25) (7.69) NONE NONE NONE lprN [Rv3495c] C798T C1016A [GenBank: HQ901094] Thr339Lys Ala266Ala (26.47) (29.09) (30.9) (31.57) (31.07) mce4F [Rv3494c] C117A C1214T [GenBank: HQ901087] Pro405Lys Thr39Thr (8.75) (9.09) (7.3) (10.52) (5.09) Frequency of single nucleotide polymorphisms detected in the genes of mce4 operon. The nucleotide

changes and the corresponding changes Staurosporine research buy in amino acids are shown here. The frequency of SNPs was Cell Cycle inhibitor calculated from 112 clinical isolates. The data has been subdivided according to the drug susceptibility profile. The single letter nucleotide designations used are as follows: A, adenine; C, cytosine; G, guanine and T, thymidine. The three letter amino acid designations used are as follows Ala, alanine; Ile, isoleucine; Pro, proline; Val, valine; Gly, glycine; Phe, phenylalanine; Compound C Thr, threonine; Arg, arginine; Ser; serine; Gln, glutamine and Lys, lysine. DS: drug sensitive, DR: drug resistant, SDR: single drug resistant, MDR TB: Multi drug resistant Effect of SNPs on codon usage in mce operons The preferential usage of codons for different amino acids in various organisms including M. tuberculosis is well known. The codon bias influences the translational efficiency in these organisms [15]. Therefore, we analysed the codon usage in M. tuberculosis for synonymous changes observed in both mce1 and mce4 operons. Analysis revealed that codons of amino acids were changed to the

next preferred codon (Table 3). It is possible that such altered preference for certain codons would alter the expression of the respective proteins. Table 3 Codon usage in mce1 and mce4 operons Operon Gene name (Accession Number) Wild type codon Polymorphic codon mce1 operon mce1A [Rv0169] TAC TA T   yrbE4A [Rv3501c] GCG ATC GC T AT A mce4 yrbE4B [Rv3500c] ATC CCC AT T CC T operon mce4A [Rv3499c] TTC TT T   lprN [Rv3495c] GCC GC T   mce4F [Rv3494c] ACC AC A The codon usage in the polymorphic regions is shown here. The synonymous changes in the nucleotide sequence, when analysed bioinformatically through Gene Runner software version 3.05 (Hastings Software, Inc.) next predicts the usage of less preferred codon which could reflect

upon the expression efficiency of the protein encoded by the gene. Nucleotide highlighted in bold indicates the altered nucleotide. Prediction of functional consequences of nonsynonymous SNPs by PolyPhen and PMut servers The functional impact of 12 nonsynonymous SNPs in proteins of mce1 and mce4 operons was analyzed using PolyPhen http://​genetics.​bwh.​harvard.​edu/​pph/​ and PMut http://​mmb2.​pcb.​ub.​es:​8080/​PMut/​ servers. Of the 12 nonsynonymous SNPs studied, 5 nonsynonymous SNPs were predicted to be deleterious to the organism by both PolyPhen and PMut programs. These nonsynonymous SNPs were located in the genes yrbE1B [Rv0168] (NN output; 0.84, PSIC score; 1.6), mce1A [Rv0169] (NN output; 0.84, PSIC score; 2.04), mce1B [Rv0170] (NN output; 0.59, PSIC score; 1.

Figure 2 The total bacterial composition

from eight intestinal tissue samples by 16S rRNA gene clone library. The γ-Proteobacteria dominated the total bacterial composition whereas the class Clostridia only accounted for a total of 7.1% Figure 3 Overview and diversity of the bacterial composition by clone library analysis. a) Shannon’s diversity index on phylum level divided the NEC infants in two groups. This difference could not be explained by antibiotic Aurora Kinase inhibitor treatments or the severity of the necrotizing enterocolitis b) The bacterial 16S rRNA gene composition from each of the eight necrotic intestinal tissue samples. Bacterial groups whose abundance were more than 10% in any sample are shown as bars. Enterococcus and Escherichia spp. were the most abundant in the samples with a low Shannon SBE-��-CD nmr diversity index where Ralstonia sp. was the most frequent group of species in the samples with a high Shannon index. The bacteria associated with the tissue in the individually neonates have the potential to reveal bacterial pathogens related to

