World Journal of Biological Chemistry 2010,1(7):209–220 PubMedCro

World Journal of Biological Chemistry 2010,1(7):209–220.PubMedCrossRef 46. Croker AK, Allan AL: Cancer stem cells: implications for the progression and treatment of

metastatic disease. J Cell Mol Med 2008,12(2):374–390.PubMedCrossRef 47. Bao S, Wu Q, McLendon RE, Hao Y, Shi Q, Hjelmeland AB, Dewhirst MW, Bigner DD, Rich JN: Glioma stem cells promote radioresistance by preferential activation of the DNA damage response. Nature 2006,444(7120):756–760.PubMedCrossRef 48. Molofsky AV, Pardal R, Morrison SJ: Diverse mechanisms regulate stem cell self-renewal. Curr Opin Cell Biol 2004, 16:700–707.PubMedCrossRef 49. Liu S, Dontu G, Mantle ID, Patel S, Ahn NS, Jackson KW, Suri P, Wicha MS: Hedgehog signaling and Bmi-1 regulate self-renewal of normal and malignant human mammary selleck compound stem cells. Cancer Res 2006,66(12):6063–6071.PubMedCrossRef 50. Korkaya H, Paulson A, Charafe-Jauffret E, Ginestier C, Brown M, Dutcher J, Clouthier SG, Wicha MS: Regulation of mammary stem/progenitor Selleck HM781-36B cells by PTEN/Akt/β-catenin signaling. PLoS Biol 2009,7(6):e1000121.PubMedCrossRef 51. Miki J, Furusato B, Li H, Gu Y, Takahashi H, Egawa S, Sesterhenn IA, McLeod DG, Srivastava S, Rhim JS: Identification of putative stem cell markers, CD133 and CXCR4, in hTERTimmortalized primary nonmalignant and malignant tumorderived human https://www.selleckchem.com/products/hmpl-504-azd6094-volitinib.html prostate epithelial cell lines and in prostate cancer specimens. Cancer Res 2007,67(7):3153–3161.PubMedCrossRef 52. Charafe-Jauffret

E, Ginestier C, Iovino F, Wicinski J, Cervera N, Finetti P, Hur MH, Diebel ME, Monville F, Dutcher J, Brown M, Viens P, Xerri L, Bertucci F, Stassi G, Dontu G, Birnbaum D, Wicha MS: Breast cancer cell lines contain functional cancer stem sells with metastatic capacity

and a distinct molecular signature. Cancer Res 2009,69(4):1302–1313.PubMedCrossRef 53. Dontu G, Abdallah WM, Foley JM, Jackson KW, Clarke MF, Kawamura MJ, Wicha MS: In vitro propagation and transcriptional profiling of human mammary stem/progenitor cells. Genes Dev 2003,17(10):1253–1270.PubMedCrossRef 54. Widschwendter M, Fiegl H, Egle D, Mueller-Holzner E, Spizzo G, Marth C, Weisenberger DJ, Campan M, Young J, Jacobs I, Laird PW: Epigenetic stem learn more cell signature in cancer. Nat Genet 2007,39(2):157–158.PubMedCrossRef 55. Al-Hajj M, Wicha MS, Benito-Hernandez A, Morrison SJ, Clarke MF: Prospective identification of tumorigenic breast cancer cells. Proc Natl Acad Sci USA 2003, 100:3983–3988.PubMedCrossRef 56. Singh SK, Hawkins C, Clarke ID, Squire JA, Bayani J, Hide T, Henkelman RM, Cusimano MD, Dirks PB: Identification of human brain tumour initiating cells. Nature 2004, 432:396–40.PubMedCrossRef 57. Galli R, Binda E, Orfanelli U, Cipelletti B, Gritti A, De Vitis S, Fiocco R, Foroni C, Dimeco F, Vescovi A: Isolation and characterization of tumorigenic, stem-like neural precursors from human glioblastoma. Cancer Res 2007, 64:7011–7021.CrossRef 58.

The WHIM descriptors

are molecular descriptors based on s

The WHIM descriptors

are molecular descriptors based on statistical indices calculated on the projections of the atoms along principal axes. They are built in such a way as to capture relevant molecular 3D information regarding molecular size shape, symmetry, and atom distribution with respect to invariant reference frames (Todeschini et find more al., 2000). In general, the obtained data indicate that hydrophobic and total molecular symmetry properties are important for antitumor activity of acridinones. These observations are in partial agreement with the data obtained by Mazerska (Mazerska et al., 1996), for which antitumor activity of imidazoacridinones is dependent on lipophilicity. However, impact of lipophilicity on the biological activity of these compounds was observed only ARS-1620 in vivo in the case of derivatives with 8-hydroxyl group, which undergo metabolic activation (Mazerska et al., 1999, 2003). Moreover, non-hydroxyl or 9-hydroxyl derivatives also exhibited lipophilic properties, but its effect was not crucial when metabolic

activation did not occur. Relocation of hydroxyl group from position 8 to 9 drastically PX-478 decreases antitumor activity (C-1311 8-hydroxyl, C-1419 9-hydroxyl). In addition, hydrophobic properties of acridinones can play important role in transport and accumulation of these compounds in cells in view of fastening of metabolic activation (Składanowski et al.,

1996). On the other hand, diaminoalkyl side chain has also crucial influence on antitumor activity of acridinones. For compounds without 8-hydroxyl group, the increase in number see more of carbon atoms between nitrogen atoms from two to three or five (C-1415, C-1176, and C-1233 two; C-1212 and C-1296 three; and C-1266 five) generally decreases antitumor activity of imidazo- and triazoloacridinones. In case of derivatives bearing 8-hydroxyl group, the increase in number of carbon atoms (C-1311, C-1263 two, C-1371 three, and C-1492 five) rather do not augment antitumor activity for imidazoacridinones, while good increase in antitumor activity is observed in case of triazoloacridinones (C-1303, C-1410 two, and C-1305 three carbon atoms).

Recently, quantitative PCR (qPCR) has been used for studying the

Recently, quantitative PCR (qPCR) has been used for studying the levels of individual indoor mold species and assay groups [18–20], but few studies have thus far explored the total indoor mycobiota using DNA-based universal community characterization methods like ribosomal DNA amplicon sequencing or metagenome analysis [21–24]. Very little is known about the effect of building characteristics on the total fungal assemblages. A recent study by Amend et al. [21] selleck products suggested that indoor fungal communities are not significantly shaped by building-specific

Epigenetics inhibitor factors like building function, ventilation system or building materials, but instead global factors like geographic location and climate are more important. Unfortunately, the presence of water damage in buildings was not included among the studied factors, even though excess water is known to be the most significant individual factor associated with elevated viable fungal counts indoors [25, 26]. The aim of the present PND-1186 concentration study was to assess the fungal communities in moisture-damaged, renovated and non-damaged buildings using culture-based

and culture-independent methods. Contaminated building materials collected from the subject buildings were analysed to determine if contaminants originating from these materials were likely to contribute to the fungal communities in the dust. In addition, we investigated the similarity of the fungal community profile revealed by sequencing, culture and a relatively large selection of targeted

qPCR assays. Results Fungal diversity and comparison of methods Fungi in dust samples A total of 1081 full-length fungal Internal Transcribed Spacer region of nuclear ribosomal DNA (nucITS) sequences were obtained from the eight dust samples. Fungal sequences clustered in 305 OTUs, of which 180 were singletons. The number of observed OTUs (corresponding roughly to fungal species) varied from 21 to 98 per sample, while the theoretical total OTU richness by ACE estimator varied from 67 to 298 per sample (Table 1). Rarefaction curves and ACE percentage coverage values indicated that mafosfamide sampling coverage was partial (Additional file 1 Fig. S1 and Table 1). Of the 305 OTUs, 33% were annotated to species, 25% to genus and 37% to class. We identified representatives of 94 genera among the OTUs that were annotated to species or genus level. Ascomycetes accounted for the majority of the total diversity in dust (52% of all OTUs, 38-88% of clones in individual libraries), the most abundant and prevalent OTUs being allied to the classes Dothideomycetes, Eurotiomycetes and Leotiomycetes. Basidiomycetes were also consistently present in the samples (44% of OTUs, 11-54% of clones), with Agaricomycetes, Exobasidiomycetes and Tremellomycetes being the most common class affiliations.

It is possible that some kinds of cell growth or division signals

It is possible that some kinds of cell growth or division signals are misread in the presence of phenol in the

colR mutant, which eventually leads to the cell lysis. In that case phenol could act as a signal, leading to the cell death, rather than being killing factor itself. Our further experiments will hopefully clarify whether phenol- and glucose-caused stresses originate from the same defect of the colR mutant or they are caused by different reasons. Conclusions Current study demonstrates the involvement of the ColRS two-component system and the TtgABC efflux pump in phenol tolerance of P. putida. Our results imply that TtgABC and ColRS systems are not directly connected ABT-888 ic50 and may affect phenol tolerance via independent pathways. Both these systems affect phenol tolerance of growing cells only but not of starving ones, indicating that ColRS and TtgABC systems affect processes occurring in metabolically active and dividing bacteria. Most tolerance mechanisms to aromatic hydrocarbons are directed toward maintaining the cell membrane intactness [2]. Given that ColRS and TtgABC systems are also implicated in membrane functions [12, 30, 38], it is reasonable to conclude that they may assist in regulation of biosynthesis and/or turnover

of membrane components, so helping to maintain membrane homeostasis during growth and division. Population structure analysis at single cell level revealed that strong cell division inhibition occurred in phenol-exposed population which check details could be considered as adaptive response to phenol stress to reduce the phenol-caused damage and to maintain membrane homeostasis. Acknowledgements We are grateful to Tiina Alamäe and Paula Ann Kivistik for critically reading the manuscript. We thank Riho Teras for plasmid pUCNotKm. Dimitri Lubenets is specially acknowledged for operating FACSAria. This work was supported by grant 7829 from the Estonian Science Foundation to R. H., and by funding of Targeted Financing Project TLOMR0031 from the Estonian Ministry of Research and Education and by grant HHMI 55005614 from the Howard Hughes

Medical Cell press Institute International Research Scholars Program to M. K. Electronic supplementary material Additional file 1: Plate assay of phenol tolerance of P. putida PaW85 (wt) and colR -deficient (colR) strains. Cells were grown on glucose (glc) minimal medium in the presence or absence of 8 mM phenol. Approximate number of inoculated bacterial cells is indicated above the figure. Bacteria were photographed after 4 days of growth. (PDF 188 KB) Additional file 2: Comparative analysis of subpopulations with different DNA content by staining of cells with SYTO9 and PI or SYTO9 alone. P. putida wild-type (wt) and ttgC-deficient (ttgC) strains were grown for 24 h on gluconate minimal selleck screening library plates supplemented with 8 mM phenol. Cells were stained with PI and SYTO9 (SYTO9+PI) or SYTO9 alone and analysed by flow cytometry.

To measure lethality, cells were grown in LB liquid medium to mid

To measure lethality, cells were grown in LB liquid medium to mid-log phase (OD600 = 0.3 ~0.5) at 37°C with shaking. Cells were split into 1-ml aliquots in test tubes, and various concentrations

of antimicrobial agents (2 × MIC99 to 30 × MIC99) were added. After incubation for 2 hr with shaking, cells were diluted in LB liquid medium, ON-01910 purchase which eliminated drug carryover, and 10 μl of aliquots from the dilutions were spotted in triplicate on drug-free LB agar plates. Colonies were counted after overnight incubation at 37°C. Lethality was expressed as percent of control relative to the CFU per ml at the time of drug addition. The dose that reduced CFU by 90% was taken as LD90. For screening the mutant library, kanamycin-resistant

colonies were manually replica-plated with toothpicks to a series of plates containing various concentrations of nalidixic acid and incubated overnight. Colonies exhibiting the same bacteriostatic susceptibility as the parental strain were saved for lethality measurement. Survival Selleck Mocetinostat for each colony was measured in liquid medium after a 2-hr incubation in nalidixic acid at 20 μg/ml and 50 μg/ml as described in the previous paragraph. Colonies that exhibited decreased survival relative to the parental strain were then retested for MIC and survival as described in the previous paragraphs. Strains confirmed to have a hyperlethal phenotype were further characterized as described below. Identification of gene insertion sites Asymmetric PCR, modified from that described previously [14–16], was used to amplify E. coli genomic sequences near the ends of Tn5 that inserted into the genome. One primer, either Tn5R10 (5′ GGG ATC CCC TAC TTG TGT AT 3′) or Tn5F4568 (5′ AGA ATT CCT CCC GAG ATC TG 3′) was complementary to the sequence at an end of Tn5; the other primer contained a 6-nucleotide random Anacetrapib sequence followed by TGGC (Ran5-29: 5′ GTT CTA CAC GAG TCA CTG CAG NNN NNN TGG C 3′). The randomized primer binds any GCCA in the genome. However,

since PCR preferentially amplifies short fragments, combination of the two primers should amplify the sequences between one Tn5 end and the first few GCCA sequence elements. For the first 5 cycles of PCR, the annealing temperature was high (58°C); consequently, the primer that was complementary to the sequence at the Tn5 end preferentially bound to the substrate, which caused one strand of the substrate to be asymmetrically amplified. This high-temperature annealing was followed by a cycle using low annealing temperature (30°C) to allow the randomized primer to bind the strand that had already been amplified. Then one high-temperature (58°C) and one moderate-temperature (44°C) cycle were alternated 12 times to amplify the sequence between the two primers. For all amplification cycles, the annealing time was 1 min, while the learn more denaturation (94°C) and extension (72°C) times were 15 sec and 2 min, respectively.

As selective antibiotics for the presence of pMAD_SpR or its deri

As selective antibiotics for the presence of pMAD_SpR or its derivative constructs, 100 µg/ml ampicillin and 100 µg/ml spectinomycin was used for E. coli TOP10 growth,

and 3 µg/ml erythromycin and 250-300 µg/ml spectinomycin for B. licheniformis growth. This vector carries a constitutively expressed β-galactosidase gene, allowing blue-white screening on plates spread with X-Gal (40 µl 40 mg/ml 5-bromo-4-chloro-3-indolyl-β-D-galactopyranoside, VWR, BDH Prolabo). This screening was, however, not always #CRT0066101 cell line randurls[1|1|,|CHEM1|]# unambiguous following long incubations of plates with B. licheniformis MW3 transformants, probably due to the natural precence of β-galactosidase in B. licheniformis DSM 13 [77]. To construct the gene replacement vector, primers (Table 2) were designed to amplify two DNA fragments, one homologous to upstream (709 bp) and one to downstream (696 bp) regions of the deletion target (567 bp) in the gerAA. Platinum Taq DNA Polymerase High Fidelity kit (Invitrogen) was used for PCR amplification

with the following amplification procedure: initial denaturation for 2 min at 94°C, 30 cycles of 30 s at 94 °C, 30 s at 50 °C and 1 min at 68 °C, and final extension at 68 °C for 10 min. Primers of the upstream and downstream amplicons Selleck H 89 contained restriction sites BamHI and EcoRI respectively (Table 2), allowing a two_step ligation into the corresponding restriction sites on either side of the (SpR)-cassette in pMAD_SpR. The Succinyl-CoA resulting gene replacement plasmid, pMAD_SpRΔgerAA, was controlled for correct orientation of the upstream and downstream fragments by PCR. pMAD_SpRΔgerAA was introduced into B. licheniformis MW3 by electroporation, and allelic exchange

of internal parts of gerAA (567 bp) with the (SpR)-cassette of pMAD_SpRΔgerAA was allowed by double crossover. The protocol was performed as described by Arnaud et al.[75], except using growth temperatures of 37 °C following initial transformation, an incubation temperature of 45 °C and spectinomycin present during plasmid curing, and an incubation temperature of 37 °C when screening for the double crossover phenotype (spectinomycin resistant and erythromycin sensitive colonies). Chromosomal DNA was purified from a candidate colony and used in PCR amplifications (as described above) with primers hybridizing outside the cloned DNA fragment and inside the spectinomycin cassette (Table 2) to verify the deletion and insertion by sequencing. The disruption mutant was named B. licheniformis MW3ΔgerAA::spc (NVH-1307) and used in the following complementation, sporulation and germination assays.

It was the aim of this study to identify the newly isolated funga

It was the aim of this study to identify the newly isolated fungal pathogen of A. angustifolia seeds and screen for rhizosphere streptomycetes which, upon germination on ground, can affect the growth of this pathogen. Furthermore, we present a list of exudate compounds produced by the fungus-inhibiting bacteria

in single culture, and alterations due to the co-culture with the fungal pathogen. Results and discussion The pathogenic fungus on A. angustifolia seedlings: effects and identification After 50 days of germination, about 30% of Araucaria seedlings were infected by a fungus that promoted Hedgehog antagonist the death of the cotyledons and interrupted the connection between the seedling and the megagametophyte (Figure 1A, B). Of these, about 50% died, and the surviving ones showed delay in plant development. After 150 days, 52.3% of surviving plants with retarded development were dead. The cause for delayed development or seedling death might be attributed to the early interruption in the carbon and nutrients selleck compound transfer from the megagametophyte to the embryonic tissues. Electron microscopy analyses showed the presence of high amounts

of starch grains in the 7-Cl-O-Nec1 chemical structure megagametophyte of infected seedlings (Figure 1C, D), compared with the non-infected tissue (Figure 1E, F). Figure 1 Neofusicoccum parvum infection of A. angustifolia seedlings (Bar = 1 cm in A, B, F). A, Seedling; B, Megagametophyte and cotyledons infected with the fungus; C, Scanning electron microscopy of infected megagametophyte tissue that surrounds the cotyledon; D, Starch grains covered by hyphae; E-F, Non infected tissues. All images were taken from plants/tissues after 50 days of germination. ct – haustorial cotyledon, se – seed, mg – megagametophyte, st – starch grain. The natural infection of the A. angustifolia seeds by the fungus might have happened during cone maturation and before seed dispersion. The fungus infected specifically the megagametophyte tissue and promoted necrosis of Unoprostone the seed-enclosed region, and the cotyledons, after their emergence. The first visible symptoms were the decay of the cotyledons and seed browning. In this species,

the cotyledons act as a haustorial organ by transferring the reserves from the megagametophyte to the embryonic axis [16], supporting the seedling growth until about 70 to 120 days [17, 18]. The early cotyledon interruption leading to seedling death or delayed plant development, significantly reduced the chances for seedling establishment. ITS sequencing of the fungal isolate with the primer pairs ITS1 and ITS4 ([19], accession number ITS [JN811822]) yielded the highest homologies (100%) with Neofusicoccum parvum/N. ribis and Botryosphaeria parva, all members of the Botryosphaeriaceae. This is due to the fact that Neofusicoccum parvum is the anamorph of Botryosphaeria parva[20]. N. parvum and N. ribis were originally considered to be part of the Botryosphaeria dothidea complex [21].

