ssDNA binding properties The purified SSB proteins were analyzed

ssDNA binding properties The purified SSB proteins were analyzed for single-stranded DNA binding activity. In these experiments, a fixed concentration of (dT)n (n = 35, 76 or 120 nucleotides in length) were incubated with various SSB concentrations and the resulting complexes were analyzed by agarose gel electrophoresis (Figure  3). When dT35 was incubated with increasing concentrations of each of the SSB proteins, a single band of reduced mobility was LY333531 observed and remained constant even at a higher protein RXDX-101 concentration (complex I). A band with the same mobility was observed for (dT)76 at a low protein concentration, but a second band with a lower mobility was observed at a high protein concentration

(complex II). When SSB:dT120 click here complexes were analyzed, a third band with a lower mobility was detected (complex

III). This implies that the length of ssDNA required for efficient protein binding is less than 35 nucleotides long. Figure 3 Binding of SSB proteins to oligo (dT). Fixed quantities (10 pmol) of 5′-end fluorescein-labelled oligonucleotides (dT)35, (dT)76 and (dT)120 were incubated with 50, 100 and 200 pmol of the SSB proteins in 20 μl reaction mixtures for 10 min at 25°C. Symbols I, II and III describe SSB:dT complexes. In order to explore the binding properties of all the proteins in question further, we used fluorescence spectroscopy. All the bacterial SSBs which have been studied to date have shown a dramatic decrease of tryptophan fluorescence when binding to ssDNA. With an excitation wavelength of 295 nm, the emission spectrum of SSB proteins at 25°C reached its maximum at 348 nm, which is consistent with tryptophan fluorescence. On the addition of a saturating quantity of (dT)76, the intrinsic fluorescence at 348 nm was quenched by 93±3% for the DpsSSB, FpsSSB, ParSSB, PcrSSB, and PtoSSB, by 90±3% for the PprSSB, and by 81±3% for the PinSSB. It was salt independent. The estimated binding site was determined as being approximately 30 ± 2 nucleotides long for the PinSSB, 31 ± 2 nucleotides

for the DpsSSB and 32 ± 2 nucleotides for the ParSSB, PcrSSB, PprSSB, and PtoSSB. Practically no binding mode transition was observed when changing the Sirolimus solubility dmso ionic strength from low to high salt (Figure  4). However, for the FpsSSB, a binding-mode transition of 31 ± 2 nucleotides at low salt concentrations and 45 ± 2 at high ones was observed. Figure 4 Inverse fluorescence titration of SSB proteins with oligo(dT) 76 . The 1.5 nmol samples of the SSB proteins under study were titrated with (dT)76 at 2 mM (Δ), 100 mM (□) and 300 mM (○) NaCl binding buffer. dsDNA melting point destabilization A destabilization of DNA double strands in the presence of SSB must be expected as a thermodynamic consequence of SSB proteins binding specifically to ssDNA and not to dsDNA.

57 PSPPH_1181 glucose ABC transporter, periplasmic glucose-bindin

57 PSPPH_1181 glucose ABC transporter, periplasmic glucose-binding protein, 4-Hydroxytamoxifen molecular weight putative 0.65 PSPPH_1211 cytochrome o ubiquinol oxidase, subunit I 0.55 PSPPH_1508 acetyltransferase, GNAT family 0.35 PSPPH_1518 ATP-dependent DNA helicase RecQ 0.53 PSPPH_1575 CAIB/BAIF family protein 0.65 PSPPH_1759 plasmid stabilization system family protein 0.53 PSPPH_1762 transcriptional regulator, AsnC family 0.54 PSPPH_1917 cation ABC transporter, periplasmic cation-binding protein 0.60 PSPPH_1921 peptidase 0.58 PSPPH_1963 electron transfer flavoprotein-ubiquinone oxidoreductase, putative 0.38 PSPPH_2053 membrane protein, putative 0.65 PSPPH_2057 2-methylcitrate synthase 0.62 PSPPH_2159 dehydrogenase,

