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91.
R. Abbott D. Albach S. Ansell J. W. Arntzen S. J. E. Baird N. Bierne J. Boughman A. Brelsford C. A. Buerkle R. Buggs R. K. Butlin U. Dieckmann F. Eroukhmanoff A. Grill S. H. Cahan J. S. Hermansen G. Hewitt A. G. Hudson C. Jiggins J. Jones B. Keller T. Marczewski J. Mallet P. Martinez‐Rodriguez M. Möst S. Mullen R. Nichols A. W. Nolte C. Parisod K. Pfennig A. M. Rice M. G. Ritchie B. Seifert C. M. Smadja R. Stelkens J. M. Szymura R. Väinölä J. B. W. Wolf D. Zinner 《Journal of evolutionary biology》2013,26(2):229-246
Hybridization has many and varied impacts on the process of speciation. Hybridization may slow or reverse differentiation by allowing gene flow and recombination. It may accelerate speciation via adaptive introgression or cause near‐instantaneous speciation by allopolyploidization. It may have multiple effects at different stages and in different spatial contexts within a single speciation event. We offer a perspective on the context and evolutionary significance of hybridization during speciation, highlighting issues of current interest and debate. In secondary contact zones, it is uncertain if barriers to gene flow will be strengthened or broken down due to recombination and gene flow. Theory and empirical evidence suggest the latter is more likely, except within and around strongly selected genomic regions. Hybridization may contribute to speciation through the formation of new hybrid taxa, whereas introgression of a few loci may promote adaptive divergence and so facilitate speciation. Gene regulatory networks, epigenetic effects and the evolution of selfish genetic material in the genome suggest that the Dobzhansky–Muller model of hybrid incompatibilities requires a broader interpretation. Finally, although the incidence of reinforcement remains uncertain, this and other interactions in areas of sympatry may have knock‐on effects on speciation both within and outside regions of hybridization. 相似文献
92.
Orly Laufman Hudson H. Freeze Wanjin Hong Sima Lev 《Traffic (Copenhagen, Denmark)》2013,14(10):1065-1077
Multiple mutations in different subunits of the tethering complex Conserved Oligomeric Golgi (COG) have been identified as a cause for Congenital Disorders of Glycosylation (CDG) in humans. Yet, the mechanisms by which COG mutations induce the pleiotropic CDG defects have not been fully defined. By detailed analysis of Cog8 deficiency in either HeLa cells or CDG‐derived fibroblasts, we show that Cog8 is required for the assembly of both the COG complex and the Golgi Stx5‐GS28‐Ykt6‐GS15 and Stx6‐Stx16‐Vti1a‐VAMP4 SNARE complexes. The assembly of these SNARE complexes is also impaired in cells derived from a Cog7‐deficient CDG patient. Likewise, the integrity of the COG complex is also impaired in Cog1‐, Cog4‐ and Cog6‐depleted cells. Significantly, deficiency of Cog1, Cog4, Cog6 or Cog8 distinctly influences the production of COG subcomplexes and their Golgi targeting. These results shed light on the structural organization of the COG complex and its subcellular localization, and suggest that its integrity is required for both tethering of transport vesicles to the Golgi apparatus and the assembly of Golgi SNARE complexes. We propose that these two key functions are generally and mechanistically impaired in COG‐associated CDG patients, thereby exerting severe pleiotropic defects. 相似文献
93.
94.
Hudson T. Pinheiro Bruno C. L. Macena Ronaldo B. Francini-Filho Carlos E. L. Ferreira Fernanda V. Albuquerque Natalia P. A. Bezerra Alfredo Carvalho-Filho Romulo C. P. Ferreira Osmar J. Luiz Thayna J. Mello Sibele A. Mendonça Diogo M. Nunes Caio R. Pimentel Alessandra M. A. Pires Abilio Soares-Gomes Danielle L. Viana Fabio H. V. Hazin Luiz A. Rocha 《Journal of fish biology》2020,97(4):1143-1153
Saint Peter and Saint Paul's Archipelago (SPSPA), one of the smallest and most isolated island groups in the world, is situated on the Mid-Atlantic Ridge, between Brazil and the African continent. SPSPA has low species richness and high endemism; nonetheless, the diversity of fishes from deep habitats (>30 m depth) had not been previously studied in detail. Several expeditions conducted between 2009 and 2018 explored the shallow and deep reefs of SPSPA using scuba, closed-circuit rebreathers, manned submersibles, baited remote underwater stereo-videos (stereo-BRUV) and fishing between 0 and 1050 m depth. These expeditions yielded 41 new records of fishes for SPSPA: 9 in open waters, 9 in shallow waters (0–30 m), 8 in mesophotic ecosystems (30–150 m) and 15 in deeper reefs (>150 m). Combined with literature records of adult pelagic, shallow and deep-reef species, as well as larvae, the database of the fish biodiversity for SPSPA currently comprises 225 species (169 recorded as adult fishes and 79 as larvae, with 23 species found in both stages). Most of them (112) are pelagic, 86 are reef-associated species and 27 are deep-water specialists. Species accumulation curves show that the number of fish species has not yet reached an asymptote. Whereas the number of species recorded in SPSPA is similar to that in other oceanic islands in the Atlantic Ocean, the proportion of shorefishes is relatively lower, and the endemism level is the third highest in the Atlantic. Twenty-nine species are listed as threatened with extinction. Observations confirm the paucity of top predators on shallow rocky reefs of the island, despite the presence of several pelagic shark species around SPSPA. Because all of the endemic species are reef associated, it is argued that the new marine-protected areas created by the Brazilian government do not ensure the protection and recovery of SPSPA's biodiversity because they allow exploitation of the most vulnerable species around the archipelago itself. This study suggests a ban on reef fish exploitation inside an area delimited by the 1000 m isobath around the islands (where all known endemics are concentrated) as the main conservation strategy to be included in the SPSPA management plan being prepared by the Brazilian government. 相似文献
95.
