Suzuki T, Miki H, Takenawa T, Sasakawa C: Neural Wiskott-Aldrich syndrome protein is implicated in the actin-based motility of Shigella flexneri. EMBO J 1998, 17:2767–2776.PubMedCrossRef

11. Kocks C, Marchand JB, Gouin E, d’Hauteville H, Sansonetti PJ, Carlier MF, Cossart P: The unrelated surface proteins ActA of Listeria monocytogenes and IcsA of Shigella flexneri are sufficient to confer actin-based motility on Listeria innocua and Escherichia coli respectively. Mol Microbiol 1995, 18:413–423.PubMedCrossRef 12. Boujemaa-Paterski R, Gouin E, Hansen G, Samarin S, Le Clainche C, Didry D, Dehoux P, Cossart P, Kocks C, Carlier MF, Pantaloni D: Listeria protein ActA mimics WASp family proteins: it activates filament barbed end branching by Arp2/3 complex. Biochemistry 2001, 40:11390–11404.PubMedCrossRef 13. EPZ-6438 mouse Baines AJ: Evolution of spectrin function in cytoskeletal and membrane networks. Raf inhibitor Biochem Soc Trans 2009, 37:796–803.PubMedCrossRef 14. Bennett V, Baines AJ: Spectrin and ankyrin-based pathways: metazoan inventions for integrating cells into tissues. Physiol Rev 2001, 81:1353–1392.PubMed 15. Baines AJ: The spectrin-ankyrin-4.1-adducin membrane skeleton: adapting eukaryotic

cells to the demands of animal life. Protoplasma 2010, 244:99–131.PubMedCrossRef 16. Baines AJ: Evolution of the spectrin-based membrane skeleton. Transfus Clin Biol 2010, 17:95–103.PubMedCrossRef 17. Li X, Matsuoka Y, Bennett V: Adducin preferentially recruits spectrin to the fast growing ends of actin filaments in a complex requiring the MARCKS-related domain and a newly defined oligomerization

domain. J Biol Chem 1998, 273:19329–19338.PubMedCrossRef 18. Ohanian V, Wolfe LC, John KM, Pinder JC, Lux SE, Gratzer WB: Analysis of the ternary interaction of the red cell membrane skeletal proteins spectrin, actin, and 4.1. Biochemistry 1984, 23:4416–4420.PubMedCrossRef 19. Beck KA, Nelson WJ: The spectrin-based membrane skeleton as a membrane protein-sorting machine. Am J Physiol 1996, 270:C1263-C1270.PubMed 20. Ruetz T, Cornick S, Guttman JA: The spectrin cytoskeleton Flavopiridol (Alvocidib) is crucial for adherent and invasive bacterial pathogenesis. PLoS One 2011, 6:e19940.PubMedCrossRef 21. Gouin E, Gantelet H, Egile C, Lasa I, Ohayon H, Villiers V, Gounon P, Sansonetti PJ, Cossart P: A comparative study of the actin-based motilities of the pathogenic bacteria Listeria monocytogenes, Shigella flexneri and Rickettsia conorii. J Cell Sci 1999,112(11):1697–1708.PubMed 22. Ruiz-Saenz A, VS-4718 Kremer L, Alonso MA, Millan J, Correas I: Protein 4.1R regulates cell migration and IQGAP1 recruitment to the leading edge. J Cell Sci 2011, 124:2529–2538.PubMedCrossRef 23. Bournier O, Kroviarski Y, Rotter B, Nicolas G, Lecomte MC, Dhermy D: Spectrin interacts with EVL (Enabled/vasodilator-stimulated phosphoprotein-like protein), a protein involved in actin polymerization. Biol Cell 2006, 98:279–293.PubMedCrossRef 24.