isocitrate/isopropylmalate family 0.60 PSPPH_2246 4-alpha-glucanotransferase Epigenetics inhibitor 0.66 PSPPH_2695 peptide ABC transporter, permease protein 0.45 PSPPH_2868 major facilitator family transporter 0.63 PSPPH_2892 TonB-dependent

siderophore receptor, putative 0.62 PSPPH_2897 yersiniabactin non-ribosomal peptide synthetase 0.40 PSPPH_2899 yersiniabactin polyketide/non-ribosomal peptide synthetase 0.58 PSPPH_2904 isochorismate synthase 0.55 PSPPH_3100 isocitrate dehydrogenase, NADP-dependent 0.63 PSPPH_3251 maleylacetoacetate isomerase 0.53 PSPPH_3528 acetate–CoA ligase 0.52 PSPPH_3558 aconitate hydratase 2 0.61 PSPPH_3782 porin D 0.42 PSPPH_3985 3-oxoacyl-[acyl-carrier protein] reductase 0.54 PSPPH_4221 unnamed protein check details product 0.44 PSPPH_4654 smtA protein 0.47 PSPPH_4703 coenzyme PQQ biosynthesis protein PqqF 0.32

PSPPH_4805 oxidoreductase FAD-binding domain/oxidoreductase NAD-binding domain/2Fe-2S iron-sulfur cluster binding domain protein 0.55 PSPPH_4833 Rhs family protein 0.33 PSPPH_4859 transporter, BCCT family 0.65 PSPPH_4869 Glutathione peroxidase cadmium-translocating P-type ATPase 0.54 PSPPH_4885 D-3-phosphoglycerate dehydrogenase 0.56 PSPPH_4938 amino acid ABC transporter, ATP-binding protein 0.61 PSPPH_4962 prophage PSPPH06, C4-type zinc finger protein, DksA/TraR family 0.35 PSPPH_5024 acetyltransferase, GNAT family 0.64 PSPPH_5027 acetyltransferase, GNAT family 0.64 PSPPH_5170 acyltransferase family protein 0.60 PSPPH_A0062 LysR-family transcription regulator SinR 0.45 PSPPH_A0083 IS801, transposase 0.64 PSPPH_A0109 sulfotransferase, putative 0.49 PSPPH_A0129 Yersinia/Haemophilus virulence surface antigen family 0.53 PSPPH_A0132 ISPsy16, transposase 0.66 PSPPH_A0145 conjugal transfer protein 0.56 PSPPH_B0004 RulB protein 0.63 PSPPH_B0050 relaxase, putative 0.65 PSPPH_B0059 exeA-like protein 0.64 The described functions were obtained from the literature. The down-regulated genes were identified using cutoff criteria ≤ 0.6 of ratio. The ratio is in relation to the expression levels obtained between 18°C and 28°C (18°C/28°C). Control: corresponds to genes obtained by PCR amplification that were printed in the microarray.

However, in silico analysis

However, in silico analysis Pexidartinib research buy of all NRPS modules present in the genome of P. syringae 1448a failed to reveal any A-domains predicted to specify alanine. One possibility may be that the variant pyoverdine species was generated as an artefact of the purification process through some unexplained mechanism; however, as the additional monomer clearly seems to fall between the chromophore and lysine residue rather than being added in a peripheral fashion, this explanation seems unlikely.

An alternative explanation is that the product of P. syringae 1448a gene Pspph1923 (the single-module NRPS predicted to incorporate L-lysine; Table 2) may possess a dual activity that enables occasional incorporation of

an additional alanine residue. Unfortunately we were unable to biochemically characterize the substrate FK228 purchase specificity of this or any other of the pyoverdine NRPS modules in in vitro assays – despite obtaining soluble protein by several different strategies, none of our purified proteins appeared to retain activity. This phenomenon is not uncommon for NRPS enzymes. We note however that in ongoing work we have verified the second module of Pspph1925 is indeed a serine-activating NRPS, as predicted by our in silico analysis (Table 2); when appropriate regions of this Thiazovivin mouse gene are swapped with the equivalent regions in module 2 of P. aeruginosa else PAO1 pvdD the substrate specificity of the recombinant gene product is converted from L-threonine [19] to L-serine, and a correspondingly modified pyoverdine product is produced (MJ Calcott, JG Owen, LW Martin, IL Lamont, DF Ackerley, unpublished data). It may be that we can employ a similar ‘recombinant genetic characterization’ strategy to interrogate the substrate specificity of Pspph1923. However, for now the precise nature of the variant P. syringae 1448a pyoverdine species (peak m/z 1212, Figure 2A) remains unknown. Although an equivalent species was not previously detected in studies of other P. syringae pathovars [35, 36], it is possible that these other pathovars also produce this form. As MALDI-TOF