Bozena Szulc Paulina Sosicka Dorota Maszczak-Seneczko Edyta Skurska Auhen Shauchuk Teresa Olczak Hudson H. Freeze Mariusz Olczak 《The Journal of biological chemistry》2020,295(48):16445
Nucleotide sugar transporters, encoded by the SLC35 gene family, deliver nucleotide sugars throughout the cell for various glycosyltransferase-catalyzed glycosylation reactions. GlcNAc, in the form of UDP-GlcNAc, and galactose, as UDP-Gal, are delivered into the Golgi apparatus by SLC35A3 and SLC35A2 transporters, respectively. However, although the UDP-Gal transporting activity of SLC35A2 has been clearly demonstrated, UDP-GlcNAc delivery by SLC35A3 is not fully understood. Therefore, we analyzed a panel of CHO, HEK293T, and HepG2 cell lines including WT cells, SLC35A2 knockouts, SLC35A3 knockouts, and double-knockout cells. Cells lacking SLC35A2 displayed significant changes in N- and O-glycan synthesis. However, in SLC35A3-knockout CHO cells, only limited changes were observed; GlcNAc was still incorporated into N-glycans, but complex type N-glycan branching was impaired, although UDP-GlcNAc transport into Golgi vesicles was not decreased. In SLC35A3-knockout HEK293T cells, UDP-GlcNAc transport was significantly decreased but not completely abolished. However, N-glycan branching was not impaired in these cells. In CHO and HEK293T cells, the effect of SLC35A3 deficiency on N-glycan branching was potentiated in the absence of SLC35A2. Moreover, in SLC35A3-knockout HEK293T and HepG2 cells, GlcNAc was still incorporated into O-glycans. However, in the case of HepG2 cells, no qualitative changes in N-glycans between WT and SLC35A3 knockout cells nor between SLC35A2 knockout and double-knockout cells were observed. These findings suggest that SLC35A3 may not be the primary UDP-GlcNAc transporter and/or different mechanisms of UDP-GlcNAc transport into the Golgi apparatus may exist. 相似文献
96.
Peter J. Kerr Matthew B. Rogers Adam Fitch Jay V. DePasse Isabella M. Cattadori Alan C. Twaddle Peter J. Hudson David C. Tscharke Andrew F. Read Edward C. Holmes Elodie Ghedin 《Journal of virology》2013,87(23):12900-12915
The evolutionary interplay between myxoma virus (MYXV) and the European rabbit (Oryctolagus cuniculus) following release of the virus in Australia in 1950 as a biological control is a classic example of host-pathogen coevolution. We present a detailed genomic and phylogeographic analysis of 30 strains of MYXV, including the Australian progenitor strain Standard Laboratory Strain (SLS), 24 Australian viruses isolated from 1951 to 1999, and three isolates from the early radiation in Britain from 1954 and 1955. We show that in Australia MYXV has spread rapidly on a spatial scale, with multiple lineages cocirculating within individual localities, and that both highly virulent and attenuated viruses were still present in the field through the 1990s. In addition, the detection of closely related virus lineages at sites 1,000 km apart suggests that MYXV moves freely in geographic space, with mosquitoes, fleas, and rabbit migration all providing means of transport. Strikingly, despite multiple introductions, all modern viruses appear to be ultimately derived from the original introductions of SLS. The rapidity of MYXV evolution was also apparent at the genomic scale, with gene duplications documented in a number of viruses. Duplication of potential virulence genes may be important in increasing the expression of virulence proteins and provides the basis for the evolution of novel functions. Mutations leading to loss of open reading frames were surprisingly frequent and in some cases may explain attenuation, but no common mutations that correlated with virulence or attenuation were identified. 相似文献
97.