Gut 2012, 61:43–52.PubMedCrossRef 18. Yan GR, Xu SH, Tan ZL, Yin XF, He QY: Proteomics characterization of gastrokine https://www.selleckchem.com/products/10058-f4.html 1-induced growth inhibition of gastric cancer cells. Proteomics 2011, 11:3657–3664.PubMedCrossRef 19. Toback FG, Walsh-Reitz MM, Musch MW, Chang

EB, Del Valle J, Ren H, Huang E, Martin TE: Peptide fragments of AMP-18, a novel secreted gastric antrum mucosal protein, are mitogenic and motogenic. Am J Physiol Gastrointest Liver Physiol 2003, 285:G344-G353.PubMed 20. Moss SF, Lee JW, Sabo E, Rubin AK, Rommel J, Westley BR, May FE, Gao J, Meitner PA, Tavares R, Resnick MB: Decreased expression of gastrokine 1 and the trefoil factor interacting protein TFIZ1/GKN2 in gastric cancer: influence of tumor histology and relationship to prognosis. Clin Cancer Res 2008, 14:4161–4167.PubMedCrossRef 21. Vogler M: BCL2A1: the underdog in the BCL2 family. Cell Death Differ 2012, 19:67–74.PubMedCrossRef Competing interests The authors declare that they have no competing interests. Authors’ contributions Mao W and Chen J performed the experiments and wrote the paper;

Peng TL and Yin XF organized the figures and collected tissue specimens and patients’ data; Chen MH designed this study and supervised the writing and discussion. All authors SIS3 purchase have read and approved the final version of this manuscript.”
“Introduction Burkitt lymphoma is a high-grade, rapidly-growing and aggressive

B-cell non-Hodgkin’s lymphoma [1]. Three forms are recognized: http://www.selleck.co.jp/products/E7080.html those endemic to Africa, sporadic forms, and those associated with immunodeficiency states. In the endemic and sporadic forms, B lymphocytes possess rearranged immunoglobulin genes and most commonly carry the (8;14) chromosomal translocation of the proto-oncogene c-myc[1]. Although Burkitt lymphoma is sensitive to chemotherapy, the different regimens used to treat this cancer are associated with varied success rates [1, 2]. Prognosis depends on the stage of the disease at diagnosis and is generally worse for children, adolescents, and patients with co-existent AIDS. Baicalin is one of several pharmacologically-active flavones present in Scutellaria baicalensis Georgi (Huang-qin or Chinese skullcap), a plant widely used in traditional Chinese herbal medicine [3]. Although baicalin is generally non-toxic to normal tissues, it exhibits strong anti-inflammatory, anti-viral, and anti-tumor activities [4, 5]. Growth of human leukemia and myeloma cells and of human hepatic, see more prostate, breast, lung, bladder, and estrogenic cancer cells is potently suppressed by this flavone. Molecular mechanisms underlying these growth-suppressive effects are thought to include changes in oxidation/reduction status, cell cycle inhibition, and induction of apoptosis [3–5].

The RpoS protein detected in the clpP/csrA mutant, however, was clearly larger when compared to the protein of the wild type and single mutants, indicating changes JSH-23 in the protein. We propose that RpoS does not function correctly

in this strain, and that this allow the strain to cope with the mutations. Since we observed an elevated level of RpoS protein with apparent normal size in the csrA (sup) mutant, the negative growth effect of RpoS is likely to be present in this strain too. However, the growth defect caused by lack of CsrA appears to be stronger since the double mutant remains severely growth affected. Expression of csrA is increased during growth at 15°C To get further insight into the essential role of csrA at

