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11.
Wood decay under the microscope 总被引:3,自引:0,他引:3
Many aspects of the interactions between host wood structure and fungal activity can be revealed by high resolution light microscopy, and this technique has provided much of the information discussed here. A wide range of different types of decay can result from permutations of host species, fungal species and conditions within wood. Within this spectrum, three main types are commonly recognised: brown rot, white rot and soft rot. The present review explores parts of the range of variation that each of these encompasses and emphasizes that degradation modes appear to reflect a co-evolutionary adaptation of decay fungi to different wood species or the lignin composition within more primitive and advanced wood cell types. One objective of this review is to provide evidence that the terms brown rot, white rot and soft rot may not be obsolete, but rigid definitions for fungi that are placed into these categories may be less appropriate than thought previously. Detailed knowledge of decomposition processes does not only aid prognosis of decay development in living trees for hazard assessment but also allows the identification of wood decay fungi that can be used for biotechnology processes in the wood industry. In contrast to bacteria or commercial enzymes, hyphae can completely ramify through solid wood. In this review evidence is provided that wood decay fungi can effectively induce permeability changes in gymnospermous heartwood or can be applied to facilitate the identification of tree rings in diffuse porous wood of angiosperms. The specificity of their enzymes and the mild conditions under which degradation proceeds is partly detrimental for trees, but also make wood decay fungi potentially efficient biotechnological tools. 相似文献
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13.
Organisms Diversity & Evolution - Chaetopteridae — the parchment worms — comprise a group of early branching annelids with a scarcely investigated neuroanatomy and neurogenesis. Due... 相似文献
14.
Haploinsufficiency for one COL3A1 allele of type III procollagen results in a phenotype similar to the vascular form of Ehlers-Danlos syndrome, Ehlers-Danlos syndrome type IV 下载免费PDF全文
Schwarze U Schievink WI Petty E Jaff MR Babovic-Vuksanovic D Cherry KJ Pepin M Byers PH 《American journal of human genetics》2001,69(5):989-1001
Mutations in the COL3A1 gene that encodes the chains of type III procollagen result in the vascular form of Ehlers-Danlos syndrome (EDS), EDS type IV, if they alter the sequence in the triple-helical domain. Although other fibrillar collagen-gene mutations that lead to allele instability or failure to incorporate proalpha-chains into trimers-and that thus reduce the amount of mature molecules produced-result in clinically apparent phenotypes, no such mutations have been identified in COL3A1. Furthermore, mice heterozygous for Col3a1 "null" alleles have no identified phenotype. We have now found three frameshift mutations (1832delAA, 413delC, and 555delT) that lead to premature termination codons (PTCs) in exons 27, 6, and 9, respectively, and to allele-product instability. The mRNA from each mutant allele was transcribed efficiently but rapidly degraded, presumably by the mechanisms of nonsense-mediated decay. In a fourth patient, we identified a point mutation, in the final exon, that resulted in a PTC (4294C-->T [Arg1432Ter]). In this last instance, the mRNA was stable but led to synthesis of a truncated protein that was not incorporated into mature type III procollagen molecules. In all probands, the presenting feature was vascular aneurysm or rupture. Thus, in contrast to mutations in genes that encode the dominant protein of a tissue (e.g., COL1A1 and COL2A1), in which "null" mutations result in phenotypes milder than those caused by mutations that alter protein sequence, the phenotypes produced by these mutations in COL3A1 overlap with those of the vascular form of EDS. This suggests that the major effect of many of these dominant mutations in the "minor" collagen genes may be expressed through protein deficiency rather than through incorporation of structurally altered molecules into fibrils. 相似文献
15.
Cadmium-induced apoptosis of primary epithelial lung cells: Involvement of Bax and p53, but not of oxidative stress 总被引:11,自引:0,他引:11
Lag M Westly S Lerstad T Bjørnsrud C Refsnes M Schwarze PE 《Cell biology and toxicology》2002,18(1):29-42
The lung is a target organ for cadmium (Cd) toxicity. Apoptosis induced by cadmium acetate (CdAc) was studied in alveolar
type 2 cells and Clara cells isolated from rat lung. Relatively low concentrations of CdAc (1–10 μmol/L) induced apoptosis
after exposure for 20 h. Type 2 cells were more sensitive than Clara cells to Cd-induced apoptosis and loss of cell viability.
