For example, the transcriptional response to ciprofloxacin [11], an inhibitor of Selleckchem C646 bacterial DNA gyrase, is clearly AZD4547 order different from that of fosfomycin, because the cell wall stress stimulon genes were not activated. Similarly, the transcriptional profile of the antiseptic compound triclosan, that targets fatty acid biosynthesis [12], confirms the specificity of the cell wall stress response. The effects of fosfomycin on S. aureus metabolism, supported by our transcription data, are schematized in Figure 6. The inhibition of MurA causes accumulation

of its substrate phosphoenolpyruvate (PEP) which is known to act as a carbon starvation signal. PEP accumulation was shown to be responsible for downregulation of several central metabolism genes and nucleic acid biosynthesis genes in different organisms including bacteria [13]. A downregulation of pur and pyr operons was observed at the latest time point. Downregulation of both operons has also been reported in the SOS response [8], acid-shock response [7],

ciprofloxacin response [11] and in the S. aureus MurF underexpression mutant [6]. Figure 6 Fosfomycin effects on S. aureus metabolism supported by transcriptional data in this study. Processes in red ovals were induced and those in green ovals were repressed by fosfomycin treatment. In order Caspase-independent apoptosis to reach target enzymes MurA and MurZ, fosfomycin has to cross the cell membrane. Because of its hydrophilic

Palbociclib in vivo nature it uses the active transport systems (ABC transport proteins), specifically the L-α-glycerophosphate and the glucose-6-phosphate uptake systems [1]. The PEP phosphotransferase system (PTS) mediates the uptake and phosphorylation of carbohydrates and controls metabolism in response to carbohydrate availability, and can therefore affect the whole cell metabolic rate [14]. GSEA shows that PTS was downregulated by fosfomycin 20 and 40 minutes after treatment. This downregulation could be a defense mechanism against the influx of fosfomycin. It has been reported that PTS mutant bacteria are highly resistant to fosfomycin [15] and that some fosfomycin-resistant E. coli isolates have altered glpT and/or uhp transport systems [16]. The downregulation of PTS genes can also contribute to PEP accumulation [13]. As shown in Figure 3 and Table 1, transport processes in general were significantly downregulated. The majority of differentially expressed genes in this group encode proteins that transport oligopeptides (opp genes), amino acids, sugars, polyamines (potABCD) and cations into the cell. Genes encoding iron transport and binding proteins, belonging to the Isd system, were also downregulated similarly as in a MurF underexpression mutant study [6]. However, a small proportion of transport genes were upregulated, including some amino acid and oligopeptide carrier genes and the sodium/hydrogen exchanger genes mnhBCDEG.

: International Society of selleck inhibitor Sports Nutrition position stand: nutrient timing. J Int Soc Sports Nutr 2008, 5:17.PubMedCrossRef 23. Wilson J, Wilson RNA Synthesis inhibitor GJ: Contemporary issues in protein requirements and consumption for resistance trained athletes. J Int Soc Sports Nutr 2006, 3:7–27.PubMedCrossRef 24. White JP, Wilson JM, Austin KG, Greer BK, St John N, Panton LB: Effect of carbohydrateproteinsupplement timing on acute exercise-induced muscle damage. J Int Soc Sports Nutr 2008, 5:5.PubMedCrossRef 25. Cribb PJ, Hayes A: Effects of supplement timing and resistance exercise on skeletal muscle hypertrophy. Med Sci Sports

Exerc 2006, 38:1918–1925.PubMedCrossRef 26. Levenhagen DK, Gresham JD, Carlson MG, Maron DJ, Borel MJ, Flakoll PJ: Postexercise nutrient intake timing in humans is critical to recovery of leg glucose and protein homeostasis. Am J Physiol Endocrinol