low temperature, we investigated whether this gene was expressed at elevated levels at low temperatures. Expression of clpP was included as a control, and the expression of this gene was not altered after a temperature downshift to 15°C compared to 37°C (data not shown). In contrast, the expression of csrA was increased several fold in the wild type and clpP mutants, both at 3 and 19 hours after the temperature downshift (Figure 3C), This supports that CsrA plays a specific role in adaptation to growth at low temperature. In the rpoS mutant after 3 hours, and in the clpP/rpoS double mutant after both 3 and 19 hours, expression of csrA was lower than in the other strains tested. After 3 hours, the level in the double mutant corresponded to the level in the rpoS mutant. csrA expression is controlled by RpoS at 37°C [13], NCT-501 mw and the results are consistent next with this also being the case at 10°C. Why the control appears to be lost after 19 hours in the single mutant is currently unknown, but it suggest that another mechanism steps in at this time point. CsrA has previously been shown to be important for induction of the typical heat shock response in Helicobacter pylori [32]. Combined with our results, this could indicate that the CsrA protein is involved in temperature-dependent regulation both at high and

low temperature, however, this has to be further investigated. clpP-mutation causes formation of filamentous cells in an RpoS dependent manner Growth by elongation of cells with incomplete separation is important in selleckchem relation to food safety. Rapid completion of separation occur when filamentous cells, produced during chilling, are transferred to 37°C, and a more than 200-fold increase in cell number can be found within four hours [33]. S. Enteritidis wild-type strains with normal RpoS level have previously been reported to produce filaments up to 150 μm at 10°C whereas strains with impaired RpoS expression are only up to 35 μm long [33,34]. Microscopic examination of cultures grown at 10°C and 15°C showed that the clpP mutant formed long filamentous cells (Figure 4A) similar to what is seen for the B. thuringiensis clpP1 mutant at 25°C [11].

Second, as shown in Figure 5, PEPCK is required to convert PEP into OAA in the partial reductive TCA (rTCA) cycle. SN-38 manufacturer without assimilating CO2 by PEPCK, carbon flux through the partial rTCA cycle cannot take place. Possible functions of PFOR and FNR during chemotrophic growth To evaluate the buy MK-4827 function of PFOR and FNR in pyruvate metabolism in darkness, we examine the culture growth in acetate-supported medium with and without the addition of HCO3 – and acetate excretion from pyruvate-grown cultures. No CO2-enhanced growth in acetate-supported

medium can be detected, and cell growth in acetate medium is extremely slow in darkness (data not shown). Also, approximately 44% of the pyruvate in pyruvate-grown cultures is converted into acetate during chemotrophic growth (Table 3). Madigan and coworkers reported a large amount of CO2 by analyzing the gas phase of chemotrophic-grown heliobacterial cultures [21]. Together, the following roles of PFOR and FNR during chemotrophic growth can be proposed (Figure 8): (1) PFOR provides energy and reducing power for cellular functions. PFOR catalyzes pyruvate fermentation to acetyl-CoA, CO2, 2 Fdred and 2 H+ (equation 1). Fdred is used for carbon and nitrogen metabolism

in Selleckchem LDN-193189 darkness (Figure 7), and 2 Fdred and 2 H+ from the oxidation of pyruvate can generate H2 by [FeFe]-hydrogenase (2 Fdred + 2 H+ → 2 Fdox + H2) (Figure 8). 2 Fdox can be then used for pyruvate fermentation. Further, acetyl-CoA can be utilized to generate acetate and produce ATP through substrate-level phosphorylation catalyzed by ACK (Table 3 and Figure 5). This

ATP production process may partially explain pyruvate being the most favorable nutrition source; and (2) FNR produces NADPH during chemotrophic growth. As mentioned above, essential genes in the oxidative pentose phosphate and ED pathways, two potential sources producing NADPH, are missing in the H. modesticaldum genome. While NADPH is generated by FNR via the light-induced Venetoclax molecular weight electron transfer during phototrophic growth, NADPH production is also required during chemotrophic growth. It is likely that some Fdred molecules produced by pyruvate fermentation in H. modesticaldum are used to produce NADPH by FNR during chemotrophic growth (equation 2). When this occurs, Fdox is regenerated for pyruvate fermentation (Figure 8). In summary, since [FeFe]-hydrogenase and FNR compete for using 2 Fdred and 2 H+ produced from pyruvate fermentation, intracellular NAD(P)H availability likely plays important role on H2 production, as well as nitrogen and carbon flux, in H. modesticaldum. Figure 8 Summary of energy metabolism of H. modesticaldum during phototrophic and chemotrophic growth described in this report. Bold curves and lines represent the proposed major pathways during phototrophic (shown in blue) and chemotrophic (shown in green) growth.

