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51.
Protein acetylation affects acetate metabolism,motility and acid stress response in
Escherichia coli 下载免费PDF全文
52.
Laurent AF Frantz Joshua G Schraiber Ole Madsen Hendrik-Jan Megens Mirte Bosse Yogesh Paudel Gono Semiadi Erik Meijaard Ning Li Richard PMA Crooijmans Alan L Archibald Montgomery Slatkin Lawrence B Schook Greger Larson Martien AM Groenen 《Genome biology》2013,14(9):R107
Background
Elucidating the process of speciation requires an in-depth understanding of the evolutionary history of the species in question. Studies that rely upon a limited number of genetic loci do not always reveal actual evolutionary history, and often confuse inferences related to phylogeny and speciation. Whole-genome data, however, can overcome this issue by providing a nearly unbiased window into the patterns and processes of speciation. In order to reveal the complexity of the speciation process, we sequenced and analyzed the genomes of 10 wild pigs, representing morphologically or geographically well-defined species and subspecies of the genus Sus from insular and mainland Southeast Asia, and one African common warthog.Results
Our data highlight the importance of past cyclical climatic fluctuations in facilitating the dispersal and isolation of populations, thus leading to the diversification of suids in one of the most species-rich regions of the world. Moreover, admixture analyses revealed extensive, intra- and inter-specific gene-flow that explains previous conflicting results obtained from a limited number of loci. We show that these multiple episodes of gene-flow resulted from both natural and human-mediated dispersal.Conclusions
Our results demonstrate the importance of past climatic fluctuations and human mediated translocations in driving and complicating the process of speciation in island Southeast Asia. This case study demonstrates that genomics is a powerful tool to decipher the evolutionary history of a genus, and reveals the complexity of the process of speciation. 相似文献53.
Henrik Aronsson 《Plant signaling & behavior》2008,3(12):1093-1095
Processes putatively dependent on the galactolipid monogalactosyldiacylglycerol (MGDG) were recently studied using the knockdown monogalactosyldiacylglycerol synthase 1 (mgd1-1) mutant (∼40% reduction in MGDG). Surprisingly, targeting of chloroplast proteins was not affected in mgd1-1 mutants, suggesting they retain sufficient MGDG to maintain efficient targeting. However, in dark-grown mgd1-1 plants the photoactive to photoinactive protochlorophyllide (Pchlide) ratio was increased, suggesting that photoprotective responses are induced in them. Nevertheless, mgd1-1 could not withstand high light intensities, apparently due to impairment of another photoprotective mechanism, the xanthophyll cycle (and hence thermal dissipation). This was mediated by increased conductivity of the thylakoid membrane leading to a higher pH in the thylakoid interior, which impaired the pH-dependent activation of violaxanthin de-epoxidase (VDE) and PsbS. These findings suggest that MGDG contribute directly to the regulation of photosynthesis-related processes.Key words: conductivity, galactolipid, light stress, photosynthesis, plastid, xanthophyllThe galactolipid monogalactosyldiacylglycerol (MGDG), the major lipid in plastids,1 is mainly synthesised in inner plastid envelopes,2 where monogalactosyldiacylglycerol synthase 1 (MGD1) catalyses the last step of its production.3 Two MGDG-deficient mutants are known: the knockdown mgd1-1 mutant, which accumulates ∼40% less MGDG than wild type,4 and the null mutant mgd1-2, which displays extremely severe defects in chloroplast and plant development.5 Thus, the mgd1-1 mutant is more suitable for assessing putative roles of MGDG in processes such as protein targeting and photoprotection.There are conflicting indications regarding the involvement of galactolipids in chloroplast protein targeting: some suggest they play an important role,6–10 but not all.11,12 The data recently collected for mgd1-1 do not support MGDG''s involvement in protein targeting, since (inter alia) the level of MGDG in mgd1-1 mutants is clearly sufficient for efficient targeting.13 Further, the galactolipid associated with the TOC complex12 is digalactosyldiacylglycerol (DGDG) and the digalactosyldiacylglycerol synthase 1 (dgd1) mutant,14 which has ∼10% of wild-type levels of DGDG, has impaired import efficiency.15,16 Hence, this may indicate that DGDG is relatively