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Julie K. De Zutter Kara B. Levine Di Deng Anthony Carruthers 《The Journal of biological chemistry》2013,288(28):20734-20744
The human blood-brain barrier glucose transport protein (GLUT1) forms homodimers and homotetramers in detergent micelles and in cell membranes, where the GLUT1 oligomeric state determines GLUT1 transport behavior. GLUT1 and the neuronal glucose transporter GLUT3 do not form heterocomplexes in human embryonic kidney 293 (HEK293) cells as judged by co-immunoprecipitation assays. Using homology-scanning mutagenesis in which GLUT1 domains are substituted with equivalent GLUT3 domains and vice versa, we show that GLUT1 transmembrane helix 9 (TM9) is necessary for optimal association of GLUT1-GLUT3 chimeras with parental GLUT1 in HEK cells. GLUT1 TMs 2, 5, 8, and 11 also contribute to a less abundant heterocomplex. Cell surface GLUT1 and GLUT3 containing GLUT1 TM9 are 4-fold more catalytically active than GLUT3 and GLUT1 containing GLUT3 TM9. GLUT1 and GLUT3 display allosteric transport behavior. Size exclusion chromatography of detergent solubilized, purified GLUT1 resolves GLUT1/lipid/detergent micelles as 6- and 10-nm Stokes radius particles, which correspond to GLUT1 dimers and tetramers, respectively. Studies with GLUTs expressed in and solubilized from HEK cells show that HEK cell GLUT1 resolves as 6- and 10-nm Stokes radius particles, whereas GLUT3 resolves as a 6-nm particle. Substitution of GLUT3 TM9 with GLUT1 TM9 causes chimeric GLUT3 to resolve as 6- and 10-nm Stokes radius particles. Substitution of GLUT1 TM9 with GLUT3 TM9 causes chimeric GLUT1 to resolve as a mixture of 6- and 4-nm particles. We discuss these findings in the context of determinants of GLUT oligomeric structure and transport function. 相似文献
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Mélody Porlier Marc Bélisle Dany Garant 《Philosophical transactions of the Royal Society of London. Series B, Biological sciences》2009,364(1523):1543-1554
Improving our knowledge of the links between ecology and evolution is especially critical in the actual context of global rapid environmental changes. A critical step in that direction is to quantify how variation in ecological factors linked to habitat modifications might shape observed levels of genetic variability in wild populations. Still, little is known on the factors affecting levels and distribution of genetic diversity at the individual level, despite its vital underlying role in evolutionary processes. In this study, we assessed the effects of habitat quality on population structure and individual genetic diversity of tree swallows (Tachycineta bicolor) breeding along a gradient of agricultural intensification in southern Québec, Canada. Using a landscape genetics approach, we found that individual genetic diversity was greater in poorer quality habitats. This counter-intuitive result was partly explained by the settlement patterns of tree swallows across the landscape. Individuals of higher genetic diversity arrived earlier on their breeding grounds and settled in the first available habitats, which correspond to intensive cultures. Our results highlight the importance of investigating the effects of environmental variability on individual genetic diversity, and of integrating information on landscape structure when conducting such studies. 相似文献
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Charles L. Nunn Peter H. Thrall Kelly Stewart Alexander H. Harcourt 《Evolutionary ecology》2008,22(4):519-543
Emerging infectious diseases threaten a wide diversity of animals, and important questions remain concerning disease emergence
in socially structured populations. We developed a spatially explicit simulation model to investigate whether—and under what
conditions—disease-related mortality can impact rates of pathogen spread in populations of polygynous groups. Specifically,
we investigated whether pathogen-mediated dispersal (PMD) can occur when females disperse after the resident male dies from
disease, thus carrying infections to new groups. We also examined the effects of incubation period and virulence, host mortality
and rates of background dispersal, and we used the model to investigate the spread of the virus responsible for Ebola hemorrhagic
fever, which currently is devastating African ape populations. Output was analyzed using regression trees, which enable exploration
of hierarchical and non-linear relationships. Analyses revealed that the incidence of disease in single-male (polygynous)
groups was significantly greater for those groups containing an average of more than six females, while the total number of
infected hosts in the population was most sensitive to the number of females per group. Thus, as expected, PMD occurs in polygynous
groups and its effects increase as harem size (the number of females) increases. Simulation output further indicated that
population-level effects of Ebola are likely to differ among multi-male–multi-female chimpanzees and polygynous gorillas,
with larger overall numbers of chimpanzees infected, but more gorilla groups becoming infected due to increased dispersal
when the resident male dies. Collectively, our results highlight the importance of social system on the spread of disease
in wild mammals. 相似文献