J Gerontol A Biol Sci Med Sci 67:13–16PubMedCrossRef 20. Fielding RA, Vellas B, Evans WJ, Bhasin S, Morley JE, Newman AB, Abellan van Kan G, Andrieu S, Bauer J, Breuille D, Cederholm T, Chandler J, De Meynard C, Donini L, Harris T, Kannt A, Keime Guibert F, Onder G, CP673451 cell line Papanicolaou D, Rolland Y, Rooks D, Sieber C, Souhami E, Verlaan S, Zamboni M (2011) Sarcopenia: an undiagnosed condition in older adults. Current consensus definition: prevalence, etiology, and consequences. International

Working Group on Sarcopenia. J Am Med Dir Assoc 12:249–256PubMedCrossRef 21. Cruz-Jentoft AJ, Baeyens JP, Bauer JM, Boirie Y, Cederholm T, Landi F, Martin FC, Michel JP, Rolland Y, Schneider SM, Topinkova E, Vandewoude M, Zamboni M (2010) Sarcopenia: European consensus on definition and diagnosis: report of the European Working Group on Sarcopenia in Older People. Age Ageing 39:412–423PubMedCrossRef 22. Stenholm S, Harris TB,

Rantanen T, Visser M, Kritchevsky SB, Ferrucci L (2008) Sarcopenic obesity: definition, cause and see more consequences. Curr Opin Clin Nutr Metab Care 11:693–700PubMedCrossRef 23. Prado CM, Wells JC, Smith SR, Stephan BC, Siervo M (2012) Sarcopenic obesity: a critical appraisal of the current evidence. Clin Nutr 31:583–601PubMedCrossRef 24. Marcus RL, Addison O, Dibble LE, Foreman KB, Morrell G, Lastayo P (2012) Intramuscular adipose tissue, sarcopenia, and mobility function in older individuals. J Aging Res. doi:10.​1155/​2012/​629637 25. Rolland Y, Lauwers-Cances V, Cristini C, van Kan GA, Janssen I, Morley JE, Vellas B (2009) Difficulties with physical function associated

with obesity, sarcopenia, and sarcopenic-selleck inhibitor obesity in community-dwelling elderly women: the EPIDOS study. Am J Clin Nutr 89:1895–1900PubMedCrossRef ID-8 26. Marcus RL, Brixner DI, Ghate S, Lastayo P (2012) Fat modulates the relationship between sarcopenia and physical function in nonobese older adults. Curr Gerontol Geriatr Res 2012:216185PubMed 27. Dufour AB, Hannan MT, Murabito JM, Kiel DP, McLean RP (2013) Sarcopenia definitions considering body size and fat mass are associated with mobility limitations: the Framingham study. J Gerontol A Biol Sci Med Sci 68:168–174PubMedCrossRef 28. Baumgartner RN, Wayne SJ, Waters DL, Janssen I, Gallagher D, Morley JE (2004) Sarcopenic obesity predicts instrumental activities of daily living disability in the elderly. Obes Res 12:1995–2004PubMedCrossRef 29. Waters DL, Hale L, Grant AM, Herbison P, Goulding A (2010) Osteoporosis and gait and balance disturbances in older sarcopenic obese New Zealanders. Osteoporos Int 21:351–357PubMedCrossRef 30. Nielson CM, Srikanth P, Orwoll ES (2012) Obesity and fracture in men and women: an epidemiologic perspective. J Bone Miner Res 27:1–10PubMedCrossRef 31.