On exposure to 10 μmol/L CdAc, the levels of the apoptosis-modulating proteins p53 and Bax were increased at 2 h and 5–12
h, respectively. The expression of p53 preceded the expression of Bax and the apoptotic process. The exposure to 10 μmol/L
CdAc did not significantly increase the formation of cellular reactive oxygen species (ROS). However, after exposure to a
high concentration of CdAc (100 μmol/L), a 30% increase of the ROS level was observed. No significant nitric oxide production
was measured following CdAc exposure. Catalase, superoxide dismutase, dimethyl sulfoxide, or tetramethylthiourea did not protect
against Cd-induced apoptosis. In conclusion, the results show that Clara cells and type 2 cells are sensitive to Cd-induced
apoptosis. Increased levels of p53 and Bax are suggested to be involved in the apoptosis. The apoptosis did not appear to
be mediated by oxidative pathways.
This revised version was published online in August 2006 with corrections to the Cover Date. 相似文献
16.
Novel pathways associated with bypassing cellular senescence in human prostate epithelial cells 总被引:8,自引:0,他引:8
Schwarze SR DePrimo SE Grabert LM Fu VX Brooks JD Jarrard DF 《The Journal of biological chemistry》2002,277(17):14877-14883
17.
Ranke MB Schweizer R Elmlinger MW Weber K Binder G Schwarze CP Wollmann HA 《Hormone research》2001,55(3):115-124
BACKGROUND: Little information is available on the relevance of parameters representing the insulin-like growth factor (IGF) system with regard to growth hormone (GH) treatment during childhood. In adults, high IGF-I levels were found to be associated with side effects and long-term risks. AIM/METHOD: Our aim was to monitor the serum levels of IGF-I, IGF-binding protein (IGFBP) 3, and IGFBP-2 during long-term GH treatment of 156 patients with GH deficiency (GHD) and of 153 non-GHD patients. We determined the extent to which the IGF parameters exceed the normal ranges and identified those parameters which are predictive of 1st-year growth. RESULTS: In prepubertal GHD children, the levels of IGF-I, IGFBP-3, and IGF-I/IGFBP-3 exceeded the 95th centile of the reference values for this age group in 2.3, 0.3, and 7.9% of the cases, respectively, whereas in prepubertal non-GHD children, the same parameters exceeded the 95th reference centile in 20.1, 3.5, and 32.2%, respectively. In pubertal GHD children IGF-I, IGFBP-3, and IGF-I/IGFBP-3 levels exceeded the 95th reference centile in 11.1, 1.5, and 15.4%, respectively. In pubertal non-GHD children, these levels also exceeded the 95th centile in 26.7, 7.0, and 41.4%, respectively. In both GHD and non-GHD groups, however, some patients had IGF parameters which were below the reference values. Our analysis showed that, in both groups, in addition to maximum GH, all IGF parameters (IGF-I, IGFBP-3, IGF-I/IGFBP-3 ratio, IGFBP-2 or derivatives) significantly extend the scope of a calculated model for predicting 1st-year height velocity. CONCLUSION: For reasons of safety and optimization of GH therapy, it is essential to follow up IGF-I, IGFBP-3, and IGFBP-2 levels regularly during childhood. 相似文献
18.
Schweizer R Ranke MB Binder G Herdach F Zapadlo M Grauer ML Schwarze CP Wollmann HA 《Hormone research》2000,53(5):228-238
The experience gained since 1987, through observation of 85 girls with Turner syndrome under growth hormone (GH) treatment, has enabled the analysis of one of the largest cohorts. Our results show that age, karyotype and height reflect the heterogeneity of the patients examined at our growth centre. In 47 girls, followed over 4 years on GH (median dose 0.72 IU/kg/week), the median age was 9.4 years and mean height SDS was -3.55 (Prader) and -0.14 (Turner-specific), while height and other anthropometrical parameters [weight, body mass index, sitting height (SH), leg length (LL) SH/LL, head circumference, arm span] were documented and compared to normative data as well as to Turner-specific references established on the basis of a larger (n = 165) untreated cohort from Tübingen. The latter data are also documented in this article. Although there was a trend towards normalization of these parameters during the observation period, no inherent alterations in the Turner-specific anthropometric pattern occurred. In 42 girls who started GH treatment at a median age of 11.8 years, final height (bone age >15 years) was achieved at 16.7 years. The overall gain in height SDS (Turner) from start to end of GH therapy was 0.7 (+/- 0.8) SD, but 0.9 (+/- 0.6) SD from GH start to onset of puberty (spontaneous 12.2 years, induced 13.9 years) and -0.2 (+/- 0.8) from onset of puberty to end of growth. Height gain did not occur in 12 patients (29%) and a gain of > 5 cm was only observed in 16 patients (38%). Height gain correlated positively with age at puberty onset, duration, and dose of GH, and negatively with height and bone age at the time GH treatment started. Final height correlated positively with height SDS at GH start and negatively with the ratio of SH/LL (SDS). We conclude that, in the future, GH should be given at higher doses, but oestrogen substitution should be done cautiously, owing to its potentially harmful effect on growth. LL appears to determine height variation in Turner syndrome and the potential to treat short stature successfully with GH. 相似文献
19.