the pathogenesis of NEC. In the δ-proteobacteria group Escherichia/Shigella genera dominated with a frequency of 45% out of all δ-proteobacteria and were present in 5 of medroxyprogesterone the 8 neonates with an average frequency of 24% (±36%). The Enterobacteriaceae group consisted of virtually one tag but it was similar to genera of Citrobacter, Enterobacter

(Klebsiella) and Erwinia and was Autophagy Compound Library supplier detected in 4 of the neonates. The taxonomic class Clostridia contained 10 different tags belonging to a variety of different genera (Table 4), the two most prominent being Clostridium and Anaerococcus detected in four and three neonates, respectively. A tag matching the potential pathogen Finegoldia was found twice in two different neonates. One of the specimen characterised histologically exhibiting pneumatosis intestinalis was also observed to include the genus Clostridium. The most prevalent tag belonged to Ralstonia being present in 7 out of 8 neonates, with an average of 9% (±5%). R. detusculanense, R. pickettii and R. insidiosa were revealed with more than 99% similarity (Figure 4). Figure 4 Phylogenetic relationship among Ralstonia detected in the tissue samples from the NEC infants. R. detusculanense, R. pickettii and R. insidiosa did all have more than 99% similarity with the matched Ralstonia tag from the 16S rRNA gene clone library from this study. The bacteria names and the accession numbers are shown.

H. capsulatum is a fungal pathogen that affects a wide range of mammal species, including the human. Autochthonous clinical cases have been reported between the latitudes 54° 05′ North (Alberta, Canada) and 38° South (Neuquén, Argentina) [1, 2]. The disease associated with this fungus is relevant in the geographical areas where histoplasmosis is endemic or epidemic, such

as the Missouri, Ohio, and Mississippi river valleys, in the United States of America MEK inhibitor clinical trial (USA), and some Latin American countries with a high frequency of outbreaks [3, 4]. In Mexico, histoplasmosis is widely distributed and case reports are rather variable [4]. Infection is caused by the inhalation

of fungal saprobe mycelial-phase propagules (infective form) that develop in special environments and are mainly found in bat guano accumulated in confined spaces such as caves and abandoned mines and buildings. The potential role of bats in spreading H. capsulatum in nature remains unclear. The high risk of natural bat infection with this fungus in Mexican caves has been well-documented [5–8]. According to their genetic diversities, H. capsulatum isolates from different geographical origins have been grouped into eight clades; seven of which are considered phylogenetic species. Among these, highlight the LAm A clade that harbours significant genetic variability Selleckchem MAPK inhibitor [9]. The genus Pneumocystis contains highly diversified fungal pathogens that are harboured by a wide range of mammal hosts [10–16]. Pneumocystis organisms, which are transmitted via host-to-host airborne route, have a marked host-species-related ZD1839 purchase diversity that is associated with close host specificity. The high divergence

among Pneumocystis species most likely resulted from a prolonged process of co-evolution with each mammal host, mostly associated with co-speciation, as suggested by Demanche et al. [12] and Hugot et al. [13]. Although most phenotypic and genotypic data supporting Pneumocystis stenoxenism derives from Selleckchem Brigatinib laboratory animal models or captive animals, reports about Pneumocystis prevalence and circulation in wild fauna are scarce [12–16]. Unpublished preliminary data by our team revealed H. capsulatum and Pneumocystis co-infection in two randomly captured bats, identifying these mammals as probable reservoirs and dispersers of both parasites in nature (Dei-Cas E and Taylor ML, comm. pers.). The study of co-infection systems, where the host (i.e. a wild host) usually harbours two or multiple parasites, requires an in-depth investigation to determine a comprehensive understanding of this multi-infectious process in regards to its dynamics and consequences. H.