is not a quantitative technique the m/z 1212 peak may actually be a very minor species that happens to ionize particularly well; and as the previous studies utilized an HPLC preparative step to yield a single pure peak, this could conceivably have resulted in other minor peaks being missed. There is evidence from a previous isoelectric focusing analysis that different P. syringae pathovars produce minor variant isoforms of pyoverdine in addition to the major pyoverdine that is synthesized by all known fluorescent P. syringae isolates [45]. It is possible that the minor isoforms include variants that possess alternative side chain constituents as well as variants that have different acyl groups attached to the chromophore.

All authors read and approved the final manuscript “

All authors read and approved the final manuscript.”
“Background Aerobic anoxygenic photoheterotrophic bacteria use light as additional energy source for mixotrophic growth and play a significant

role in the microbial ecology of marine environments [1, learn more 2]. Members of this physiological group belonging to the Alphaproteobacteria have been intensively studied (for review see e.g.[3, 4]), but so far little is known on the phenotypic diversity of representatives belonging to the Gammaproteobacteria. The existence of aerobic anoxygenic photoheterotrophic gammaproteobacteria in marine environments was first postulated in a study by Béjà et al. [5], who could identify photosynthesis genes in partial genome sequences of gammaproteobacteria retrieved from seawater off the coast of California (USA). A few years later the two marine isolates HTCC2080 and KT71T were independently identified as aerobic anoxygenic photoheterotrophic gammaproteobacteria by proteomic analyses [6] and genome sequencing [7], respectively. Strain KT71T was subsequently characterized in detail and described as Congregibacter litoralis (C. litoralis) by Spring click here et al. [8], thereby representing the first photoheterotrophic bacterium of this group with a validly

published name. Phylogenetically, C. litoralis is affiliated to a large coherent cluster of 16S rRNA gene sequences, which were mainly retrieved by cultivation-independent aminophylline methods from marine habitats around the world. This sequence cluster was recognized as a distinct lineage within the class Gammaproteobacteria and designated as OM60 [9, 10] or NOR5 clade [11]. Metabolic active bacteria representing

this clade could be detected in numerous environmental selleck inhibitor samples by using fluorescence in situ hybridization experiments [12, 13]. Based on these findings it is assumed that the OM60/NOR5 clade of Gammaproteobacteria is of significant ecological importance due to its widespread occurrence in the euphotic zone of saline ecosystems and high abundance especially in coastal waters [6, 13, 14]. A phylogenetic lineage closely related to the OM60/NOR5 cluster was originally defined by a 16S rRNA gene sequence retrieved from deep sea sediment and designated BD1-7 [13]. In recent years reports about the isolation of additional strains belonging to the OM60/NOR5 group have accumulated. Some of these strains were described as mixotrophs containing photosynthetic pigments [6, 15] or proteorhodopsin (PR) [16]. In contrast, no photosynthetic pigments were reported in members of the genus Haliea[17–19] or Halioglobus[20].