Requirements for Construction of a Functional Hybrid Complex of Photosystem I and [NiFe]-Hydrogenase
Alexander Schwarze Marta J. Kopczak Matthias R?gner Oliver Lenz 《Applied and environmental microbiology》2010,76(8):2641-2651
The development of cellular systems in which the enzyme hydrogenase is efficiently coupled to the oxygenic photosynthesis apparatus represents an attractive avenue to produce H2 sustainably from light and water. Here we describe the molecular design of the individual components required for the direct coupling of the O2-tolerant membrane-bound hydrogenase (MBH) from Ralstonia eutropha H16 to the acceptor site of photosystem I (PS I) from Synechocystis sp. PCC 6803. By genetic engineering, the peripheral subunit PsaE of PS I was fused to the MBH, and the resulting hybrid protein was purified from R. eutropha to apparent homogeneity via two independent affinity chromatographical steps. The catalytically active MBH-PsaE (MBHPsaE) hybrid protein could be isolated only from the cytoplasmic fraction. This was surprising, since the MBH is a substrate of the twin-arginine translocation system and was expected to reside in the periplasm. We conclude that the attachment of the additional PsaE domain to the small, electron-transferring subunit of the MBH completely abolished the export competence of the protein. Activity measurements revealed that the H2 production capacity of the purified MBHPsaE fusion protein was very similar to that of wild-type MBH. In order to analyze the specific interaction of MBHPsaE with PS I, His-tagged PS I lacking the PsaE subunit was purified via Ni-nitrilotriacetic acid affinity and subsequent hydrophobic interaction chromatography. Formation of PS I-hydrogenase supercomplexes was demonstrated by blue native gel electrophoresis. The results indicate a vital prerequisite for the quantitative analysis of the MBHPsaE-PS I complex formation and its light-driven H2 production capacity by means of spectroelectrochemistry.Molecular hydrogen (H2) is often discussed as an alternative source of energy (13, 22, 26, 41). It is a highly energetic, renewable, and zero-carbon dioxide emission fuel; however, it is produced mainly from fossil resources. One intriguing possibility for sustainable H2 production is the development of cellular systems in which the light-driven oxygenic photosynthesis is efficiently coupled to hydrogen production by hydrogenase (1, 21, 36).During the process of oxygenic photosynthesis, photosystem II (PS II), a thylakoid membrane (TM)-embedded multiprotein complex, utilizes solar energy to oxidize water into dioxygen (O2), protons, and electrons. The electrons released by PS II are further conducted through an electron transport chain consisting of plastoquinones, the cytochrome b6f complex, and either plastocyanin or cytochrome c6 to the chlorophyll (Chl) dimer P700 in photosystem I (PS I) (20, 48). During light-induced charge separation in PS I, P700 is oxidized, leading to the reduction of the adjacent cofactor A0 (Chl a). From there, the electrons are transmitted to the phylloquinone A1 and subsequently to the Fe4S4 clusters FX, FA, and FB (9) that are located at the acceptor site of PS I. The acceptor site is composed of the PsaC subunit, which harbors the iron-sulfur clusters FA and FB, and the two additional cofactor-free extrinsic subunits PsaD and PsaE. In the final step, the electrons are transferred from FB to the ferredoxin (PetF), which has a midpoint potential of −412 mV (see Fig. Fig.1B)1B) (8, 9).Open in a separate windowFIG. 