In addition to the versatility of L casei, it possesses probioti

In Anlotinib nmr addition to the versatility of L. casei, it possesses probiotic properties making it an even more attractive vaccine delivery system i.e., immunization with L. casei expressing VP4-LTB elicited potent anti-VP4 IgA responses. Testing the efficacy in a porcine vaccination and infection model is a next step in testing the efficacy of this vaccine formulation. Methods Strains and culture conditions L. casei ATCC 393 (a kind gift of Jos Seegers, NCT-501 manufacturer NIZO, The Netherlands) was grown anaerobically in MRS broth (Sigma, St, Louis, MO) at 37°C without shaking. To analyze protein expression, transformed L. casei were grown in basal MRS medium (10 g peptone, 8 g beef extract,

4 g yeast extract, 2 g potassium phosphate, 5 g sodium acetate, 1 ml Tween 80, 2 g diammonium citrate, 0.2 g magnesium sulfate, and selleck products 0.05 g manganese sulfate per liter) supplemented with 2% xylose. L. casei was plated on MRS medium with 1.5% agar. The antibiotic concentration used for the selection of lactobacilli transformants was 10 μg/ml of chloromycetin (Cm; Sigma). Porcine rotavirus JL94 (belonging to P[7]) was conserved in the laboratory. Mice Balb/c mice (female)

weighing 25-30 g (7 weeks of age) were obtained from the inbred colony maintained at the Harbin Veterinary Research Institute. Each experimental and control group consisted of 10 mice. The animals were fed balanced rodent food and water ad libitum. The mice were handled and maintained under strict ethical conditions according to the international recommendations for animal welfare and the Ethical Committee for animals sciences of HeiLongJiang province (032/2006).

Mouse anti-VP4 antibodies The mouse anti-VP4 antibodies used in Western-blot and immunofluorescence analysis had been prepared and stored in our laboratory. The recombinant plasmid VP4-pGEX-6P-1 was constructed and transformed click here into E. coli BL21(Yan Song). The recombinant strain was induced with IPTG. The serum was obtained from the Balb/c mice immunized with the purified VP4 protein. Western-blot test and neutralization test circumstantiate the expressed protein has biological activity(data not shown). Expression plasmid construction The pPG612.1 plasmid is an expression vector containing an ssUsp signal peptide secretion sequence (kindly supplied by Jos Seegers, NIZO, The Netherlands). Nucleic acid manipulation and cloning procedures were performed according to standard procedures [42]. All DNA manipulations were performed according to standard procedures [43]. A gene fragment about 756 bp (VP8) encoding the main structural polypeptide of VP4 (obtained from the genome of PRV strain JL94) was amplified by polymerase chain reaction (PCR) using forward primer 5′-CAGGGATCCAATGGCTTCGCTCA-3′(BamHI site underlined) and the reverse primer 5′-GGCCTCGAGAGCTCTTGTGTGCA-3′(XhoI site underlined) (Figure 8).

Tukey’s honestly significant difference (HSD) was performed in th

Tukey’s honestly significant difference (HSD) was performed in the event of a significant F ratio. Two-tailed statistical significance was accepted at p < 0.05. When significant differences are stated, the mean difference plus the 95% confidence interval (CI) of the mean difference are provided [10]. Results Acid-Base Balance There were

significant interactions (p < 0.01) and main effects for condition (p < 0.001) and time (p < 0.001) for all acid-base variables (pH, , & BE). Decomposition of the interactions indicated significant elevation in blood alkalosis for only the B condition when compared to both P and EG from 15 to 120 min during the this website ingestion period (Figure 1). Across this time frame, mean differences between pH for the B and EG trials were 0.013 (smallest) to 0.045 (largest) with 95%CI ranging between 0.01 to 0.07. This distribution was similar between the B and P trials (mean difference between 0.010 (smallest) to 0.040 selleck inhibitor (largest) with 95%CI ranging between 0.01 and 0.06). Following this profile, changes between B and EG trials ranged from the smallest selleck mean difference of 1.6 mmol·L-1 to the largest of 4.3 mmol·L-1 (95%CI between 0.01 to 5.98 mmol·L-1), while B

