Am J Epidemiol 137:1001–1005PubMed 16. Kanis JA, Oden A, Johnell O, De Laet C, Jonsson B, Oglesby AK (2003) The components of excess mortality after hip fracture. Bone 32:468–473PubMedCrossRef 17. Blake GM, Fogelman I (2007) Role of dual-energy X-ray absorptiometry in the diagnosis and treatment of osteoporosis.

J Clin Densitom 10:102–110PubMedCrossRef 18. Engelke K, Gluer CC (2006) Quality and performance measures in bone densitometry: part 1: errors and diagnosis. Osteoporos Int 17:1283–1292PubMedCrossRef 19. Gluer CC, