuzin, which occur in alternating tandemly arranged pairs (1, 2). Amastin is an abundant glycoprotein on the surface of amastigotes. Less is understood about tuzin's function or location, but it possesses sequence similarity to a heterotrimeric G-protein. Most tandem genes in T. cruzi and other trypanosomatids, such as Leishmania species and African trypanosomes, do not have recognizable upstream promoters and are transcribed into polycistronic precursor RNAs (3-6). The 5Ј ends of the resulting mature monocistronic mRNAs are defined by the trans-splicing of a 39-nucleotide ...
Searching for an alien haven in the heavens T he first few articles in this issue of PNAS constitute the beginning of a two-part Special Feature dedicated to the study of astrobiology. Astrobiology is not an autonomous or self-sustaining discipline. Rather, it is a hybrid subject emerging at the crossroads of astronomy, geology, paleontology, physics, and biology. What at first pass may seem like an amalgamation of disparate fields, upon further review, is a clear and increasingly defined discipline. The roots of astrobiology are found in the 10 distinct goals set by the National Aeronautics and Space Administration (NASA) Astrobiology Institute. These objectives can be summarized into three branches: How does life begin and develop? Does life exist elsewhere in the universe? What is life's future on Earth and beyond? Some preliminary answers to these questions were addressed at the first large scientific conference dedicated entirely to astrobiology, held April 25-26, 2000 at the Ames Research Center at Moffett Field, CA. A few months later an international ''Frontiers of Life'' conference was held in France's Loire Valley. Sessions at those meetings ranged from ''Water-the Sine Qua Non of Life,'' which covered the water reservoirs on Jupiter's moon Europa; ''Environment,'' which covered snowball earth, life in extreme environments, the evolution of biochemisty, and interstellar quinones; ''Life Detection Methods and Biosignatures''; and ''Detection Methods for Extrasolar Planets.'' Many of these topics are expounded in this issue of PNAS, and it is clear that the two premier conferences marked the official beginning of a wave of discourse that undoubtedly has as many opinions as voices. Early astrobiology had some high-profile skeptics like French biologist Jacques Monod who in 1971 categorically dismissed the field. He reasoned that the ''unfeeling immensity of the Universe'' left one to conclude that biological organization emerged alone and by chance in a phenomenal chemical fluke (1). In 1964 American
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