and P trials followed a similar pattern (smallest mean difference = 1.3 mmol·L-1; largest mean difference = 4.2 mmol·L-1; 95%CI between 0.4 to 5.9 mmol·L-1). Finally, base excess changes between the B and EG trials ranged from the smallest mean difference of 3.8 meq·L-1 to the largest of 4.6 meq·L-1 (95%CI between 0.13 to 6.24 meq·L-1), while B and P trials again were similar (smallest mean difference = 2.4 meq·L-1; largest mean difference = 3.9 meq·L-1; 95%CI between 0.7 to 5.5 meq·L-1). Figure 1 Represented are the acid-base responses for

Energised Greens™ (9 g) (EG), 0.1 g·kg -1 BW sodium bicarbonate (NaHCO 3 ) or flour placebo (Placebo) conditions over 120 min RANTES post ingestion. For all three acid-base variables, only the NaHCO3 condition resulted in significant elevation (*) in blood alkalosis between 15 and 120 min (p < 0.01) when compared to both Placebo and EG. GI Discomfort A large degree of intra-subject variability was evident in both the incidence and severity of GI discomfort (Figure 2). There were no significant interactions (p > 0.98) or main effects for condition (p > 0.80) or time (p > 0.57) for either incidence or severity. Figure 2 Represented in the following figure are mean ± SD scores for both incidence and severity of symptoms over 120 minutes after ingestion of either Energised Greens™ (9 g) (EG), 0.1 g·kg -1 BW sodium bicarbonate (NaHCO 3 ) or flour placebo (Placebo). Conclusions The aim of the current investigation was to profile the differences in acid-base response following both acute fruit and vegetable extract (EG) consumption and a standard, low dose of sodium bicarbonate. Our findings suggest that acute EG supplementation only induces minimal blood alkalosis (Figure 1).

In conclusion, distinct solid tumor cells secrete GRP-78 thereby

In conclusion, distinct solid tumor cells secrete GRP-78 thereby gaining resistance to bortezomib. These learn more findings describe a hitherto unknown mechanism of resistance to proteasome inhibitors and may offer a novel strategy to increase

the susceptibility of solid tumor cells to bortezomib. Poster No. 154 The Effect of Platycodin D on Breast Cancer-Induced Bone Destruction Sun Kyoung Lee 1,2 , Kwang-Kyun Park1,2, Yeong-Shik Kim3, Young-Wan Ha3, Won-Yoon Chung1,2 1 Department of Oral Biology, Oral Cancer Research Institute, Oral Science Research Institute, Brain Korea 21 Project, College of Dentistry Yonsei University, Seoul, Korea Republic, 2 Department of Applied Life Science, The Graduate School, Yonsei University, Seoul, Korea Republic, 3 Natural Products Research Institute, College of Pharmacy, Seoul National University, Seoul, Korea Republic Breast cancer is the most common cancer

affecting women in the United States and other countries. In individuals with breast cancer, the MNK inhibitor frequency of bone metastasis is much higher than other organ metastases. Breast cancer cells secrete osteolytic factors, such as parathyroid hormone-related protein (PTHrP), interleukin (IL)-1β, -6 and -11. These factors stimulate stromal/osteoblastic cells to over-express receptor activator of nuclear factor-kappa B ligand (RANKL), which is required to induce osteoclast CH5424802 concentration formation/activation. Over-expression of RANKL results in increased osteoclast formation and bone resorption. The subsequent bone resorption induces the release of various growth factors from the bone matrix, such as transforming growth factor (TGF)-β, insulin-like growth

factor Cytidine deaminase (IGF)-Iand -II. The released growth factors stimulate the proliferation of cancer cells. The interaction between tumor cells and bone cells, called to ‘vicious cycle’, is crucial for the initiation and promotion of skeletal metastasis. We found that platycodin D (PD), a major constituent of triterpene saponins found in the root of Platycodon grandiflorum, inhibited the viability of human breast cancer MDA-MB-231 cells, in a dose-dependent manner. However, PD did not influence the secretion of osteolytic factors in MDA-MB-231 cells and RANKL/OPG ratio in osteoblasts treated with conditioned media of MDA-MB-231 cells. PD suppressed RANKL-induced osteoclast formation/activation through down-regulation of c-Fos and nuclear factor of activated T cells 1 (NFATc1) in mouse bone marrow-derived macrophage (BMM) cells. PD also induced apoptosis in osteoclasts. Consistent with the in vitro effect, PD showed the inhibitory effect on tumor growth and tumor-induced bone destruction in vivo.