more important for chloroplast import than MGDG.The prolamellar bodies (PLBs) of etioplasts have high lipid-to-protein ratios compared to thylakoids. Their major lipid and protein are MGDG and NADPH:Pchlide oxidoreductase (POR), respectively,17 and MGDG putatively plays an important role, interactively with POR, in the formation of PLBs.18–20 The transformation of PLBs into thylakoids involves phototransformation of photoactive Pchlide (F656), a precursor of chlorophyll. Non-photoactive Pchlide (F631) is susceptible to photooxidative damage, but POR is believed to suppress this.21,22 After excitation at 440 nm, mgd1-1 mutants display distinctly higher fluorescence emission peaks corresponding to photoactive Pchlide than wild type counterparts and (hence) higher photoactive:non-photoactive Pchlide ratios.13 These changes may be photoprotective responses that favour formation of photoactive Pchlide and optimize the plants'' opportunities to use light for chlorophyll production, enabling the transformation of etioplasts into chloroplasts.Interestingly,the xanthophyll cycle, another photoprotective mechanism, is impaired in mgd1-1.13 Normally, the xanthophyll cycle pigment violaxanthin is de-epoxidized into antheraxanthin, and then into zeaxanthin, by the enzyme VDE (Fig. 1), which is dependent on MGDG.23 MGDG is also an integral component of photosynthetic complexes.24–26 Thus, since mgd1-1 mutants have reduced total amounts of xanthophyll and chlorophyll pigments, but increased chlorophyll a/b ratios, their photosynthesis capacity is unsurprisingly reduced, even though the organization of their electron transport chains is not strongly affected by the MGDG deficiency.13Open in a separate windowFigure 1Reactions of the xanthophyll cycle (adapted from ref. 29). VDE, violaxanthin de-epoxidase; ZE, zeaxanthin epoxidase.During short-term high light stress, antheraxanthin and zeaxanthin are thought to facilitate dissipation of excess light energy in the PSII antenna bed by non-photochemical quenching.27,28 Upon high light stress the pH decreases, triggering photoprotective mechanisms via changes in the PSII antenna system. The PsbS protein, which is involved in thermal dissipation, is protonated and initiates a conformational change in the PSII antenna bed. This change is further stabilized by the de-epoxidation of violaxanthin to zeaxanthin by the luminal VDE.28 However, the thermal dissipation is impaired in mgd1-1 mutants at high light intensities (>1000 µmol m−2 s−1) making them more susceptible to light stress. Surprisingly, this is not mediated by direct effects on VDE and PsbS activities, but by changes in the proton conductivity of the thylakoid membrane.13The steady-state capacity of the xanthophyll cycle is reduced in mgd1-1 mutants, due to a ∼40% reduction in the proton motive force (pmf) across their thylakoid membranes, indicating that they have impaired capacities to energize these membranes. Nevertheless, the pmf is more or less equal to wild type under light-limited conditions (200 µmol m−2 s−1 light); it is only the increase in pmf in high light intensities that is impaired in the mutants.13 This leads to the thylakoid lumen being less acidic in mgd1-1 than in wild type, hampering full activation of VDE and PsbS. Thus, the thylakoid lumen pH is above the threshold level required for full activation of PsbS and VDE under steady-state conditions and so de-epoxidation rates are retarded and the equilibrium between zeaxanthin and violaxanthin starts to shift slightly towards violaxanthin (Fig. 2).13 Thus, increased conductivity of the thylakoid membranes is probably responsible for the diminished non-photochemical quenching in mgd1-1, and the findings strongly indicate that MGDG is required for efficient photosynthesis and photoprotection, in addition to being a physical membrane constituent.Open in a separate windowFigure 2Schematic diagram illustrating the normal mode of action of the xanthophyll cycle. In standard light conditions, V is bound to the photosynthetic complexes and harvests light. In strong light, V is released from the complexes and converted to Z by VDE, which is unable to access V when it is associated with the photosynthetic complexes. The newly formed Z then binds to the photosynthetic complexes (at the PsbS protein), where it dissipates excess energy through NPQ. V, violaxanthin; A, antheraxanthin; Z, zeaxanthin; VDE, violaxanthin de-epoxidase; ZE, zeaxanthin epoxidase. Arrows indicate the directions of reactions. 相似文献
54.