A p ≤ 0 05 decision rule was utilized as the null hypothesis

A p ≤ 0.05 decision rule was utilized as the null hypothesis

rejection criterion for the individual adjusted statistical tests. SAS version 9.2 (SAS Institute Inc, Cary, NC, USA) was used to conduct the data analyses. Results Safety There were no serious adverse events during the study period. Subjects reported unusual urine oder (n = 1), tiredness (n = 1), dry mouth (n = 1), headaches (n = 2), and nausea (n = 1) while on StemSport supplementation and tiredness/headaches (n = 1) while on the placebo. There were no subject dropouts. Pain and tenderness Perceived ratings of muscle pain and tenderness were significantly increased in both conditions for 72 hours post-exercise (p < 0.001; Figure 2A and B). There were no differences in pain or tenderness ratings between conditions at any time point (baseline adjusted comparison of the mean change in pain and tenderness at 24, 48, 72, and 168 hours

see more post-exercise, p = 0.99). Biceps girth, a measure of local tissue Citarinostat in vitro swelling, was increased for 48-hours post-exercise Emricasan research buy in both conditions (p < 0.03; Figure 2C). Figure 2 Baseline adjusted comparison of the mean change (±SEM) in (A) elbow flexor pain and (B) tenderness, and (C) biceps girth between StemSport and placebo at 24, 48, 72 and 168 hours post-DOMS exercise. *Perceived ratings of muscle pain and tenderness were significantly increased in both conditions for 72 hours post-exercise (p < 0.001; A and B). Measures of muscle function Biceps peak force was decreased for 72 hours in both the placebo (p < 0.02; Figure 3A) and StemSport condition (p < 0.05; Figure 3A). Significant decrements in elbow extension range of motion were observed for 72 hours during the placebo (p < 0.001; Figure 3B), and range of motion tended to be reduced during StemSport supplementation (p < 0.14; Figure 3B). Elbow flexion range of motion was significantly reduced in both groups for 72 hours (p < 0.03; Figure 3C). The only significant

difference in muscle function between conditions was elbow extension range of motion (placebo, 10 degree decrement in elbow extension PRKD3 range of motion at 48 hours post-exercise versus StemSport, 2 degree decrement in elbow extension range of motion; p = 0.003; Figure 3B). Overall, less extension range of motion decrement post-exercise was found with supplementation of StemSport versus the placebo up to 72-hrs post exercise. All measures of muscle function returned to baseline values 1 week post-exercise (p > 0.07; Figure 3A-C). Figure 3 Baseline adjusted comparison of the mean change (±SEM) in (A) biceps peak force, (B) elbow extension range of motion, and (C) elbow flexion range of motion between StemSport and placebo at 24, 48, 72 and 168 hours post-DOMS exercise. *p = 0.003, significantly different from placebo. For biceps peak force, 0.91 kg equates to 2 pounds or 8.9 Newtons.

0 Å resolution structure of photosystem II Nature 438:1040–1044P

0 Å resolution structure of photosystem II. Nature 438:1040–1044PubMedCrossRef Metz JG, Nixon PJ, Rogner M, Brudvig GW, Diner BA (1989) Directed alteration of the D1 polypeptide of photosystem II: evidence that tyrosine-161 is the redox component, Z, connecting the oxygen-evolving complex to

the primary electron donor, P680. Biochemistry 28:6960–6969PubMedCrossRef Nixon PJ, Boehm M, Michoux F, Yu J, Komenda J (2010) Recent AZD3965 solubility dmso advances in understanding the assembly and repair of Photosystem II. Ann Bot 106:1–16 Niyogi KK (1999) Photoprotection revisited: genetic and molecular approaches. Annu Rev Plant Phys 50:333–359CrossRef Noren GH, Raf inhibitor Boerner RJ, Barry BA (1991) EPR characterization of an oxygen-evolving photosystem II preparation from the transformable cyanobacterium