1.Models of the hydrogenase and photosystem I complexes used in this study. (A) Membrane-bound hydrogenase (MBHwt) of Ralstonia eutropha H16. (B) Wild-type photosystem I (PS I) from Synechocystis sp. PCC 6803. (C) MBHstop protein lacking the C-terminal anchor domain of HoxK. (D) MBHPsaE and PS IΔPsaE.Hydrogenases of the NiFe and FeFe types catalyze the reversible cleavage of H2 into protons and electrons (18, 63). For most hydrogenases, this reaction is highly sensitive to O2 and leads to the reversible or even irreversible inactivation of the enzyme (49, 66, 67). A prominent exception is the oxygen-tolerant membrane-bound [NiFe]-hydrogenase (MBH) from Ralstonia eutropha H16, which catalyzes H2 conversion in the presence of O2 (42, 65). The MBH consists of large subunit HoxG (67 kDa), harboring the NiFe active site, and small subunit HoxK (35 kDa), bearing three FeS clusters (Fig. (Fig.1)1) (32). Both cofactor-containing subunits are completely assembled within the cytoplasm and become subsequently translocated through the cytoplasmic membrane by the twin-arginine translocation (Tat) system. This transport is guided by a specific Tat signal peptide that is located at the N terminus of small subunit HoxK (53). The MBH is then connected to the membrane via the hydrophobic C-terminal “anchor” domain of HoxK, which provides the electronic connection to the diheme cytochrome b, HoxZ (5, 57). All structural, accessory, and regulatory genes for the synthesis of active MBH are arranged in a large, megaplasmid-borne operon (7, 11, 14, 29, 33, 38, 58).The concept of light-driven hydrogen production has been investigated in numerous studies (for reviews, see references 3, 21, and 23), including one involving direct electron transfer from PS I to the free form of hydrogenase in vitro (45). In a preliminary attempt, the MBH from R. eutropha was recently directly fused to PsaE (creating MBHPsaE) (28). The fusion protein was partially purified and subjected to in vitro reconstitution with PS I lacking PsaE (PS IΔPsaE) (54) for light-driven hydrogen production. This concept was based on the previous observation that PS I lacking the peripheral subunit PsaE is fully reconstituted in vitro simply by the addition of independently purified PsaE protein (12).In the present communication, we describe a novel purification procedure for R. eutropha MBHPsaE that yields homogeneous, functionally active MBHPsaE. Additionally, a new method for efficient and fast purification of Synechocystis sp. PCC 6803 (hereafter referred to as Synechocystis) His-tagged PS I was established. Finally, the pure proteins MBHPsaE and PS IΔPsaE were successfully subjected to in vitro reconstitution. 相似文献
20.
Helena E. Christiansen Ulrike Schwarze Shawna M. Pyott Mohammed Al Balwi Melanie G. Pepin David R. Eyre 《American journal of human genetics》2010,86(3):389-398
Osteogenesis imperfecta (OI) is characterized by bone fragility and fractures that may be accompanied by bone deformity, dentinogenesis imperfecta, short stature, and shortened life span. About 90% of individuals with OI have dominant mutations in the type I collagen genes COL1A1 and COL1A2. Recessive forms of OI resulting from mutations in collagen-modifying enzymes and chaperones CRTAP, LEPRE1, PPIB, and FKBP10 have recently been identified. We have identified an autosomal-recessive missense mutation (c.233T>C, p.Leu78Pro) in SERPINH1, which encodes the collagen chaperone-like protein HSP47, that leads to a severe OI phenotype. The mutation results in degradation of the endoplasmic reticulum resident HSP47 via the proteasome. Type I procollagen accumulates in the Golgi of fibroblasts from the affected individual and a population of the secreted type I procollagen is protease sensitive. These findings suggest that HSP47 monitors the integrity of the triple helix of type I procollagen at the ER/cis-Golgi boundary and, when absent, the rate of transit from the ER to the Golgi is increased and helical structure is compromised. The normal 3-hydroxylation of the prolyl residue at position 986 of the triple helical domain of proα1(I) chains places the role of HSP47 downstream from the CRTAP/P3H1/CyPB complex that is involved in prolyl 3-hydroxylation. Identification of this mutation in SERPINH1 gives further insight into critical steps of the collagen biosynthetic pathway and the molecular pathogenesis of OI. 相似文献