Plant J.2002,32:375–390.PubMedCrossRef 32. Jacobs AK, Lipka V, Burton RA, Panstruga R, Strizhov N, Schulze-Lefert P, Fincher GB:An Arabidopsis callose synthase, GSL5, is required for wound and papillary callose formation. Plant Cell.2003,15(11):2503–2513.PubMedCrossRef 33. Qutob D, Kamoun S, Gijzen M:Expression of a Phytophthora sojae necrosis-inducing protein occurs during transition from biotrophy to www.selleckchem.com/products/apr-246-prima-1met.html necrotrophy. Plant J.2002,32:361–373.PubMedCrossRef

34. Guide to GO Evidence Codes[http://​www.​geneontology.​org/​GO.​evidence.​shtml] 35. Kamoun S, van West P, Vleeshouwers VG, de Groot KE, Govers F:Resistance of Nicotiana benthamiana to Phytophthora infestans is mediated by the recognition of the elicitor protein INF1. Plant Cell.1998,10(9):1413–1426.PubMedCrossRef

36. Torto-Alalibo TA, Collmer CW, Lindeberg M, Bird D, Collmer A, Tyler BM:Common PDGFR inhibitor and contrasting themes in effectors from bacteria, fungi, oomycetes and nematodes. BMC Microbiology2009,9(Suppl 1):S3.PubMedCrossRef 37. Lindeberg M, Biehl BS, Glasner JD, Perna NT, Collmer A, Collmer CW:Gene Ontology annotation highlights shared and divergent pathogenic strategies of type III effector proteins deployed by the plant pathogen Pseudomonas syringae pv tomato DC3000 and animal pathogenic Escherichia coli strains. BMC Microbiology2009,9(Suppl 1):S4.PubMedCrossRef 38. White FF, Yang B, Johnson LB:Prospects for understanding avirulence gene function. Curr Opin Plant Biol.2000,3(4):291–298.PubMedCrossRef 39. Roulston A, Marcellus RC, Branton PE:Viruses and apoptosis. Annu Rev Microbiol.1999,53:577–628.PubMedCrossRef 40. Gao L-Y, Kwaik YA:The modulation of host cell apoptosis by intracellular bacterial pathogens. Trends Microbiol.2000,8(7):306–313.PubMedCrossRef 41. Fischer SF, Vier J, Müller-Thomas C, Häcker G:Induction of apoptosis by Legionella pneumophila in mammalian cells GSK2126458 molecular weight requires the mitochondrial pathway for caspase activation. Microbes Infect.2006,8:662–669.PubMedCrossRef 42. Fink SL, Cookson BT:Pyroptosis and host cell death

responses during Salmonella infection. Cell Microbiol.2007,9(11):2562–2570.PubMedCrossRef 43. Rajavelu P, Das SD:A correlation between phagocytosis Temsirolimus order and apoptosis in THP-1 cells infected with prevalent strains of Mycobacterium tuberculosis.Microbiol Immunol.2007,51(2):201–210.PubMed 44. McCann HC, Guttman DS:Evolution of the type III secretion system and its effectors in plant-microbe interactions. New Phytol.2008,177:33–47.PubMedCrossRef 45. Tseng T-T, Tyler BM, Setubal JC:Protein secretion systems in bacterial-host associations, and their description in the Gene Ontology. BMC Microbiology2009,9(Suppl 1):S2.PubMedCrossRef 46. Abramovitch RB, Kim Y-J, Chen S, Dickman MB, Martin GB:Pseudomonas type III effector AvrPtoB induces plant disease susceptibility by inhibition of host programmed cell death. EMBO J.2003,22(1):60–69.PubMedCrossRef 47.

[22]. Briefly, the heights of each vertebra (i.e., anterior (Ha), middle (Hm), and posterior (Hp)) were measured by placement of six points using a

cursor R428 manufacturer and backlit digitizing board. Vertebral morphometric fractures were defined using ratios of vertebral height: the Ha/Hp (wedge) ratio, the Hm/Hp ratio, and the ratio of posterior heights of adjacent vertebrae Hpi/Hp i + 1 and Hpi/Hp i − 1 (crush). A vertebral body is considered fractured when at least one of its ratios falls below 3 SDs from normative mean values. Statistical analyses The baseline characteristics of Southern Chinese postmenopausal women who had a vertebral fracture were compared with women who did not have a vertebral fracture using t tests for continuous variables and χ2 tests for categorical variables. Logistic regression models

were applied to determine the odds ratios (OR) of vertebral fracture and the 95% CI for each SD decrease in BMD, bone mineral Adriamycin concentration content (BMC), and bone mineral apparent density (BMAD). The relationship between BMD and prevalent vertebral fracture was determined using different models with adjustment for age alone, age and body weight, and a multivariable model of risk factors. Clinical risk factors were included in the multivariable model if they were associated with vertebral fractures (p ≤ 0.1). In the PI3K Inhibitor Library multivariable model, we adjusted for age (≥65 years), body mass index (BMI < 19 kg/m2), menarche age (>14 years), years since menopause (>5 years), current smoker or drinker, daily calcium intake (<400 mg/day),

history of fracture (excluding clinical spine fracture), and fall in the last 12 months. To compare the discriminative value of various measurements, we analyzed the areas under receiver operating characteristic (ROC) curves using the C statistics. Finally, the prevalence of vertebral fractures by age and number of risk factors were determined. ROC curve analysis was conducted using MedCalc package version 9.3 (MedCalc, Mariakerke, Belgium). All statistical Tolmetin analyses were performed using SPSS for Windows version 15.0 statistical software (SPSS, Chicago, IL, USA). Results Two hundred and ninety nine (22%) subjects were found to have prevalent vertebral fractures. Table 1 summarizes the baseline characteristics of the studied subjects. Compared with women who did not have a prevalent vertebral fracture, women with prevalent vertebral fractures were older, had a later menarche age, had longer time since menopause, and had a higher prevalence of smokers and alcohol drinkers. Furthermore, these women were more likely to fall during the previous 12 months, to fracture after age of 45 years, to report clinical spine fracture, and to have BMD T-score ≤−2.5 at anyone skeletal site.

Stromata were nearly dry at collection times and may be more reddish PLX-4720 cell line brown when fresh, as suggested

by the red colour after rehydration. Dry stromata may be confounded with those of H. neorufa and H. neorufoides, which differ in a yellow colour when young, in darker and more compact dry stromata, in yellow perithecial walls, and in many culture and anamorph characteristics. The dark brown dry stromata of H. petersenii lack violet tones. T. petersenii sporulates well on all media, grows well at 30°C and grows substantially faster on all media than T. subeffusum. The large coilings on the surface of larger colonies of T. subeffusum on CMD close to the distal margin have been detected in all isolates. They have not been seen in any other Hypocrea anamorphs in Europe so far, i.e. they are characteristic for this species. In addition, T. subeffusum is one of the few species that sporulate well on CMD, but poorly on SNA. Hypocrea valdunensis Jaklitsch, sp. nov. Fig. 24 Fig. 24 Teleomorph of Hypocrea valdunensis (WU 29516). a–c. Fresh stromata. d–k. Dry stromata (d–f. immature). l. Rehydrated mature stroma. m. Stroma in 3% KOH after rehydration. n. Rehydrated stroma surface showing ostiolar openings and inhomogeneous pigment. o. Perithecium in section. p. Cortical and subcortical tissue in section.

FDA approved Drug Library concentration q. Subperithecial tissue in section. r. Stroma base in section. s. Ascus with ascospores in cotton blue/lactic acid. t, u. Hairs on stroma surface. v. Tubercular stroma surface in section. w. Stroma surface in face view. Scale pentoxifylline bars: a–c = 2 mm. d, h, j, k = 1 mm. e, f, i, m = 0.3 mm. g = 0.2 mm. l = 0.7 mm. n = 70 μm. o, r, v = 25 μm. p, q, t, u = 15 μm. s, w = 10 μm MycoBank MB 5166708 Anamorph:

Trichoderma valdunense Jaklitsch, sp. nov. Fig. 25 Fig. 25 Cultures and anamorph of Hypocrea valdunensis (CBS 120923). a–c. Cultures (a. on CMD, 19 days; b. on PDA, 19 days; c. on SNA, 21 days). d, e. Conidiation tufts (CMD; d. 27 days, stereo-microscope. e. 11 days, compound microscope, 10× SU5402 ic50 objective). f–m. Conidiophores (f–h, k–m. CMD, 6–8 days; i, j. MEA, 10 days). n. Phialides (CMD, 8 days). o–r. Conidia (o. MEA, 10 days; p. from tuft, CMD, 27 days; q, r. CMD, 6 days). a–r. All at 25°C. Scale bars: a–c = 15 mm. d, e. = 80 μm. f, g = 20 μm. h–k = 15 μm. l–n = 10 μm. o, p = 5 μm. q, r = 3 μm MycoBank MB 5166709 Differt a Hypocrea viridescente ascosporis minoribus, incremento tardiore et conidiis glabris. Ascosporae bicellulares, hyalinae, verruculosae vel spinulosae, ad septum disarticulatae, pars distalis (sub)globosa, (3.0–)3.3–3.7(–4.0) × (2.8–)3.0–3.5 μm, pars proxima oblonga, (3.5–)3.8–4.5(–5.0) × (2.3–)2.5–3.0 μm. Phialides divergentes, lageniformes, (4.5–)6–11(–14) × (1.8–)2.2–2.8(–3.2) μm. Conidia ellipsoidea vel ovalia, luteo-viridia in agaro CMD, glabra, (2.7–)3.2–3.8(–4.0) × (2.3–)2.5–2.8(–3.0) μm.

Figure 2 M. bovis BCG clearance and mycobacterial-induced lung pathology is not influenced by an established or successive T. muris infection. (A) Viable pulmonary M. bovis BCG CFU numbers at experimental AZD2014 concentration endpoint in co-infected (black) Foretinib in vivo and BCG-only (clear) infected BALB/c mice infected according to experimental design as shown in Figure 1A. Data display mean ± SEM, representing 3 individual experiments of 5–6 animals per group. (B) Viable pulmonary M. bovis BCG CFU numbers at experimental endpoint in co-infected (black) and BCG-only (clear) infected BALB/c mice infected according to experimental design as shown

in Figure 1B. Data display mean ± SEM, representing 3 individual experiments of 5–6 animals per group. (C) Viable pulmonary M. bovis BCG CFU growth curve data of co-infected (black) and BCG-only (clear) infected mice at days 14, 24 and 35 post BCG infection (D) Representative histological H&E stained lung sections captured at 10x magnification illustrating the differences in histopathology between BCG/T.muris co-infected, PF-6463922 manufacturer BCG-only infected, uninfected

and T. muris-only infected BALB/c mice infected according to experimental design as shown in Figure 1A. (E) Pulmonary histopathological scoring was performed in a blinded fashion according to the degree of peribronchiolitis (b), perivasculitis (v), interstitial pneumonitis (i) and alveolitis (a) per lung. Average pulmonary scores of BALB/c mice infected according to experimental design as shown in Figure 1A. Groups included

naive (circle), T. muris-only (diamond), BCG-only (triangle) and co-infected (square) mice. Data display mean ± SD, representing 2 individual experiments of 5–6 animals per group. P values <0.05 were considered statistically significant. (*p ≤ 0.05, ns = non significant). Previously established BCG infection delays T. muris expulsion in co-infected animals The influence of M. bovis BCG co-infection on eradication of T. muris in BALB/c mice was evaluated as worm expulsion for both experimental protocols (Figure 1A and B). In each case, susceptible IL-4KO mice with disrupted protective TH2 responses, were included as controls of delayed worm clearance [33]. Following the infection strategy in Figure 1A, the helminth burden at experimental Metformin supplier completion demonstrated that almost half (44%; 4/9) of mice with an established chronic BCG infection, that were subsequently co-infected with a low dose of helminth eggs, still presented with T. muris, whereas significantly more animals (88%; 7/8) from the T. muris-only infected group had cleared all helminths (Figure 3A). Both groups displayed significantly lower worm burdens compared to IL-4KO mice infected with T. muris only (Figure 3A). Similar results were observed in experimental repeats using a high dose of helminth eggs, showing helminth clearance in (100%; 0/9) T. muris-only infected BALB/c mice, whereas T. muris expulsion failed in (40%; 4/10) M.