Metab 2001, 280:E982-E993.PubMed 27. Tipton GSK872 manufacturer KD, Ferrando AA, Phillips SM, Doyle D Jr, Wolfe RR: Postexercise net protein synthesis in human muscle from orally administered amino acids. Am J Physiol 1999, 276:E628-E634.PubMed 28. Tipton KD, Ferrando AA: Improving muscle mass: response of muscle metabolism to exercise, nutrition and anabolic agents. Essays Biochem 2008, 44:85–98.PubMedCrossRef 29. Tipton KD, Rasmussen BB, Miller SL, Wolf SE, Owens-Stovall SK, Petrini BE, Wolfe RR: Timing of amino acid-carbohydrate ingestion alters anabolic response of muscle to resistance exercise. Am J Physiol see more Endocrinol Metab 2001, 281:E197-E206.PubMed 30. Hopkins WG, Marshall SW, Batterham AM, Hanin J: Progressive statistics for studies in sports medicine and exercise science. Med Sci Sports Exerc 2009, 41:3–13.PubMed 31. Batterham AM, Hopkins WG: Making meaningful inferences about magnitudes. Int J Sports Physiol Perform 2006, 1:50–57.PubMed 32. Chrusch MJ, Chilibeck PD, Chad KE, Davison KS, Burke DG: Creatine supplementation combined with resistance training in older men. Med Sci Sports Exerc 2001, 33:2111–2117.PubMedCrossRef

33. Percario S, Domingues SP, Teixeira LF, Vieira JL, de Vasconcelos F, Ciarrocchi DM, Almeida ED, Conte M: Effects of creatine supplementation on oxidative stress profile of athletes. J Int Soc Sports Nutr 2012, 9:56.PubMedCrossRef 34. Jagim AR, Oliver JM, Sanchez A, Galvan E, Fluckey J, Riechman S, Greenwood M, Kelly K, Meininger C, Rasmussen C, Kreider RB: A buffered form of creatine does not promote greater changes in muscle creatine content, body composition, or training adaptations than creatine monohydrate. J Int Soc Sports Nutr 2012, 9:43.PubMedCrossRef 35. Souza-Junior TP, Willardson JM, Bloomer R, Leite RD, Fleck SJ, Oliveira PR, Simao R: Strength and hypertrophy responses to constant and decreasing rest intervals in trained men using creatine supplementation. J Int Soc Sports Nutr 2011, 8:17.PubMedCrossRef 36. Willoughby DS, Rosene J: Effects of oral creatine and resistance training on myosin heavy chain expression. Med Sci Sports Exerc 2001, 33:1674–1681.

The structural appearance of adhesive discs is essentially identical, not only for different G. lamblia assemblages but also for other species such as G. muris [37, 39, 40]. Immunofluorescence assays using anti-β giardin mAb and confocal microscopy showed that β-giardin localized in the VX-680 cost ventral disc of WB permeabilized trophozoites (Figure 3A). We have extended the analysis to other Assemblages A isolates (WB clone A6 and Portland-1) and we found no

differences with the localization seen in WB 1267 trophozoites (data not shown). The distinctive fluorescence intensity detected at the margins of the ventral disc has been previously reported in Giardia trophozoites transfected with GFP-tagged β-giardin or using polyclonal Smad3 phosphorylation antibodies [41, 42]. Some authors have suggested that β-giardin also localizes in the median body selleck products of WB trophozoites [43]. However, we did not observe any labeling of the median body, although a large population of trophozoites was analyzed. These differences in localization may suggest that it could

be modified, taking into account that Palm et al. found three isoforms of this protein in a proteomic assay [23]. Interestingly, the immunolocalization of β-giardin at the ventral disc in GS trophozoites was rather different, with β-giardin being specifically organized into a radial array that surrounded the half ring of the ventral ADP ribosylation factor disc, resembling a horseshoe (Figure 3B). Also, at the center of the ventral disc, an asymmetrical grid could be observed. Figure 3 Immunolocalization