cereus 10987 in the presence of DSF signal using microarray assay

cereus 10987 in the presence of DSF signal using microarray assay. It was revealed that addition of DSF signal significantly decreased the transcripts levels of the genes encoding a series of drug efflux systems and drug resistance proteinsof B. cereus (selleckchem Additional file 1: Figure S1, Additional file 1: Table S1), which may likely reduce the antibiotic-resistant activity. We then tested the effect

of DSF signal on B. cereus growth and biofilm formation. As shown in Figure 4, the growth rate of B. cereus was only slightly reduced with addition of 50 μM DSF signal, whereas the bacterial biofilm formation was substantially inhibited. NVP-HSP990 Intriguingly, we also discovered that DSF signal remarkably reduced the persistence of B. cereus (Figure 4C). Addition of 50 μM DSF signal decreased the persistence rate of B. cereus by 5.5- and 8.7- fold after 4 h and 8 h incubation, respectively (Figure 4C). As bacterial biofilm and persisters are highly tolerant to different types of antibiotics, inhibition of biofilm formation and persistence may likely alter bacterial antibiotic susceptibility. In combination, our results suggest that DSF signal could exert multifaceted effect on B. cereus, such as reducing the drug-resistant activity, inhibiting biofilm formation and attenuating bacterial persistence,

which might lead to altered bacterial AZD9291 in vitro susceptibility to antibiotics. Figure 4 Influences of exogenous addition of DSF signal on the bacterial growth rate (A) biofilm formation (B), and persistence Ureohydrolase (C) of B. cereus . For measurement of growth rate, the bacterial cells were grown in the absence or presence of 50 μM DSF; while for test of persistence, the bacterial cells were treated with10 μg/ml gentamicin (Gm) in the absence or presence of 50 μM DSF signal. For biofilm formation assays, DSF signal was added at different final concentrations as indicated. Data shown are means of three replicates and error bars indicate the standard deviations. The differences between the samples with DSF and without DSF

are statistically significant with *p < 0.05, as determined by using the Student t test. The combination effect of DSF signal with antibiotics on other bacterial species To study whether DSF could also influence the antibiotic susceptibility of other bacterial species, the signal was used to test the synergistic effect with antibiotics against a few bacterial species in our collection, including Bacillus thuringiensis, Staphylococcus aureus, Mycobacterium smegmatis, Neisseria subflava, and Pseudomonas aeruginosa. Among them, B. thuringiensis belongs to B. cereus group and has been used as a biopesticide for many years [31]. It is closely related to the other two member of B. cereus group, i.e., B. anthracis and B. cereus, which are important human pathogens to cause anthrax and foodborne illness, respectively [32]. S. aureus is frequently found in human respiratory tract and on the skin.

Jain RK: The next frontier of molecular medicine:

Jain RK: The next frontier of molecular medicine: R428 purchase delivery of therapeutics. Nature Medicine 1998, 4: 655–57.CrossRefPubMed 23. Heldin CH, Rubin K, Pietras K,

Ostman A: High interstitial fluid pressure – an obstacle in cancer therapy. Nature Rev Cancer 2004, 4: 806–13.CrossRef 24. Akiri G, Sabo E, Dafni H, Vadasz Z, Kartvelishvily Y, Gan N, Kessler O, Cohen T, Resnick M, Neeman M, Neufeld G: Lysyl oxidase-related protein-1 promotes tumor fibrosis and tumor progression in Vivo . Cancer Research 2003, 63: 1657–1666.PubMed 25. Bjorn MJ, Groetsema G, Scalapino L: Antibody-Pseudomonas Exotoxin A Conjugates Cytotoxic to Human Breast Cancer Cells in Vitro . Cancer Research 1986, 46: 3262–3267.PubMed find more 26. Lanteri M, Ollier L, Giordanengo V, Lefebvre JC: Designing a HER2/neu promoter to drive α1,3 galactosyltransferase expression for targeted anti-αGal antibody- mediated tumor cell killing. Breast Cancer Research 2005, 7: R487-R494.CrossRefPubMed Competing interests The authors declare that they have no competing interests. Authors’ contributions ZPZ and JZ prepared mimetic and fusion molecules, measured in vitro