1 was used. A negative control was

included for each LAMP run. PCR As a comparison, two sets of PCR reactions were performed, one using LAMP outer primers (F3 and B3) and the other one using the toxR-PCR primers (Table 2) published previously [18]. Each PCR mix in a 25 μl total volume contained 1 × PCR buffer, 0.2 mM of each dNTP, 1.5 mM of MgCl2, 0.5 μM of each forward and reverse primer, 0.625 U of GoTaq Hot Start Polymerase (Promega, Madison, WI), and 2 μl of DNA template. The PCR reactions were conducted using initial denaturation at 95°C for 5 min followed by 30 GSK1210151A nmr cycles of denaturation at 94°C for 1 min, primer annealing at 60°C (50°C for F3/B3 primers) for 1 min, extension at 72°C for 1 min, and a final extension at 72°C for 7 min in a Bio-Rad ACP-196 C1000 Thermal Cycler (Hercules, CA). Aliquots Dabrafenib (10 μl) of PCR products were analyzed by electrophoresis on 1.5% agarose gel containing ethidium

bromide, and visualized under UV light. Gel images were documented by a Gel Doc XR system (Bio-Rad). LAMP specificity and sensitivity Seventy-five bacterial strains (Table 1) were used to determine the LAMP specificity. DNA templates were made from fresh overnight bacterial cultures and aliquots (2 μl) were subjected to both LAMP and PCR amplifications. Specificity tests were repeated twice. To determine LAMP sensitivity, serial 10-fold dilutions (ca. 108 CFU/ml to extinction) of a mid-log phase V. parahaemolyticus ATCC 27969 culture grown in TSB were prepared in phosphate buffered saline (PBS; BD Diagnostic Systems) and quantified using the standard plating method. DNA templates were prepared from each dilution by the boiling method described above and aliquots (2 μl) were subjected to both LAMP and PCR amplifications. Sensitivity tests were repeated six times and the lower limits of detection

(CFU/reaction) were reported. Standard curves were generated Sucrase by plotting Ct (cycle threshold; for the real-time PCR platform) or Tt (time threshold; for the real-time turbidimeter platform) values against log CFU/reaction and the linear regression was calculated using the Microsoft Excel Software (Seattle, WA). LAMP testing in experimentally inoculated oyster samples Oyster samples were obtained from local seafood restaurants and determined to be V. parahaemolyticus-negative as described previously [10]. Oyster samples were processed following a previous study with slight modifications [11]. Briefly, 25 g of oyster sample was mixed with 225 ml of alkaline peptone water (APW; BD Diagnostic Systems) and homogenized in a food stomacher (Model 400; Tekmar Company, Cincinnati, OH) for 90 s to generate 1:10 oyster in APW homogenate. Serial 10-fold dilutions of a mid-log phase V. parahaemolyticus ATCC 27969 culture were prepared in PBS as described above. Aliquots (100 μl) of each dilution were inoculated into 900 μl of the 1:10 oyster in APW homogenate.

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Table  1 also shows that the two different electrolyte formulas have the same variation trends as the used voltage increases. As the voltage was changed from 0.00 to -0.50 V, the ratios of Bi and Sb elements in (Bi,Sb)2 – x Te3 + x compositions increased. Two reasons are believed to cause those results. First, the reduced reactions

of Bi3+, Sb3+, and Te4+ ions start at -0.23, -0.23, and 0.20 V (Figure  2). For that, as 0.00 to -0.20 V is used, the main element in the deposited materials is Te. As the voltage is smaller than -0.30 V, the driving forces of reduction for Bi3+ and Sb3+ ions increase LY3009104 datasheet and the ratios of Bi and Sb elements in the deposited compositions increase. Second, the driving force for mass KU-60019 order transfer is typically a difference in chemical potential, though other thermodynamic gradients may couple to the flow of mass and drive it as well. As the voltage value is more negative (means the applied voltage is larger than the needed reduction voltage), the mass transfer effect will influence the compositions of the deposited (Bi,Sb)2 – x Te3 + x materials. A chemical species moves from areas of high chemical potential to areas of low chemical potential. Thus, the maximum theoretical extent of a given mass transfer is typically determined by the point at which