maltophilia by electrospray ionization mass spectrometry (ESI-MS)

maltophilia by electrospray ionization mass spectrometry (ESI-MS) and gas chromatography and mass spectrometry (GC-MS analysis) [7]. Functional analysis of rpfF or rpfC mutants in different bacterial species suggests that the general Selleckchem BVD-523 role of the DSF-signaling system in the modulation of virulence seems to be conserved, but the regulatory mechanisms and DSF-dependent traits may differ among taxa [8, 15–17]. Xanthomonas oryzae pv. oryzae (Xoo) is a causal

agent of bacterial blight disease of rice [18]. Xoo enters either through wounds or hydathodes, XAV-939 clinical trial multiplies in the epitheme and moves to the xylem vessels where active multiplication results in blight disease symptoms on rice leaves. Similar to Xcc, Xoo also produces a range of virulence factors, including EPS, extracellular enzyme, iron-chelating siderophores, and the Sepantronium nmr type III-secretion dependent effectors, which are collectively essential for virulence [19–23]. Null mutation of rpfC in Xoo wild type strain T3000 substantially affects the EPS synthesis and virulence [24]. The rpfF mutants of an Indian Xoo wild type isolate BXO43 are attenuated in virulence and defective in

growth under low iron conditions [15]. More recently, a report showed that mutations in the core rpf genes rpfB, rpfF, rpfC and rpfG reduced the EPS levels, xylanase activity, motility, and virulence of Xoo strain KACC10331 [25]. These findings suggest that DSF signalling

system in Xoo much is involved in the regulation of virulence factor production. However, little is known about the chemical structure of the DSF-family signals in Xoo and the factors influencing the signal production. In this study, the comparative genomics analysis revealed that Xoo genome shares the key components of DSF biosynthesis and signalling with Xcc. The DSF production assay of rpfF, rpfC, rpfG mutants showed that Xoo uses a similar autoregulation mechanism as Xcc to control DSF biosynthesis. We further found that Xoo produces three DSF-family signals: DSF, BDSF and a novel signal with two double bonds, which was designated as CDSF. All the three DSF-family signals induce the EPS production and extracellular xylanase activity in the rpfF mutant of Xoo with variable efficiencies. Moreover, we found that the production and the ratio of the DSF-family signals are affected by the culture medium composition. Results Xoo uses the similar mechanism of Xcc in autoregulation of DSF biosynthesis In Xcc, the rpf cluster is involved in DSF biosynthesis, signal sensing and response. RpfF, a putative enoyl-CoA hydratase, is a key enzyme involved in DSF biosynthesis and mutation of rpfF abolishes DSF production [4]. RpfC negatively controls DSF biosynthesis by binding to RpfF at low cell density [10], and disruption of rpfC results in a 16-fold higher DSF accumulation than the wild-type Xcc [5, 11].

After being rinsed with deionized water, they were soaked in etha

After being rinsed with deionized water, they were soaked in ethanol for 30 min, rinsed with deionized water again, and dried in the oven at 50°C for 30 min. Then, an Au film whose thickness was about 50 nm was deposited on