of β-giardin in WB and GS trophozoites. Reactivity of 12G5 mAb on WB and GS Giardia trophozoites was determined by indirect immunofluorescence in permeabilized trophozoites. (A) Upper panel: immunofluorescence assays showing the labelling in the ventral disc of the trophozoites. Lower panels: high magnification showing the immunostaining in the ventral disc of WB trophozoites, with more intensity on the margins. (B) Upper panel: immunofluorescence of β-giardin in GS trophozoites. Lower panels: high magnification showing immunofluorescence specifically organized into a radial array surrounding the half ring of the ventral disc and also at the centre of it. Scale bar: 10 μm. The singular localization of β-giardin in WB and GS trophozoites was unexpected, considering that the amino acid sequence of β-giardin is 100% identical in the two assemblages (Additional File 1). Complementary assays utilizing non-permeabilized WB or GS trophozoites showed no fluorescence, showing intracellular β-giardin localization. Related to this, in studies performed on G. muris trophozoites, β-giardin was described as a surface protein, based on surface protein biotinilation assays [44].

One anti-tumoral compound isolated from several plant-derived products is cinnamic acid. Cinnamic acid and its associated compounds can be found in coffee, apples, citric Poziotinib mouse fruits, vegetable oils, propolis and wine. Cinnamic acid has a long history of human use as a component of plant-derived scents and flavoring agent [13]. Liu et al. [5] found that this compound induced tumor cell differentiation by modulating the expression of genes implicated in tumor metastasis and immunogenicity in cultured human melanoma cells. Several researchers have also demonstrated the antioxidant activity of caffeic acid and its derivatives

[14, 15], which may be associated with cell death. Lee et al. [8] demonstrated that natural antioxidant compounds in diet, such as polyphenols in green tea, activate the MAPK pathway. Moreover, at high concentrations, these substances activate the caspase signaling

R428 solubility dmso cascade, which induces apoptosis in normal cells [8]. Lamartiniere et al. [16] showed that soy isoflavones such as genistein (another polyphenolic compound) act as chemopreventive agents against prostate and mammary cancers. One of the chemopreventive mechanisms against cancer is the induction of irreversible DNA damage, which results in cell death via apoptosis [17]. Impaired function of p53 increases the probability of proliferating cells with genetic abnormalities in some conditions [18, 19]. This is due to the activation of p53 in response to unfavorable treatments, which results in genetic abnormalities such as DNA breakages Osimertinib price [20, 21], disruption PI3K Inhibitor high throughput screening of microtubules [22], lack of chromosome

segregation at mitosis [23] or the incorrect termination of cell division, which can result in micronuclei formation [22]. The micronucleus test is widely used to detect chromosomal aberrations because micronuclei can originate from chromosomal fragments or disruptions in the mitotic spindle [24, 25]. This assay has been used to evaluate the exposure levels of the human population to mutagenic or genotoxic agents [26–30] as well as in cell cultures to determine the mutagenic potential of drugs and/or natural compounds [31–33]. The screening of new compounds with anti-microbial and anti-inflammatory activities has resulted in the discovery of anti-tumor and chemopreventive properties of cinnamic acid and its derivatives [5, 34–36]. Selective cytotoxicity in tumor cells is an important role to be analyzed to compare drug effects in cultured cells [37, 38]. This study aimed to compare the cytotoxic and genotoxic potential of cinnamic acid in both a human melanocyte cell line of blue nevus and in cultured melanoma human cells. Materials and methods Cell cultures HT-144 cell line, derived from malignant cutaneous melanoma, was obtained from American Type Culture Collection (ATCC). NGM cell line, derived from melanocytes of blue nevus, was obtained from Cell Bank of Rio de Janeiro (Brazil).

e., DNA methylation directs click here histone modification and histone modification recruits Wnt signaling more DNA methylation. All of these observations suggest a reciprocal crosstalk between DNA methylation and histone modification. Indeed, these epigenetic regulators can communicate and benefit each other to reinforce epigenetic gene silencing. In

this scenario, miRNAs are becoming a crucial factor in the faithful transmission of different patterns of epigenetic modulation (Figure  2). Figure 2 The role of miRNAs in mediating the crosstalk between epigenetic regulators. DNMT1 contributes to miR-1 silencing in HCC cells, thereby promoting the accumulation of its target HDAC4. The miR-29, which targets DNMT3, is down-regulated by