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in photosystem II. Biochemistry 36:11351–11359PubMedCrossRef Shinopoulos KE, Brudvig GW (2012) Cytochrome b 559 and cyclic electron transfer within photosystem II. Biochim Biophys Acta: Bioenergetics 1817:66–75CrossRef Siegbahn PEM (2006) O-O bond formation in the S4 state of the oxygen-evolving complex in photosystem II. Chem Eur J 12:9217–9227PubMedCrossRef Sproviero EM, Gascón JA, McEvoy JP, Brudvig GW, Batista VS (2008) Computational studies of the O2-evolving complex of photosystem II and biomimetic oxomanganese complexes. Coordin Chem Rev 252:395–415CrossRef Stewart DH, Brudvig GW (1998) Cytochrome b 559 of photosystem II. Biochim Biophys Acta: Bioenergetics 1367:63–87CrossRef Stewart DH, Cua A, Chisholm DA, Diner BA, Bocian DF, Brudvig GW (1998) Identification of histidine pentoxifylline 118 in the D1 polypeptide of photosystem II as the axial ligand to chlorophyll Z. Biochemistry 37:10040–10046PubMedCrossRef Stewart DH, Nixon PJ, Diner BA, Brudvig GW (2000) Assignment of the Qy absorbance bands of photosystem II chromophores by low-temperature optical spectroscopy of wild-type and mutant reaction centers. Biochemistry 39:14583–14594PubMedCrossRef Tan Q, Kuciauskas D, Lin S, Stone S, Moore AL, Moore TA, Gust D (1997) Dynamics of photoinduced electron transfer in a carotenoid–porphyrin–dinitronaphthalenedicarboximide molecular triad.

Afr J Biotechnol 2010, 9:604–611

Afr J Biotechnol 2010, 9:604–611. MLN2238 mw 6. Bohach GA, Fast DJ, Nelson RD, Schlievert PM: Staphylococcal and streptococcal pyrogenic toxins involved in toxic shock syndrome and related illnesses. Crit Rev Microbiol 1990, 17:251–272.PubMedCrossRef 7. Breneman DL: Bacterial infection of the skin and soft tissues and their treatment. Curr Opin Infect Dis 1993, 6:678–682.CrossRef 8. Murray DL, Ohlendorf DH, Schlievert PM: Staphylococcal and streptococcal superantigens: their role in human diseases. ASM News 1995, 61:229–235. 9. Dinges MM, Orwin PM, Schlievert PM: Exotoxins of Staphylococcus aureus . Clin Microbiol Rev 2000, 13:16–34.PubMedCrossRef 10.

Barg NL, Harris T: Toxin-mediated

syndromes. In The staphylococci in human disease. Edited by: Crossley KB, Archer GL. New York: Churchill Livingstone; 1997:527–544. 11. Durupt F, Mayor L, Bes M, Reverdy ME, Vandenesch F, Thomas L, Etienne J: Prevalence of Staphylococcus aureus toxins and nasal carriage in furuncles and impetigo. Br J Dermatol 2007, 157:1161–1167.PubMedCrossRef 12. Gladstone GP, Van Heyningen WE: Staphylococcal leucocidins. Br J Exp Pathol 1957, 38:123–137.PubMed 13. Woodin AM: Fractionation of a leucocidin from Staphylococcus aureus . Bioch J 1959, 73:225–237. 14. Szmigielski S, Sobiczewska E, Prévost G, Monteil H, Colin DA, Jeljaszewicz J: Effect of purified staphylococcal GANT61 cost leukocidal toxins on isolated blood polymorphonuclear mTOR inhibitor cancer leukocytes and peritoneal macrophages in vitro . Zentralbl Bakteriol 1998, 288:383–394.PubMedCrossRef 15. Hongo I, Baba T, Oishi K, Morimoto Y, Ito T, Hiramatsu K: Phenol-soluble modulin alpha 3 enhances the human neutrophil lysis mediated by Panton- Valentine leukocidin. J Infec

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It appears that in the end all Lhca’s transfer a similar amount o

It appears that in the end all Lhca’s transfer a similar amount of excitations to the core (Wientjes et al. 2011b). To directly check the influence of the red forms on the trapping time, Wientjes et al. also measured a PSI-LHCI complex which is identical to that of the WT but in which Lhca4 had been substituted with Lhca5 GSK1838705A purchase that does not contain red forms. The fastest decay component becomes slower in the presence of Lhca5 (it goes from 20 to 26 ps), but the corresponding amplitude is strongly increased as compared to WT PSI

(with Lhca4), whereas the amplitude of the slow component, which corresponds to a red spectrum, has concomitantly decreased. This clearly indicates that the transfer from the “blue” antenna Lhca5 to the core is extremely fast. This experiment also shows that the fast decay

component commonly seen in the EET MI-503 in vivo measurements of PSI, is not only due to the trapping from the core, but also from the “blue” antennae. The slow decay originates from Lhca4 and Lhca3. The data show that these red forms together slow down the transfer by a factor of two, in agreement with previous suggestions (Engelmann et al. 2006; Slavov et al. 2008). A scheme of the energy transfer in PSI-LHCI based on Wientjes et al. (2011b) is shown in Fig. 4. Fig. 4 Schematic presentations of energy transfer and trapping in PSI-LHCI based on Wientjes et al. (2011b).