and in vivo killing activity and did pathological assays; SYZ did DNA scanning and SDS-PAGE.”
“Background Hepatitis B virus (HBV) is the prototype of hepadnaviridae. It is estimated that around 350 million people are carriers of hepatitis B surface antigen (HBsAg) worldwide [1, 2]. Persistent HBV infection leads to chronic hepatitis, and is closely associated with the PI3K Inhibitor Library supplier development of liver cirrhosis and hepatocellular carcinoma (HCC) [3]. Three forms of viral particles can be detected in the serum of HBV infected patients, namely, 42 nm diameter mature virion particles, 22 nm diameter spherical particles and 22 nm diameter filamentous particles [4]. Uniquely, 22 nm subviral particles, which are composed of HBsAg and do not contain viral DNA, usually outnumber the virions in patient serum by a factor of 1000-fold or more [5]. Though HBsAg has been identified as the neutralizing antigen of HBV and has been used as the major component of preventive vaccine for viral hepatitis B, persistence

of HBsAg in serum of patients has been recognized as a high risk factor for development of HCC [6, 7]. The possible roles of HBV envelope proteins LHBs (Pre-S1/Pre-S2/S) Tolmetin and MHBs (Pre-S2/S) in HCC development have been reported [8, 9]. However, the role of major HBsAg in tumorigenesis has not been studied in detail. By microarray study of cells transfected with the S gene coding for HBsAg, we have previously shown that marked up-regulation of lymphoid enhancer-binding factor 1 (LEF-1), a transcriptional factor in Wnt pathway, was closely correlated with HBsAg expression [10]. Furthermore, the expression level and cellular distribution of LEF-1 protein, mainly the dominant negative truncated isoform, was changed by the expression of HBsAg.

In case of chlororespiratory-induced active NPQ in the dark, the

In case of chlororespiratory-induced active NPQ in the dark, the second light increment would not have induced a NPQ down-regulation. A down-regulation of NPQ upon light exposure implies active NPQ mechanisms during growth PF conditions, and very slow de-activation kinetics, or NPQ activation in the dark. We checked whether the observed decrease in NPQ during the first 4 min of the high light exposure could be caused by a state II–state I transition, thus by transition from the high fluorescent to a low fluorescent state. The fact that we observed a decrease in the functional PSII cross

BI 2536 section (σPSII′) corroborates this, although the kinetics follow a completely different pattern (we come back to this later). Low-temperature fluorescence excitation scans were performed to check on the occurrence of state-transitions. Although the spectra shown in this study deviate from spectra found in higher plants and other algae (Harnischfeger 1977; Satoh et al. 2002), our results are in good comparison to other studies using D. tertiolecta (Gilmour et al. 1985; Vassiliev et al. 1995; Casper-Lindley and Björkman 1996). Torin 1 state-transitions operate on the time scale of minutes (Allen and Pfannschmidt 2000). Kinetics this website of the initial NPQ transient shown in

Fig. 2 operate on the same time scale. However, when the PF is increased stepwise very rapid fluctuations are observed at the lowest two PFs, and these seem too fast to be explained by state-transitions, suggesting that the observed NPQ phenomenon is not caused CYTH4 by a state-transition. Low temperature fluorescence excitation scans of D. tertiolecta showed that during the first 10 min of exposure to high light the PSII:PSI ratio did not change, and then subsequently increased from 3.5 to ~4. This suggests an increase in the PSII absorption cross section during the second half of the

light exposure. This shift was absent in NPQ and σPSII′. When the cells were transferred from 660 μmol photons m−2 s−1 to darkness the PSII:PSI ratio first decreased, and then restored itself, which was not detected by room temperature fluorescence measurements using FRRF. If only qT would have caused the change in calculated NPQ, F m would decrease as a response to the light–dark transfer, whereas the opposite was observed. Therefore, it must be concluded that state-transitions did not show up in the fluorescence measurements in this study and state-transitions signals were overshadowed by other processes, probably qE. Photoinhibition (qI) can also affect fluorescence signals. Recovery from qI requires repair of PSII reaction centres proteins, especially D1 (Ohad et al. 1994). This occurs on a time scale of hours. Hence, an effect of photoinhibition (qI) can be excluded based on the quick recovery of F v /F m values in this study.