the chemical potential is uniform. For multiphase systems, chemical species will often prefer one phase over the others and reach a uniform chemical potential only when most of the chemical species has been H 89 nmr absorbed into the preferred phase, while the actual rate of mass transfer will depend on additional factors including the flow patterns within the system

and the diffusivities of the species in each phase. As shown in Table  1, because the Te4+ ions have lower concentration in the two electrolyte formulas, it will easily reach the mass transfer condition because of higher consumption and then Te4+ ions will reach a saturation value (about 44 at.% for electrolyte formula (a) and 30 at.% for electrolyte formula (b)) even larger negative voltage is used. As compared for Bi3+ and Sb3+ ions, they have the larger negative reduced voltage and lower consumption, the mass transfer effect will not happen. For that, the concentrations of Bi and Sb elements will increase with increasing bias voltage (large negative voltage). Ergoloid When the potentiostatic deposition process is used, the obtained results prove that as more negative voltage is used as bias, the electrolyte concentrations (or ion diffusion effect) will influence the compositions of the deposited (Bi,Sb)2 – x Te3 + x materials. If we control the diffusion of ions (Bi3+, Sb3+, and Te4+), we can regulate the compositions of the deposited (Bi,Sb)2 – x Te3 + x materials. For that, the pulse deposition process is used to deposit the electrolyte formula of 0.015 M Bi(NO3)3-5H2O, 0.005 M SbCl3, and 0.0075 M TeCl4. The bias voltage was set at -0.40 V, the bias on time (t on) was set at 0.

0398). Table 2 Correlation between gene expression and GEM efficacy in patients with pancreatic cancer receiving GEM monotherapy.     GEM efficacy   Gene Expression* Evofosfamide   Effective§ Non-effective P ¶-value hENT1 High 4 9 >0.9999   Low 8 14   hENT2 High 6 9 0.5374   Low 6 14   dCK High 8 7 0.0398   Low 4 16   DCD High 3 9 0.4765   Low 9 14   CDA High 4 9 >0.9999   Low 8 14   5′-NT High 4 12 0.2882   Low 8 11   RRM1 High 4 8 >0.9999   Low 8 15   RRM2 High 4 8 >0.9999   Low 8 15   GEM, gemcitabine *Gene expression was determined as high or low based on mean values of 35 EUS-FNA samples. §Effective, partial response by imaging study

or stable disease by imaging study with 50% or more decrease in tumor markers compared to pretreatment value ¶ P, examined by chi-squared test (Fisher’s exact test) Discussion EUS-FNA is widely used as a cytological and histological diagnostic method for pancreatic cancer [8, 11].

However, there have been few reports on gene analysis of pancreatic cancer using EUS-FNA samples [7, 8, 12]. In contrast, a number of https://www.selleckchem.com/products/INCB18424.html studies have demonstrated the feasibility of DNA microarray analysis using samples obtained by FNA in other malignancies, such as breast cancer and lung cancer [13–15]. At least 10 μg of total RNA is required for DNA microarray analysis [10]. Due to the low volume of biopsy specimens obtained by EUS-FNA, it is typically impossible to selleck inhibitor perform DNA microarray analysis using the raw RNA extracted from these samples. However, a high-fidelity RNA amplification protocol has recently been established [10, 16] that allows analysis of gene expression profiles using small volumes RNA, such as those obtained by EUS-FNA. In our series, only 0.1 – 3.0 μg of total RNA was extracted from EUS-FNA biopsy samples. The objective response rate of GEM monotherapy for pancreatic cancer has been reported to be 5–12% [1, 17, 18]. In this study, PR was observed in 5 of 35 (14%) patients treated with GEM monotherapy, which corresponds

with the response rates reported previously. The number of patients in the GEM-effective group was too these small to evaluate for correlations between GEM efficacy and mRNA expression. Therefore, SD patients with a 50% or more decrease in abnormal serum levels of tumor markers compared to baseline were included in the GEM-effective group. CA 19-9 has been shown to be correlated with clinical efficacy of GEM in pancreatic cancer [19]. In this study, the GEM-effective group had a significantly better prognosis than the non-effective group, indicating that the grouping based on GEM efficacy was appropriate. GEM is transported into the cell largely via hENT1 and partly via hENT2 [4].