Increasing thickness of the arrows indicates selleck inhibitor increasing rates. The transfer rate between Lhca2 and Lhca4 could not be estimated from the target analysis in that study, but based on structural data, it has been suggested to be similar to the Farnesyltransferase intradimer transfer rates In conclusion, PSI-LHCI in plants the trapping time is around 50 ps. The most red forms are associated with the outer antenna. All Lhca’s transfer excitation energy to the core, the blue Lhca’s (1 and 2) very rapidly and the red ones (Lhca3 and 4) somewhat slower. PSI-LHCI-LHCII supercomplex In all conditions in which PSII is preferentially excited, part of the LHCII population moves to PSI to increase its antenna size, forming the PSI-LHCI-LHCII supercomplex (e.g., Lemeille and Rochaix 2010). This is considered to be a short-term acclimation mechanism that allows maintaining the excitation balance between the two photosystems upon rapid changes in light quality/quantity. However, it has recently been shown that the association of LHCII to PSI occurs also upon long-term acclimation, and it is in fact the most common state in A. thaliana (Wientjes et al. 2013). In normal light conditions (100 μmol/photons/m2) around 50 % of the PSI complexes is complemented by one LHCII trimer, while this value increases in low light and decreases in high light.

However, we cannot exclude that the lack of JamB expression also

However, we cannot exclude that the lack of JamB expression also favors a

better control of metastasis by the immune system since our results show that metastasis of B16F10 expressing ovalbumin are totally cured by cytolytic T cells directed against ovalbumin without the need of priming. Ongoing experiments ABT-263 molecular weight aim to define whether JamB and/or JamC are involved in cytolytic T cell recruitment and activation at metastatic sites. This will help to decipher if preventing metastasis with anti-JamC treatment will be counter-balanced by adverse effects on the immune system. 1 M. Aurrand-Lions et al., J Immunol 174 (10), (2005). 2 C. Lamagna et al., Cancer research 65 (13), (2005). 3 C. Zimmerli et al., J Immunol 182 (8), (2009). 4 C. Fuse et al., J Biological Chemistry 282 (11), (2007). O48 Epstein Barr Virus Infection in Hodgkin’s Lymphoma: A Mechanism Facilitating Induced Regulatory T Cells Recruitment Violaine Francois1, Olivier Morales1, Céline Miroux1, Stéphane Depil1, Anne-Valérie Decouvelaere2,

Pauline Lionne-Huyghe3, Hervé Groux4, Claude Auriault4, Yvan De Launoit1, Véronique Foretinib research buy Pancre1, Nadira Delhem 1 1 CNRS, UMR 8161, Institut de Biologie de Lille, Lille, France, 2 Service d’Anatomo-Pathologie, Pôle Biologie Pathologie, Eurasanté, Lille, France, 3 Service des Maladies du sang, CHRU, Lille, France, 4 UMR 6097, IPMC, Nice, France Purpose: CD4+ helper and

regulatory T cells play important but opposing roles in regulating host immune responses against Hodgkin’s Lymphoma (HL). Fludarabine purchase In 20–40% of patients with HL, Epstein Barr Virus (EBV) is present in the neoplastic cells, however very little is known about regulatory mechanisms induced in presence of EBV. Here, we described associations of regulatory T cells (Treg) with EBV-positive and EBV-negative Hodgkin’s lymphoma. Methods: In a retrospective, population-based study, patients with Hodgkin’s lymphoma were reclassified according to the WHO classification, and EBV status was assessed by in-situ hybridisation of EBV-encoded small RNAs. Using quantitative real time PCR, we first analyzed gene expression of chemokines, immunosuppressive cytokines and regulatory T cells markers on RNA isolated from nodes of 20 EBV-positive HL patients and from 20 EBV-negative HL patients. We also investigated presence of regulatory T cell markers in PBMCs and sequential tonsil biopsies of HL patients. Results: We described in nodes of EBV-positive HL patients, a significant increase of gene expression for the major immunosuppressive cytokine: IL-10 which was correlated with an increased gene expression of several markers of regulatory T cells (CD4+CD25+, Fox P3,CTLA4, GITR). This increase was confirmed by immunohistochemical on frozen nodes biopsies and by flow cytometry on PBMCs of HL patients.