Touré A Clemente EJ Ellis P Mahadevaiah SK Ojarikre OA Ball PA Reynard L Loveland KL Burgoyne PS Affara NA 《Genome biology》2005,6(12):R102-15
Background
The male-specific region of the mouse Y chromosome long arm (MSYq) is comprised largely of repeated DNA, including multiple copies of the spermatid-expressed Ssty gene family. Large deletions of MSYq are associated with sperm head defects for which Ssty deficiency has been presumed to be responsible. 相似文献55.
Stig Aronsson 《Acta zoologica》1984,65(2):95-103
The distribution and occurrence of the aminergic structures of the hypothalamus and the hypophysis of the investigated species are very similar, except for the pars distalis. In the tadpoles of the anuran species Rana temporaria, R. arvalis, R. dalmatina, R. escutenta, Bufo bufo and B. calamita, the pars distalis is aminergically innervated (the Falck-Hillarp technique), but these nerves disappear at the metamorphic climax. In the larvae of the urodelan species Triturus cristatus and T. vulgaris, the pars distalis is devoid of such nerves. Electron microscopical studies of R. temporaria, B. bufo and T. cristatus confirm these observations. A discussion of the functional significance of the pars distalis nerves and the phylogenetic role of the difference between anuran and urodelan species is given. 相似文献
56.
Henrik Aronsson Christer Sundqvist Michael P. Timko Clas Dahlin 《Physiologia plantarum》2001,111(2):239-244
The homologous import and membrane association of a key enzyme for chlorophyll biosynthesis, the NADPH:protochlorophyllide (Pchlide) oxidoreductase (POR, EC 1.6.99.1) into pea chloroplasts was investigated in vitro. The co-factor, NADPH, decreased binding of the precursor protein (pPOR) to the envelope membranes in the presence of ATP. The decrease of the binding reaction with NADPH was not observed with the precursor of the small subunit of Rubisco (pSS).
To investigate possible substrate-dependency for the import reaction, internal Pchlide concentrations in the plastids were raised by either an addition of δ -aminolevulinic acid to isolated plastids or etiolation of the seedlings prior to plastid isolation. Increased amounts of plastid-bound Pchlide gave no observable differences in POR import.
The capacity of POR and 11 different POR mutants, carrying charged-to-alanine scanning substitutions, to form a catalytically active POR-Pchlide-NADPH complex and to associate with the thylakoid membranes in a protease-resistant way were tested. Wild-type POR, as well as the mutants with charge substitutions in the N-terminal region of the protein, exhibited higher catalytic activity than the POR mutants carrying substitutions in the C-terminal region. Formation of a catalytically active complex did not, however, increase the association efficiency onto the thylakoids. We can, therefore, postulate that the import of pea POR into pea chloroplasts was not substrate-dependent, nor did formation of catalytically active complexes stimulate or inhibit the membrane association reaction of POR. 相似文献
To investigate possible substrate-dependency for the import reaction, internal Pchlide concentrations in the plastids were raised by either an addition of δ -aminolevulinic acid to isolated plastids or etiolation of the seedlings prior to plastid isolation. Increased amounts of plastid-bound Pchlide gave no observable differences in POR import.
The capacity of POR and 11 different POR mutants, carrying charged-to-alanine scanning substitutions, to form a catalytically active POR-Pchlide-NADPH complex and to associate with the thylakoid membranes in a protease-resistant way were tested. Wild-type POR, as well as the mutants with charge substitutions in the N-terminal region of the protein, exhibited higher catalytic activity than the POR mutants carrying substitutions in the C-terminal region. Formation of a catalytically active complex did not, however, increase the association efficiency onto the thylakoids. We can, therefore, postulate that the import of pea POR into pea chloroplasts was not substrate-dependent, nor did formation of catalytically active complexes stimulate or inhibit the membrane association reaction of POR. 相似文献
57.