The band offset between ZnO and ZnSe together with the resulted effective band gap of ZnO/ZnSe core/shell heterojunctions is favorable for improving the transport of both electrons and holes ABT-888 as well as extending the light absorption region to match the solar spectrum. Meanwhile, the staggered band alignment in type-II heterojunctions facilitates the separation of photogenerated electrons and

holes, which is an essential procedure in a photovoltaic device and quite significant to find more enhance the conversion efficiency of solar cells. In this work, we studied the optical properties corresponding to the respective excitonic band gaps of wurtzite ZnO and zinc blende ZnSe for ZnO/ZnSe heterojunctions MGCD0103 mw in the form of ZnO/ZnSe core/shell NRs. Aligned virgulate ZnO/ZnSe NRs composed of wurtzite ZnO

cores and zinc blende ZnSe shells were fabricated by pulsed laser deposition of ZnSe coatings on the surfaces of hydrothermally grown ZnO NRs. The optical properties of the samples were studied by photoluminescence (PL) measurements which show a significant reduction in the emission from ZnO and co-appearance of the near band edge (NBE) emissions of both ZnO and ZnSe. The former suggests the suppression of radiative recombination of photogenerated carriers, while the latter reveals an extended photoresponse which was further confirmed by optical transparency measurement. Both are favorable for photovoltaic applications. Methods Sample fabrication Prior to the growth of ZnO NRs, a dense nanocrystalline ZnO (NC-ZnO) film (approximately 20 nm) was first deposited on a chemically cleaned Si (100) substrate by plasma-assisted 17-DMAG (Alvespimycin) HCl pulsed laser deposition. ZnO NRs were grown on the NC-ZnO-seeded Si substrate by hydrothermal reaction. The deposition of NC-ZnO film and the growth of ZnO NRs have been described previously [13]. Serving as the cores, the prepared ZnO

NRs were transferred to a vacuum chamber and fixed on a rotating table for the deposition of ZnSe coatings as the shells. The second harmonic of a Q-switched Nd:YAG laser was used to ablate a ZnSe target after being focused by a spherical lens. The laser wavelength, pulse duration, and repetition rate were 532 nm, 5 ns, and 10 Hz, respectively. The focused laser beam with a spot size of 1.2 mm2 was incident on the target surface at an angle of 45°. The laser fluence on the target surface was 2 J/cm2. ZnSe was deposited at a base pressure of approximately 10−4 Pa for 30 min. The deposition of ZnSe coatings were performed at room temperature (RT) or at an elevated temperature of 500°C. The ZnO/ZnSe core/shell NRs obtained by depositing ZnSe at RT were annealed at 500°C in a flowing N2 atmosphere (approximately 105 Pa) for 1 h.

Following these events, most of the energy provided in the consecutive cycles is dissipated through the thin formed filaments that in turn cause their fusing via Joule heating [13]. This event occurred during the eighth and seventh cycles for the cases A and B, respectively, when there is a sharp resistance increase; their corresponding network topologies are shown in Figure 2d,k. From then on, both cases A and B experienced similar state evolution (switching events III, IV, and