Photosynth Res 92(1):109–120 Portis AR Jr, Parry MAJ (2007) Disco

Photosynth Res 92(1):109–120 Portis AR Jr, Parry MAJ (2007) Discoveries in Rubisco (Ribulose 1,5-bisphosphate carboxylase/oxygenase): a historical Cyclosporin A purchase perspective. Photosynth Res 94(1):121–143 Trebst A (2007) Inhibitors in the functional dissection of the photosynthetic electron transport system. Photosynth Res 92(2):217–224 Wada H, Murata N (2007) The essential role of phosphatidylglycerol in photosynthesis. Photosynth Res 92(2):205–215 Walker DA (2007) From Chlorella to chloroplasts: a personal note. Photosynth Res 92(2):181–185 2006 Forti G, Agostiano A, Barbato R, Bassi R, Brugnoli E, Finazzi G, Garlaschi FM, Jennings RC, Melandri BA, Trotta M. Venturoli G, Zanetti G, Zannoni

D, Zucchelli G (2006) Photosynthesis Research in Italy: a review. Photosynth Res 88(3):211–240 Giacometti GM, Giacometti G (2006) Twenty years of biophysics of photosynthesis in Padova, Italy (1984–2005): a tale of two brothers. Photosynth Res 88(3):241–258 Gorham PR, Nozzolillo CG (2006) Photosynthesis research in Canada from 1945 to the early 1970s. Photosynth Res 88(1):83–100 Govindjee (2006) Celebrating 20 years of historical papers in photosynthesis research. Photosynth Res 87(2):151–158 Zeinalov Y (2006) A brief history of the investigations on photosynthesis in Bulgaria. Photosynth Res 88(2):195–204 2005 Williams RJP (2005) The discovery of the nature of ferredoxin in photosystems: a recollection. Photosynth

Res 85(2):247–250 2004 Allen JP (2004) My daily constitutional in Martinsried. Photosynth Res 80(1–3):157–163 Bauer C (2004) Regulation Selleck AZD1480 of photosystem synthesis in Rhodobacter

capsulatus. Photosynth Res 80(1–3):353–360 Bendall DS (2004) The unfinished story of cytochrome f. Photosynth Res 80(1–3):265–276 Camm EL, Green BR (2004) How the chlorophyll-proteins got their names. Photosynth Res 80(1–3):189–196 Chance B (2004) The stopped-flow method and chemical intermediates in enzyme reactions—a personal Resveratrol essay. Photosynth Res 80(1–3):387–400 Cogdell RJ, Hashimoto H, Gardiner AT (2004) Purple bacterial light-harvesting complexes: from dreams to structures. Photosynth Res 80(1–3):173–179 Cramer WA (2004) Ironies in photosynthetic electron transport: a personal perspective. Photosynth Res 80(1–3):293–305 Crofts AR (2004) The Q-cycle—a personal perspective. Photosynth Res 80(1–3):223–243 Dilley RA (2004) On why thylakoids energize ATP formation using either deCompound C mw localized or localized proton gradients—a Ca2+ mediated role in thylakoid stress responses. Photosynth Res 80(1–3):245–263 Ellis RJ (2004) From chloroplasts to chaperones: how one thing led to another. Photosynth Res 80(1–3):333–343 Fajer J (2004) Chlorophyll chemistry before and after crystals of photosynthetic reaction centers. Photosynth Res 80(1–3):165–172 Fromme P, Mathis P (2004) Unraveling the photosystem I-reaction center: a history, or the sum of many efforts.