HDACs in AML. Likewise, miR-26a and miR-137 selleck are silenced by promoter CpG island hypermethylation, which induces the up-regulation of the target gene LSD1 in colorectal adenomas and EZH2 in prostate cancer. The miR-26a can be silenced by DNMTs in prostate cancer, which induces the accumulation of its target gene EZH2 and changes the global DNA methylation status [41], supporting the idea that miRNAs can mediate the interplay between epigenetic regulators. The miR-137 is another important mediator, which is silenced by promoter CpG island hypermethylation and targets lysine-specific demethylase 1 (LSD1) in colorectal adenomas [42]. Because LSD1 can stabilize DNMT1, a positive feedback loop exists between them. Besides the crosstalk between DNA and histone methylation, indirect crosstalk between DNA methylation

and histone deacetylation also occur through miRNA mediation, such as miR-1 and miR-29. The miR-1, which targets HDAC4, is down-regulated in human HCC cells because of its CGI hypermethylation by DNMT1, thereby promoting the expression of HDAC4 [43]. Likewise, HDACs can induce miR-29 silencing in acute myeloid leukemia (AML), which in turn increases the expression of its target gene DNMT3 [15, 44]. These findings indicate that epigenetic information can flow from one modulation to a miRNA, and then from the miRNA to another epigenetic pattern. As a member of epigenetic machinery, miRNAs can also contribute to the conversation Interleukin-2 receptor between other epigenetic events. Controlling miRNA expression with epigenetic drugs The frequent dysregulation of miRNAs and their interplay with epigenetic regulators in cancer make them attractive biomarkers and prospective therapeutic targets in clinical applications. The therapeutic application of miRNAs in cancer involves two strategies: 1) inhibition of oncogenic miRNAs by using miRNA antagonists, such as anti-miRs or antagomiRs; or 2) introduction of tumor suppressor miRNAs through either synthetic miRNA mimics or by stable and vector-based transfection of genes coding for miRNAs [45].

Mol Plant Pathol 2003, 4:31–41.PubMedCrossRef 39. Bowden CG, Smalley E, Guries RP, Hubbes M, Temple B, Horgen PA: Lack of association between cerato-ulmin production and virulence in Ophiostoma novo-ulmi . Mol Plant-Microbe Interact 1996, 9:556–564.PubMedCrossRef 40. van Wetter MA, Wosten HA, Wessels JG: SC3 and SC4 hydrophobins have distinct roles in formation of aerial structures in dikaryons of Schizophyllum commune . Mol Microbiol 2000, 36:201–210.PubMedCrossRef 41. Wösten HA, Schuren FJ, Wessels JG: Interfacial

self-assembly of a hydrophobin into an amphipathic protein membrane mediates fungal attachment to hydrophobic surfaces. EMBO J 1994, 13:5848–5854.PubMed 42. Bork P, Letunic I, Doerks T: SMART 6: recent updates and new developments. Nucleic Acids Res 2009, 37:D229-D232.PubMedCentralPubMedCrossRef 43. Quevillon E, Silventoinen V, Pillai S, Harte Selleckchem MK 8931 N, Mulder N, Apweiler R, Lopez R: InterProScan: protein domains identifier. Nucleic Acids Res 2005, 33:W116-W120.PubMedCentralPubMedCrossRef 44. Marchler-Bauer A,

Lu S, Anderson JB, Chitsaz F, Derbyshire MK, DeWeese-Scott C, Fong JH, Geer LY, Geer RC, Gonzales NR, Gwadz M, Hurwitz DI, Jackson JD, Ke Z, Lanczycki CJ, Lu F, Marchler GH, Mullokandov M, Omelchenko MV, Robertson CL, Song JS, Thanki N, Yamashita RA, Zhang D, Zhang N, Zheng C, Bryant