the substrate. High-purity Zn powders (99.999%) were placed in the quartz boat, and then, the quartz boat was put in the center of the tube furnace. The substrate was placed about 5 cm away from the quartz boat. Previous to the growth, the tube furnace was pumped to 5 Pa. Subsequently, the temperature of tube furnace was raised to 650°C for 30 min under the protection of Ar (120 sccm). Then, O2 (80 sccm) was introduced into the furnace. The growth lasted for 40 min. Then, the whose system was cooled to 25°C. After that, the ZnO C188-9 in vivo nanorod arrays were grown on the surface of the stainless steel mesh. find more Lastly, the as-prepared sample was stored in the dark room for 2 weeks before it was measured. selleck inhibitor The surface morphology of the ZnO nanorod was studied using scanning electron microscope (SEM, Hitachi S4700, Chiyoda-ku, Japan). The phase identification of the ZnO nanorod was carried out with X-ray diffraction (XRD, Cu Kα). The contact angles on the as-grown sample were measured by contact angle meter (DSA100, KRÜSS, Hamburg, Germany).

Results and discussion Figure 1 indicates the SEM images of the as-grown sample. As shown in Figure 1a, the surface of stainless steel mesh was covered uniformly with the ZnO nanorod arrays.

It can be found that the highly uniform and densely packed ZnO nanorods were grown on a stainless steel wire; the average diameter of the ZnO nanorod is about 85 nm (Figure 1b,c). Figure 1d shows the cross-sectional view of the ZnO nanorod arrays. We can found that the ZnO nanorod arrays are almost vertical to the surface of the stainless steel wire, and the heights are about 4 μm. Figure 2 shows the XRD pattern of the ZnO nanorod arrays coated on stainless steel mesh. Three peaks (100), (002), and (101) can be deduced. The intensities of (100) and (101) peaks are much lower than the (002) peak. Dehydratase This indicates that the as-grown sample is a polycrystalline wurtzite ZnO and along [001] direction. Figure 1 SEM images of the as-grown ZnO nanorod arrays on the stainless steel mesh. (a) Large-area view of the coated mesh, (b) top images of the ZnO nanorod arrays on a stainless steel wire, (c) high-magnification ZnO nanorod arrays on a stainless steel wire, and (d) SEM side views of the ZnO nanorod arrays with height about 4 μm. Figure 2 XRD patterns of the as-grown sample. The slow-growing planes usually have low surface free energy [18]. The growth rates of the ZnO crystal were reported to be [−100] > [−101] > [001] ≈ [00–1] [19]. Figure 2 shows that the surface of the ZnO nanorod is the (001) plane.

05); these observations correlated

with a significant red

05); these observations correlated

with a significant reduction in lesion intensity (p < 0.001) on mushrooms treated with 2.9 × 106 and 1.4 × 107 PFU B. bacteriovorus Nutlin-3a clinical trial HD100 (mean = 0.010 1/PV in both cases) compared with mushrooms inoculated with P. tolaasii 2192T alone (mean = 0.014 1/PV). Despite this significant reduction in lesion intensity, the total number of CFU recovered from B. bacteriovorus HD100 treated mushrooms onto King’s Medium B was high, suggesting that the bacteria recovered from seemingly similar, beige-coloured colonies on the King’s Medium B plates were not solely pathogenic P. tolaasii 2192T, but might include other species indigenous to the mushroom pileus surface that are not well preyed upon by B. bacteriovorus HD100, as observed in SEM images of mushroom tissue to which King’s medium B broth was added alone. Figure 4 Bacterial CFU numbers recovered from P. tolaasii -inoculated mushrooms in the presence and absence of Bdellovibrio . Lesion intensities and number of bacterial colony forming units (CFU) recovered from mushroom pilei subject to three different treatments detailed to the right. Each P. tolaasii

2192T inoculation contained 1.7 × 106 CFU. Images of mushrooms with typical: high, mean, and low intensity lesions in each group are shown below the graph. Horizontal black bars indicate the mean values for Crenolanib mouse lesion intensity/CFU count in each treatment group. Student’s t-test of significance between B .bacteriovorus-treated and non-treated mushrooms inoculated with P. tolaasii 2192T: *p <0.05, ***p <0.001. Enterobacterspecies are present on the surface of some commercially produced supermarket mushrooms The number of CFU recovered from the mushrooms that were treated with B. bacteriovorus HD100 after inoculation