V), but unlike the first two switching events (I and II), cases A and B require the same activation energy for forming and rupturing the percolation filaments in the following switching events. Detailed resistive switching events occurred at cycles 9, CAL-101 mw 10, and Crenigacestat in vivo 11 with corresponding filament distribution illustrated in Figure 2e,f,g and Figure 2m,n,o for cases A and B, respectively. Finally, both cases A and B remain at similar LRS which is consistent with the measured results, since the conductive TiO2-x is dominant in active cores after a number of programming cycles and the selleck products devices are approaching their endurance limits. It is worthy to point out that for specific switching events, the set or reset transition could be closely related to its previous state [8, 9]. Nonetheless,

as illustrated in Figure 2, the corresponding defect distributions in cycle 15 (Figure 2h,p) are Etomidate very

dissimilar for the two studied cases (A and B), yet they exhibit identical LRS. Clearly, if a reverse biasing polarity was used to reset the device in both cases to HRS, similar stochastic switching trends to the ones depicted in Figure 3 will most probably be exhibited. It should be noted that the above switching dynamics may only hold for the assumed current percolation circuit model. In practical ReRAM devices, multiple filaments may be formed and ruptured concurrently, which result in a much more complex behavior where antagonistic bipolar and unipolar switching occurs stochastically. It is also worthy pointing out that the stochastic switching characteristics could be correlated to the cell size [7] and ambient temperature [12, 13]. It is anticipated that scaling the devices in submicron dimensions would in principle restrict the defect density and distribution variances, while at the same time, heat accumulation due to ambient temperature could accelerate the switching process. Conclusion In conclusion, we have experimentally demonstrated that practical TiO2-based ReRAM devices with identical initial resistive states could exhibit very dissimilar switching dynamics. Although identical devices could possess phenomenologically similar initial states, we have demonstrated experimentally that their resistive switching occurs at different programming cycles.

It was estimated that τ trap = 180 ps and τ mig = 150 ps. This migration time is a factor of 4–5 longer than for the PSII membranes Selleck CHIR-99021 above, which contained 2.4–2.5 trimers per RC. Therefore, it is clear that the extra trimers are connected less well to the RCs. These results indicate that at the level of the thylakoid membrane trap-limited models are certainly not valid. At this point, it is also worth mentioning that different supercomplexes are functionally connected to each other and the domain size (how far does/can an excitation travel?) was estimated to be 12–24 LHCII trimers by Lambrev et al.(Lambrev et al. 2011). In (Wientjes et al.

2013) it was studied for A. thaliana how the time-resolved fluorescence kinetics depends on the distribution of LHCII over PSI and PSII. In most light conditions some LHCII is attached to PSI (at most one LHCII trimer per PSI, on average around half a trimer). PSI and PSI-LHCII contribute only to the fastest (87 ps in this study) component to which also PSII contributes. Lifetimes of 0.26 and

0.54 ns are due to PSII and are very OSI-027 similar to the lifetimes reported above, namely 0.25, and 0.53 ns (van Oort et al. 2010) The longest lifetime Torin 2 is only observed in the presence of “extra” LHCII and is for instance not found for supercomplexes or PSII membranes with only 2.5 LHCII trimers per RC (see above). Upon relocation of LHCII from PSII to PSI the relative amplitude of the 87 ps component increases at the expense of the 0.26 and 0.54 ns components. This is explained by a decreased contribution Digestive enzyme of the “extra” LHCIIs to the “slow” PSII fluorescence decay, and an increased contribution to the ~87 ps component by PSI-LHCII, thereby shortening the

average fluorescence lifetime of the thylakoids. Where to go? At the level of the individual pigment-protein complexes the functioning of the outer light-harvesting complexes of PSII seems to be relatively well understood (“”Outer antenna complexes”" section). When it comes to the PSII core, there is more uncertainty (“”The PSII core”" section, ). Different labs are able to obtain very similar experimental results on the same samples but there is strong disagreement about the interpretation. Moreover, there seem to be differences between the “performance” of core complexes in vitro and in vivo and striking differences exist between core preparations from plants and cyanobacteria, although it is generally assumed that these cores are very similar. However, the cores in plants are surrounded by outer light-harvesting complexes, which is not the case in cyanobacteria. It is clear from the work on PSII supercomplexes that the intrinsic performance of the core of PSII is improving when the supercomplexes increase in size (“”PSII supercomplexes”" section).