SH: CDD: a conserved domain database for the functional annotation of proteins. Nucleic Acids Res 2011, 39:D225–229.PubMedCentralPubMedCrossRef 45. Selleck Captisol Larkin MA, Blackshields G, Brown NP, Chenna R, McGettigan PA, McWilliam H, Valentin F, Wallace IM, Wilm A, Lopez R, Thompson JD, Gibson TJ, Higgins DG: Clustal W and Clustal X version Interleukin-3 receptor 2.0. Bioinformatics 2007, 23:2947–2948.PubMedCrossRef 46. Petersen TN, Brunak S, von Heijne G, Nielsen H: SignalP 4.0: Discriminating signal peptides from transmembrane regions. Nat Methods 2011, 8:785–786.PubMedCrossRef 47. Gasteiger E, Gattiker A, Hoogland C, Ivanyi I, Appel RD, Bairoch A: ExPASy: the proteomics server for in-depth protein knowledge and analysis. Nucleic Acids Res 2003, 31:3784–3788.PubMedCentralPubMedCrossRef 48. Anisimova M, Gil M, Dufayard JF, Dessimoz C, Gascuel O: Survey of branch support methods demonstrates accuracy, power, and robustness of fast likelihood-based approximation schemes. Syst Biol 2011, 60:685–699.PubMedCrossRef 49. Le SQ, Gascuel O: An improved general amino acid replacement matrix. Mol Biol Evol 2008, 25:1307–1320.PubMedCrossRef 50. Tzelepis GD, Melin P, Jensen DF, Stenlid J, Karlsson M: Functional analysis of glycoside hydrolase family 18 and 20 genes in TPCA-1 research buy Neurospora crassa . Fungal Genet Biol 2012, 49:717–730.PubMedCrossRef 51.

Mechanistically, it was reasonable to postulate that the collapse of the ΔΨm was mediated by ROS generation in the treated parasites. In this context, the fluorescent probe DHE was used for intracellular ROS detection, and AA was added as a positive control because it inhibits the electron flow through the electron transport

chain, leading to the accumulation of superoxide [33]. Among the four NQs tested, only NQ8 led to a discrete increase in the percentage of DHE + epimastigotes, giving addition evidence for the strong effect of this quinone on the parasite ΔΨm. Indeed, the pool of MK0683 in vitro anti-oxidant defenses in epimastigotes Selleck GSI-IX that includes trypanothione, tryparedoxin peroxidase and other

redox enzymes leads to a protective effect in this parasite stage, as previously described [34]. Thus, one plausible hypothesis to explain the absence of oxidative stress triggered by NQ1, NQ9 and NQ12 could be the existence of more than one mechanism of action involved in the trypanocidal find more activity of these compounds, leaving ROS generation suppressed by the detoxification system of the parasite. Possibly, the strong redox effect of NQ8 could be associated to the presence of the acetyl group in its structure facilitating quinone reduction, as previously demonstrated by electrochemical analysis [35]. Further experiments using different biochemical and molecular

approaches must be performed to better characterize ROS participation in the mechanism of action of these compounds. Electron microscopy evidence of induction of the autophagic pathway by naphthoquinones and their derivatives has also been previously reported [24–26, 28]. The presence of large profiles of endoplasmic reticulum surrounding 3-oxoacyl-(acyl-carrier-protein) reductase different cellular structures, such as lipid droplets and organelles, and the appearance of bizarre membranous structures with a myelin-like aspect are the most common characteristics. The autophagic process represents a fundamental constitutive pathway in eukaryotic cells that is responsible for remodeling cellular structures and maintaining homeostasis. In trypanosomatids, other roles for autophagy have been proposed, including in the parasite’s differentiation [36]. In a great variety of cell models, the loss of the balance between anabolic and catabolic processes leads to non-apoptotic death [37]. In the last decade, it has been demonstrated that the induction of autophagy in T. cruzi trypanosomatids is triggered by several classes of drugs, in particular naphthoquinones and their derivatives [25, 26, 38]. Our transmission electron microscopy analysis suggested the involvement of endoplasmic reticulum and cytosolic membranous structures in pre-autophagosomal formation, as previously postulated by Yotimitsu & Klionsky [39].