Hudson Meadwell 《Ethnic and racial studies》2013,36(3):309-328
This article identifies a set of assumptions that underlie culturalist approaches to ethnic nationalism and it assesses these assumptions from a particular instrumentalist point of view ‐ collective‐choice theory. It is argued that cultural approaches are structuralist, leaving little room for intentional explanations and, when agent‐centred explanations are used, they are typically embedded within a moral economic theory of groups. In contrast, collective‐choice theory is intentionalist and political‐economic in orientation. From the perspective of these different approaches, the article examines a common dilemma of mobilization in nationalist movements ‐ how popular support can be mobilized by activists who, for entrepreneurial or ideological reasons, have formed a nationalist organization. Empirical illustrations are drawn from interwar Brittany and contemporary Quebec. 相似文献
98.
Newborn kittens and piglets show some notable similarities in suckling‐associated behaviours. Both develop a pattern of teat use in which each member of the litter predominantly occupies one or two particular nipples or teats, both show agonistic behaviour towards littermates during suckling, and both are born with ‘weapons’–kittens with sharp claws and piglets with sharp needle teeth. Traditionally, the differential use of nipples or teats has been thought to be due to differential quality of the mammary glands. However, neither our findings in kittens nor an examination of the literature on piglets support this view. As mammary glands usually are of equal quality and as there are normally more glands than young, there seems little reason for littermates to fight. Furthermore, there is also little evidence that individual performance in suckling contests or use of ‘weapons’ is related to weight gain or to dominance relations. Given the present lack of satisfying adaptive explanations for the seemingly aggressive behaviour and use of weapons by kittens and piglets, we suggest these to be epiphenomena of developmental processes anticipating the use of these behaviours and structures in later adaptive contexts. 相似文献
99.
Proteins are complex macromolecules with dynamic conformations. They are charged like colloids, but unlike colloids, charge is heterogeneously distributed on their surfaces. Here we overturn entrenched doctrine that uncritically treats bovine serum albumin (BSA) as a colloidal hard sphere by elucidating the complex pH and surface hydration-dependence of solution viscosity. We measure the infinite shear viscosity of buffered BSA solutions in a parameter space chosen to tune competing long-range repulsions and short-range attractions (2 mg/mL ≤ [BSA] ≤ 500 mg/mL and 3.0 ≤ pH ≤ 7.4). We account for surface hydration through partial specific volume to define volume fraction and determine that the pH-dependent BSA intrinsic viscosity never equals the classical hard sphere result (2.5). We attempt to fit our data to the colloidal rheology models of Russel, Saville, and Schowalter (RSS) and Krieger-Dougherty (KD), which are each routinely and successfully applied to uniformly charged suspensions and to hard-sphere suspensions, respectively. We discover that the RSS model accurately describes our data at pH 3.0, 4.0, and 5.0, but fails at pH 6.0 and 7.4, due to steeply rising solution viscosity at high concentration. When we implement the KD model with the maximum packing volume fraction as the sole floating parameter while holding the intrinsic viscosity constant, we conclude that the model only succeeds at pH 6.0 and 7.4. These findings lead us to define a minimal framework for models of crowded protein solution viscosity wherein critical protein-specific attributes (namely, conformation, surface hydration, and surface charge distribution) are addressed. 相似文献
100.
Nathan E. Hudson Feng Ding Igal Bucay E. Timothy O’Brien III Oleg V. Gorkun Richard Superfine Susan T. Lord Nikolay V. Dokholyan Michael R. Falvo 《Biophysical journal》2013
Fibrin fibers form the structural scaffold of blood clots. Thus, their mechanical properties are of central importance to understanding hemostasis and thrombotic disease. Recent studies have revealed that fibrin fibers are elastomeric despite their high degree of molecular ordering. These results have inspired a variety of molecular models for fibrin’s elasticity, ranging from reversible protein unfolding to rubber-like elasticity. An important property that has not been explored is the timescale of elastic recoil, a parameter that is critical for fibrin’s mechanical function and places a temporal constraint on molecular models of fiber elasticity. Using high-frame-rate imaging and atomic force microscopy-based nanomanipulation, we measured the recoil dynamics of individual fibrin fibers and found that the recoil was orders of magnitude faster than anticipated from models involving protein refolding. We also performed steered discrete molecular-dynamics simulations to investigate the molecular origins of the observed recoil. Our results point to the unstructured αC regions of the otherwise structured fibrin molecule as being responsible for the elastic recoil of the fibers. 相似文献