Henrik Aronsson 《Traffic (Copenhagen, Denmark)》2016,17(10):1125-1138
Peripheral vesicles in plastids have been observed repeatedly, primarily in proplastids and developing chloroplasts, in which they are suggested to function in thylakoid biogenesis. Previous observations of vesicles in mature chloroplasts have mainly concerned low temperature pretreated plants occasionally treated with inhibitors blocking vesicle fusion. Here, we show that such vesicle‐like structures occur not only in chloroplasts and proplastids, but also in etioplasts, etio‐chloroplasts, leucoplasts, chromoplasts and even transforming desiccoplasts without any specific pretreatment. Observations are made both in C3 and C4 species, in different cell types (meristematic, epidermis, mesophyll, bundle sheath and secretory cells) and different organs (roots, stems, leaves, floral parts and fruits). Until recently not much focus has been given to the idea that vesicle transport in chloroplasts could be mediated by proteins, but recent data suggest that the vesicle system of chloroplasts has similarities with the cytosolic coat protein complex II system. All current data taken together support the idea of an ongoing, active and protein‐mediated vesicle transport not only in chloroplasts but also in other plastids, obviously occurring regardless of chemical modifications, temperature and plastid developmental stage. 相似文献
58.
Mats X. Andersson Anders K. Nilsson Oskar N. Johansson Gülin Bozta? Lisa E. Adolfsson Francesco Pinosa Christel Garcia Petit Henrik Aronsson David Mackey Mahmut T?r Mats Hamberg Mats Ellerstr?m 《Plant physiology》2015,167(1):251-261
Plants defend themselves against microbial pathogens through a range of highly sophisticated and integrated molecular systems. Recognition of pathogen-secreted effector proteins often triggers the hypersensitive response (HR), a complex multicellular defense reaction where programmed cell death of cells surrounding the primary site of infection is a prominent feature. Even though the HR was described almost a century ago, cell-to-cell factors acting at the local level generating the full defense reaction have remained obscure. In this study, we sought to identify diffusible molecules produced during the HR that could induce cell death in naive tissue. We found that 4-methylsulfinylbutyl isothiocyanate (sulforaphane) is released by Arabidopsis (Arabidopsis thaliana) leaf tissue undergoing the HR and that this compound induces cell death as well as primes defense in naive tissue. Two different mutants impaired in the pathogen-induced accumulation of sulforaphane displayed attenuated programmed cell death upon bacterial and oomycete effector recognition as well as decreased resistance to several isolates of the plant pathogen Hyaloperonospora arabidopsidis. Treatment with sulforaphane provided protection against a virulent H. arabidopsidis isolate. Glucosinolate breakdown products are recognized as antifeeding compounds toward insects and recently also as intracellular signaling and bacteriostatic molecules in Arabidopsis. The data presented here indicate that these compounds also trigger local defense responses in Arabidopsis tissue.Plants are constantly challenged by pathogenic microorganisms and have developed several detection and defense systems to protect themselves against the invaders. Preformed defenses include the waxy cuticle, thick cell walls, and antimicrobial compounds. After recognition of microbe-associated patterns, defense responses are induced, which include the fortification of cell walls and the production of phytoalexins (Monaghan and Zipfel, 2012). Overcoming the preformed and induced defenses of the plant hosts requires adaptation by the pathogen. Pathogenic bacteria use type III secretion to inject proteins (so-called effectors) into the host cytosol in order to overcome plant defense responses (Bent and Mackey, 2007). In turn, plants have developed systems to recognize the pathogenic effectors and mount defense. Recognition of type III effectors by plant resistance (R) proteins induces robust defense responses that frequently include the hypersensitive response (HR).The HR is a complex defense reaction characterized by the induction of programmed cell death (PCD) in the local host tissue as well as the activation of other defense responses in both local and systemic tissue (Mur et al., 2008; Shah, 2009). Oomycetes and true fungi also secrete proteinaceous effectors that can be recognized by host R proteins (Coates and Beynon, 2010; Hückelhoven and Panstruga, 2011; Feng and Zhou, 2012). The lesions formed during the HR vary in size between different host-pathogen pairs; however, a lesion induced at one or a few cells can spread to surrounding cells (Mur et al., 2008). Since pathogens inducing HR typically fail to proliferate, the first infected cell likely releases a compound that promotes PCD in surrounding cells. This is especially clear in models with oomycete and fungal pathogens, where the localization of the pathogen and the spread of cell death around the infection site can be clearly visualized (Mur et al., 2008; Coates and Beynon, 2010). Trailing necrosis is an incomplete resistance phenotype characterized by cell death that trails, but fails to contain, the filamentous growth of the pathogen. One explanation for trailing necrosis is a failure of infected cells to produce a putative mobile defense signal required to enhance defense in neighboring cells. Farther from the site of PCD, other defense pathways are activated and systemic tissue is primed for defense.The hunt for systemically acting compounds has been intense, and several candidates for this signal have been presented (Dempsey and Klessig, 2012). In contrast, even though the phenomenon of HR as a defense reaction was described almost a century ago (Stakman, 1915; Mur et al., 2008), compounds acting on the local tissue scale of the HR have attracted little attention. We set out to find substances released from cells undergoing the HR that could induce cell death in naive tissue. We report that leaf tissue of the model plant Arabidopsis (Arabidopsis thaliana) releases the reactive electrophilic compound sulforaphane after bacterial effector recognition. Mutants affected in sulforaphane production as well as other glucosinolate breakdown products showed delayed or reduced cell death after the recognition of pathogenic effectors and decreased resistance to an oomycete pathogen. Moreover, pretreatment of plants with sulforaphane enhanced resistance against a virulent oomycete isolate. Thus, we interpret this as that sulforaphane and likely similar compounds might both possess direct antimicrobial properties and, through a cytotoxic mechanism, act directly on plant cells to trigger defense responses. 相似文献
59.