Methodological issues In this study, we excluded the relatively unhealthy workers at baseline from the study subjects of this study. The results of the sensitivity tests in the two alternative study groups supported the validity of the decision, despite a loss of statistical power. Including them into study subjects of this study (alternative study group 1) would have significantly CHIR-99021 concentration underestimated the synergistic effects between job control and social support at work in both men and women. At the same time, the results in the

group (Table 6) suggests that a statistical adjustment of the baseline health conditions was not enough to remove their impact on the psychological job characteristics and general psychological distress at follow-up. We reported AZD8931 molecular weight the two (80 and 95%) CIs of the Rothman’s synergy index in consideration of a potential Type II error. In this study, all of the synergy indexes between job control and social support at work on psychological distress were non-significant at the alpha level of 0.05. However, they were significant

at the alpha level of 0.20 in women (Tables 4, 5). Also, in men, when the sample size was almost doubled (i.e., in the alternative study group 1), the 80% CIs of the synergistic indexes Selleckchem Dinaciclib became clearly above or below unity (Table 6). All of these indicate that an injudicious application of the typical alpha PLEKHB2 level (0.05) to interaction significance tests could obscure a possible synergism. As mentioned before, low statistical power in interaction tests (Greenland 1993; Marshall 2007; Selvin

1996) should be considered. In addition, Rothman (1978) warned that a quantitative interval estimation of synergy index should not be confused with a significance test (in which typically the alpha level of 0.05 is employed). Hogan et al. (1978) also reported that the CIs of synergy index based on a simple asymptotic approach (Hosmer and Lemeshow 1992) could be unduly conservative in comparison with alternative approaches. More importantly, we think that a synergism between two exposures should be judged based on an array of information such as a strong theoretical hypothesis, a significant difference between the results under no-interaction assumption and under an interaction assumption as presented in Tables 3, 4 and 5, and confidence intervals considering a type II error, not solely based on the significance test (at the alpha of 0.05) of synergy index. Implications for risk assessment, job stress models, and interventions The most important lesson from this study is that the risk assessment of the combination of low job control, high job demands, and low social support at work on common mental disorders needs to be conducted with full consideration of their interactions and study context (Johnson and Hall 1996; Kasl 1996; Schaubroeck and Fink 1998).

The development of phages for therapy has been hampered by concerns over the potential for immune response, rapid toxin release

by the lytic action of phages, and difficulty of dose determination in clinical situations [5]. Phages multiply logarithmically in infected bacterial cells, and the selleck kinase inhibitor release of progeny phage occurs by lysis of the infected cell at the end of the infection cycle, which involves the holin-endolysin system [6, 7]. Holins create a lesion in the cytoplasmic membrane through which endolysins gain access to the murein layer selleck products [7]. Endolysins are peptidoglycan hydrolases that degrade the bacterial cell wall, leading to cell lysis and release of progeny phages [8]. An undesirable side effect of this phenomenon from a therapeutic perspective is the development of immunogenic reactions due to large uncontrolled amounts of phages in circulation [9]. Such concerns must be addressed before phage therapy can be widely accepted [5, 10]. This work features engineered bacteriophages that are incapable of lysing bacterial cells because they lack endolysin enzymatic activity. We previously produced, as a model, a recombinant lysis-deficient version of T4 bacteriophage that infects Escherichia coli [11, 12]. Phages have also been engineered to be non- replicating or to possess additional desirable

properties [13–15]. In an experimental E. coli infection model, the improved survival rate of rats treated Selleck ABT 737 with lysis-deficient T4LyD phage was attributed to lower endotoxin release [16]. We wished to generate an endolysin-deficient phage against a gram-positive bacterium, and chose S. aureus