with P. tolaasii was relatively high compared to mushrooms inoculated with P. tolaasii alone. To confirm the identity of the bacteria seen in Figures 3d and e and recovered from supermarket mushroom tissue pre-treated with B. bacteriovorus HD100 before P. tolaasii 2192T at both 2.9 × 106 and 1.4 × 107 PFU ml−1, 20 colonies taken from the King’s medium B agar plates used to enumerate bacterial CFU, recovered from the treated mushroom tissue of two mushrooms in each group, were grown on buy PF-02341066 Coliform Chromogenic agar (oxoid). This agar contains two chromogenic substrates that turn almost purple when cleaved by the enzymes glucorinidase and galactosidase, which are both present in coliforms such as E. coli, and absent from Pseudomonads (including P. tolaasii); all 20 colonies were pigmented purple indicating them as coliform, closely related to E. coli, and therefore as indigenous species to the mushroom pileus, and distinctly different to P. tolaasii 2192T , which produced straw coloured colonies on the agar. Three of these coliform isolates were identified by 16 s rDNA sequencing as members of the Enterobacter genus using the BLAST online tool (http://​blast.​ncbi.​nlm.​nih.​gov/​Blast.

1 – 5% of culturable

1 – 5% of culturable

buy Ferrostatin-1 soil bacterial species can carry out denitrification [34]. This conclusion is supported by our BLASTN results, which found only two sequences from either metagenome that matched with a N metabolism gene. With the BLASTX comparison to the SEED BAY 11-7082 database, however, over 1% of our sequences from each metagenome matched with nitrogen metabolism subsystems. The fact that we found no differences in nitrogen metabolism EGT relative abundance after NO3- addition suggests that microbial populations involved in N cycling did not shift in the 20 hours following exposure to a NO3- pulse. This lack of treatment response could be due to insufficient time between treatment initiation and sampling (i.e. populations were slow to respond to selleck chemical the treatment). However, we did see other EGT changes, suggesting that some microbial populations grew and experienced a detectable community shift in response to acute changes in NO3- concentration. The initial microbial community response to NO3- in our metagenomes was toward organisms that contained stress response, carbohydrate, and fatty acids, lipids, and isoprenoid EGT matches (Figure 1). The stress response EGT that was higher in the +NO3- metagenome was for an alkyl hydroperoxide reductase subunit C-like protein. The gene

for alkyl hydroperoxide reducates, subunit C is upregulated by NO3- exposure after only 30 minutes in Desulfovibrio vulgaris, suggesting that such increases in this and other oxidative stress genes may be a general stress response by the bacteria [35]. Within the carbohydrates category, one EGT match that was higher in the +NO3- metagenome was for fermentation. Recently, there has been evidence for fermentation that is coupled to NO3- reduction in both bacteria and fungi [36, 37]. Fermentation in the +NO3- microcosms may have been particularly prominent for the fungi, because a switch to NO3- -coupled fermentation as the primary source of energy for soil fungi under anoxic conditions has been suggested [36]. The sequencing effort described here

also showed changes to the proportional representation of taxonomic EGTs. There were highly significant increases in the relative abundance of Alphaproteobacteria and Acidobacteria EGTs in the +NO3- metagenome. Similarly, using freshwater microcosms, Barlett and Leff [38] found an increase in Alphaproteobacteria abundance when NO3- was present as a N source and suggested a competitive advantage to this group of organisms under these conditions. Under anoxic conditions, such as our microcosms, higher physiological activity and substrate uptake have been reported in several Alphaproteobacteria species when NO3- or NO2- were present as an electron acceptor [39]. Therefore, in our microcosms, there could have been a competitive advantage to the Alphaproteobacteria due to greater growth compared to other facultative organisms in an anoxic environment with abundant NO3-.