Wong CW Heng CL Wan Yee L Soh SW Kartasasmita CB Simoes EA Hibberd ML Sung WK Miller LD 《Genome biology》2007,8(5):R93
DNA microarrays used as 'genomic sensors' have great potential in clinical diagnostics. Biases inherent in random PCR-amplification, cross-hybridization effects, and inadequate microarray analysis, however, limit detection sensitivity and specificity. Here, we have studied the relationships between viral amplification efficiency, hybridization signal, and target-probe annealing specificity using a customized microarray platform. Novel features of this platform include the development of a robust algorithm that accurately predicts PCR bias during DNA amplification and can be used to improve PCR primer design, as well as a powerful statistical concept for inferring pathogen identity from probe recognition signatures. Compared to real-time PCR, the microarray platform identified pathogens with 94% accuracy (76% sensitivity and 100% specificity) in a panel of 36 patient specimens. Our findings show that microarrays can be used for the robust and accurate diagnosis of pathogens, and further substantiate the use of microarray technology in clinical diagnostics. 相似文献
60.
Elaine A Dunlop Sara Seifan Tijs Claessens Christian Behrends Miriam AF Kamps Ewelina Rozycka Alain J Kemp Ravi K Nookala John Blenis Barry J Coull James T Murray Maurice AM van Steensel Simon Wilkinson Andrew R Tee 《Autophagy》2014,10(10):1749-1760
Birt-Hogg-Dubé (BHD) syndrome is a rare autosomal dominant condition caused by mutations in the FLCN gene and characterized by benign hair follicle tumors, pneumothorax, and renal cancer. Folliculin (FLCN), the protein product of the FLCN gene, is a poorly characterized tumor suppressor protein, currently linked to multiple cellular pathways. Autophagy maintains cellular homeostasis by removing damaged organelles and macromolecules. Although the autophagy kinase ULK1 drives autophagy, the underlying mechanisms are still being unraveled and few ULK1 substrates have been identified to date. Here, we identify that loss of FLCN moderately impairs basal autophagic flux, while re-expression of FLCN rescues autophagy. We reveal that the FLCN complex is regulated by ULK1 and elucidate 3 novel phosphorylation sites (Ser406, Ser537, and Ser542) within FLCN, which are induced by ULK1 overexpression. In addition, our findings demonstrate that FLCN interacts with a second integral component of the autophagy machinery, GABA(A) receptor-associated protein (GABARAP). The FLCN-GABARAP association is modulated by the presence of either folliculin-interacting protein (FNIP)-1 or FNIP2 and further regulated by ULK1. As observed by elevation of GABARAP, sequestome 1 (SQSTM1) and microtubule-associated protein 1 light chain 3 (MAP1LC3B) in chromophobe and clear cell tumors from a BHD patient, we found that autophagy is impaired in BHD-associated renal tumors. Consequently, this work reveals a novel facet of autophagy regulation by ULK1 and substantially contributes to our understanding of FLCN function by linking it directly to autophagy through GABARAP and ULK1. 相似文献