because of FER its clinical relevance. S. aureus is a major pathogen responsible for a variety of diseases ranging from minor skin infections to life-threatening conditions such as sepsis. This pathogen is often resistant to all β-lactam antibiotics; vancomycin-resistant strains may become untreatable [17–19]. This organism is the most common cause of nosocomial infections, and nasal carriage is implicated as a risk factor [20]. In the United States alone, invasive methicillin-resistant S. aureus (MRSA) infections occur in approximately 94,000 people each year, causing nearly 19,000 deaths [21]. Understandably, the progressive multidrug resistance of bacteria has motivated the re-evaluation of phages as therapy for diverse bacterial infections [22]. We report here that the recombinant endolysin-deficient S. aureus phage P954 kills cells without causing cell lysis and forms plaques on a host that expresses a plasmid-encoded heterologous endolysin, enabling its large-scale production. The recombinant phage P954 was evaluated for in vivo efficacy in an experimental mouse model and found to protect mice from fatal S. aureus infection.

Upon a dark–light transient, it would be expected that maximal fluorescence signals would decrease as a result of elevated non-photochemical fluorescence quenching (Krause and

Weis 1991; Campbell et al. 1998). In this study, however, F m ′ values increased compared to F m in the block light treatment (Fig. 2). The F m ′ increase (and therefore NPQ down-regulation) was induced after approximately 1 min of actinic light onset, continued for ca 2.5 min, and was followed by a somewhat slower, but steady, decline until the signal was perturbed by addition of 160 μM DIC. learn more F m ′ correlated strongly with F′ (m = 1.39; r 2 = 0.91–0.96). A strong correlation between F′ and F m ′ in FRRF measurements suggests a change in the absorption cross section of PSII during the transient, although the functional absorption cross section was found to be stable throughout the actinic light phase (Fig. 2b). The initial rise in F m ′ might be an indication of the dissipation of chlororespiration, but the following decrease in both F′ and F m ′ might be due to both induction of qE or a change in the absorption cross section of PSII due to a state-transition. We applied low-temperature chlorophyll fluorescence emission spectra to investigate the occurrence

of state-transitions. 77 K Metabolism inhibitor emission spectra Figure 4 shows a typical chlorophyll fluorescence emission spectrum in D. tertiolecta. Fluorescence emission peaks were not very distinct, with a small contribution at 695 nm

(F 695) (PSII reaction centre). Emission at 715 nm (F 715) is regarded as a contribution from PSI, F 730 is considered as a vibration, while the origin of F 702 remains unclear. Emission spectra were normalised to the fluorescence yield at F 685 (light harvesting complexes of PSII). Murakami (1997) showed that the PSI/(PSII + PSI) ratio determined with biochemical techniques Flucloronide could be estimated accurately from the F PSI/(F PSII + F PSI) ratio for different algal species. We used the F 685/F 715 ratio as a proxy for changes in the ratio of PSII to PSI. Fig. 4 Representative fluorescence emission spectrum measured at 77 K (a) and residuals remaining after de-convolution (b). A minimum of three measurements per sample were averaged and baseline corrected. The fit was forced through peaks at 685 nm (light harvesting compounds of PSII), 695 nm (PSII reaction core), 702 nm (origin not clear), 715 nm (PSI) and 730 nm (PSI, or vibration). Top curve: dots data points, line selleck products resulting fit from de-convolution. Although the origin of the F 702 is obscure, leaving it out resulted in poor fits. Spectra were normalised to F 658 nm. Residuals (b) show the quality of the fit and remained below 0.05 for all samples analysed. Emission peak height data were used for PSII/PSI ratio (F 685/F 715 nm). Excitation wavelength was 435 nm F 685/F 715 ratios F 685/F 715 ratio remained relatively constant at approximately 3.4 during the dark to light transient (Fig. 5).