The experiment was done in duplicates shown by filled and empty symbols. Note that only the UV radiation curve is shown in graph B since the visible light curve is the same as in graph A. Black arrows indicate the time point of the shift. White and black bars indicate light and dark periods. The dashed line indicates the growth irradiance curve (right axis). Abbreviations as in Fig. 1. Table 2 Growth parameters of PCC9511 batch Nutlin3a cultures shifted from LL to HL during 12 h/12 h L/D cycles. Growth Parameters* Cycle 1 (LL) Cycle 2 (HL) Cycle 3 (HL) μcc (d-1) 0.43 ± 0.03 0.67 ± 0.01

0.62 ± 0.01 μnb (d-1) 0.37 ± 0.04 0.59 ± 0.09 0.58 ± 0.05 TG1 (h) 30.8 ± 3.1 16.7 ± 0.3 18.8 ± 0.2 TS (h) 4.12 ± 0.01 5.15 ± 0.14 5.53 ± 0.12 TG2 (h) 3.89 ± 0.01 2.85 ± 0.14 Selleck JQ1 2.47 ± 0.12 Sr 20.8 ± 1.7 32.4 ± 0.4 29.8 ± 0.3 Values shown are averages (± mean deviation) of two biological replicates * Growth rates per day calculated from: cell cycle data (μcc) or cell numbers (μnb); TG1, TS, TG2: cell cycle phase duration in hours; Sr: rate of synchronization estimated from the ratio

(TS+TG2)/(TG1+TS+TG2) In the second shift experiment, HL acclimated PCC9511 cultures were sampled during one complete L/D cycle, then on the following two days were subjected to a modulated L/D cycle Apoptosis inhibitor of HL+UV radiations. As for the HL+UV acclimated cells, UV exposure seemed to cause a delay in the initiation of DNA replication, but with the peak of S cells occurring 3 to 4 h after the LDT (Fig. 2B), instead of 2 h. Furthermore, although the UV dose received by the cells was the same in the UV acclimation and UV shift experiments, UV irradiation was clearly much more stressful for the cells in the second case, as they reacted by dramatically decreasing their growth rate (Table 3), an effect which was even more marked on the second day after switching the UV lamps on. Table 3 Growth parameters of PCC9511 batch cultures shifted from HL to HL+UV during 12 h/12

h L/D cycles. Growth Parameters* Cycle Pyruvate dehydrogenase lipoamide kinase isozyme 1 1 (HL) Cycle 2 (HL+UV) Cycle 3 (HL+UV) μcc (d-1) 0.69 ± 0.02 0.61 ± 0.01 0.45 ± 0.00 μnb (d-1) 0.64 ± 0.05 0.45 ± 0.02 0.1 ± 0.02 TG1 (h) 18.0 ± 0.6 21.4 ± 0.3 29.3 ± 0.2 TS (h) 3.67 ± 0.14 3.72 ± 0.09 6.25 ± 0.03 TG2 (h) 2.33 ± 0.14 2.28 ± 0.09 1.75 ± 0.03 Sr 25.0 ± 0.7 21.9 ± 0.2 21.5 ± 0.1 Values shown are averages (± mean deviation) of two biological replicates *Growth rates per day calculated from: cell cycle data (μcc) or cell numbers (μnb); TG1, TS, TG2: cell cycle phase duration in hours; Sr: rate of synchronization estimated from the ratio (TS+TG2)/(TG1+TS+TG2) Comparative cell cycle dynamics of acclimated P.