The superoxide dismutase

(SOD) identified as interacting

The superoxide dismutase

(SOD) identified as interacting with SSG-1 belongs to a family of enzymes that catalyze the dismutation of oxygen radical to hydrogen peroxide eliminating superoxide anions generated in aerobic respiration [47, 48]. Many SOD genes have been identified in fungal genomes [49]. SODs have been shown to contribute to growth and survival of fungi under oxidative stress conditions, specifically inside macrophages. In C. neoformans, SOD1 mutants were observed to be less virulent while SOD2 mutants had increased susceptibility to oxidative stress and showed decreased growth at elevated temperatures [50, 51]. Virulence in C. neoformans variety gattii has been reported to be dependent on both SOD1 and SOD2 [32, 33]. In C. albicans the null mutant of mitochondrial SOD2 was more sensitive than wild-type cells to stress [52] Fedratinib and the SOD1 null mutant had attenuated virulence [53]. S. schenckii superoxide dismutases have not been studied. In fact, this is the first report of the presence of a member of this protein family in this fungus. Analysis of the amino acid sequence of SsSOD against the Homo

sapiens database using BLAST shows that it is homologous to the human manganese superoxide dismutase SOD2 family with 32% identity. This same analysis, using the fungal databases revealed that SsSOD is phylogenetically selleck compound closely related to SODs of the filamentous fungi with the sequence identity being in the range of 23-43%.

Also SsSOD has a calculated molecular Vorinostat weight of 35.44 kDa, very close to that of other fungal homologues. The specific role of SOD2 in S. schenckii stress and pathogenesis has yet to be addressed. Fungal SODs have two main locations: cytosolic or mitochondrial [49]. Analysis using PSORT II [39] and TargetP [40] suggests that SsSOD isolated by the yeast two-hybrid analysis is a mitochondrial SOD. Being a mitochondrial protein does not disqualify SsSOD as an interacting partner of SSG-1. It is important to note that Gαi subunits can be present not only in the cytoplasm but also in the mitochondria [54]. Also, SODs acquire the metal ion during protein synthesis and this seems to occur in the cytoplasmic face of the mitochondrial membrane. It is also of interest Resminostat to note that another mitochondrial protein was also found to interact with SSG-1 (unpublished results). This protein belongs of the mitochondrial metal transporter protein family (Mtm family) that is known to be involved in the acquisition of the metal ion by SODs [55, 56]. These results together with the interactions of SSG-1 and the metal ion transporters SsNramp and SsSit, discussed below suggest a possible role of SSG-1 in SODs metal acquisition. Metals are essential nutrients and important co-factors of a variety of proteins and enzymes; they are required for the survival of all organisms. Fungi have developed multiple strategies to acquire metals from the environment [57].

The reduced fungal burden indicates that the aPDT treated cells a

The reduced fungal burden indicates that the aPDT treated cells are potentially damaged and thus the survival might be altered by the addition of another cell membrane directed bombarding compound, a structure important for the maintenance of cell wall integrity. Hence, we investigated the effects of combined treatment of aPDT with fluconazole, a compound that targets P450 and affects ergesterol synthesis, a major component of the cell membrane. This antifungal agent is used extensively because of its low host toxicity to treat fungal infections. One of the mechanisms that can be used by C. albicans to develop resistance

selleck chemical to fluconazole is related to the overexpression of cell membrane multidrug efflux systems [23, 24]. Based on the hypothesis that aPDT could damage the cell membrane of C. albicans, producing

increased membrane permeability [25] and possibly damaging efflux pumps, we used G. mellonella-C. albicans system to Lazertinib mw assess the sequential combination of PDT with fluconazole. G. mellonella were inoculated with 1.41 × 106 CFU/larva to infect the larvae with the fluconazole-resistant C. albicans strain (C. albicans Can37). Larvae treated only with PDT or only NCT-501 with fluconazole did not show significantly prolonged larval survival. The sequential combination with fluconazole, before or after PDT, significantly increased larvae survival in both assays (Figure  4). These results suggest that aPDT increases PD184352 (CI-1040) the susceptibility of C. albicans Can37 to fluconazole. Figure 4 Killing of G. mellonella larvae after infection by C. albicans Can37 fluconazole resistant. The larvae received an injection of 1.4x106CFU/larva and were maintained at 37°C. a) administration of fluconazole (14 mg/kg) or PBS (Control), b) antimicrobial PDT or only MB (Control), c) administration of fluconazole

followed by aPDT in a combined therapy or PBS (Control), d) administration of aPDT followed by fluconazole in a combined therapy or PBS (Control), e) administration of aPDT or fluconazole + PDT, f) administration of aPDT or fluconazole + PDT. There was no significant difference on larvae survival when treatment was done only by injecting of fluconazole (P = 0.584) or aPDT alone (P = 0.102). The combined treatment by application of aPDT followed or before fluconazole injection resulted in significantly lower death rates when compared to a control groups (P = 0.0010 to aPDT followed by fluconazole, and P = 0.0018 when aPDT was applied after fluconazole injection). A significant difference in survival was observed for combined treatment compared to aPDT alone (P = 0.0062 for aPDT followed by fluconazole, and P = 0.0068 when aPDT was applied after fluconazole injection). Discussion and conclusion In this study we used the invertebrate model G. mellonella for the in vivo study of antifungal PDT. We verified that aPDT prolonged the survival of G. mellonella caterpillars infected by C.

The availability of molecular tools will prompt and yield a large

The availability of molecular tools will prompt and yield a large number of new and highly interesting results in the near

future. Acknowledgements I am very grateful to Prof. Dr. K. Hyde (Mae Fah Luang University, Thailand) for initiating this review and for his suggestions to improve the manuscript. Prof. Dr. J.Y. Zhuang and Prof. Dr. L. Guo (Institute this website of Microbiology, Chinese Academy of Sciences, China) are acknowledged for the identification of my collections of rusts and smuts respectively. Prof. Dr. M. Piepenbring (J. W. Goethe-Universität Frankfurt, Frankfurt/Main, Germany) is acknowledged for providing an image of Entorrhiza casparyana. This study was supported by the Joint Funds of the National Natural Science Foundation of China and Yunnan Provincial Government (No. U0836604), the National Basic Research Program of China

(No. 2009CB522300), and the Hundred Talents Program of the Chinese Academy of Sciences. Open Access This article is distributed under the terms SC79 solubility dmso of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited. References Aanen DK, Eggleton P, Rouland-Lefèvre C et al (2002) The evolution of fungus-growing termites and their mutualistic fungal symbionts. Proc Natl Acad Sci USA 99:14887–14892PubMed Agnarsson I, Kuntner M (2007) Taxonomy in a changing PDK4 world: seeking solutions for a science in crisis. Syst Biol 56:531–539PubMed

Aime MC, Matheny PB, Henk D et al (2007) An overview of the higher-level classification of Pucciniomycotina based on combined analyses of nuclear large and small subunit rDNA sequences. Mycologia 98:896–905 Ainsworth GC, Sparrow FK, Sussman AS (eds) (1973) The fungi, an advanced treatise. Vol. IV B, a taxonomic review with keys: basidiomycetes and lower fungi. Academic, New York Albee-Scott SR (2007) Does secotioid inertia drive the evolution of false-truffles? Mycol Res 111:1030–1039PubMed Bartnicki-Garcia S (1968) Cell wall chemistry, morphogenesis, and taxonomy of fungi. Annu Rev Microbiol 22:87–108PubMed Bas C (1975) A comparison of Torrendia(Gasteromycetes)with Amanita (Agaricales). In: Bigelow HE, Thiers HD (ed.) Studies on higher fungi. Nova Hedwigia Beiheft 51:53–60 Bauer R, Oberwinkler F, Vánky K (1997) Ultrastructural markers and ACY-738 mouse systematics in smut fungi and allied taxa. Can J Bot 75:1273–1314 Bauer R, Begerow D, Oberwinkler F et al (2001) Ustilaginomycetes. In: McLaughlin DJ, McLaughlin EG, Lemke PA (eds) The Mycota. VII (B). Systematics and evolution. Springer, Berlin, pp 57–83 Bauer R, Begerow D, Sampaio JP et al (2006) The simple-septate basidiomycetes: a synopsis. Mycol Prog 5:41–66 Begerow D, Göker M, Lutz M et al (2004) On the evolution of smut fungi on their hosts.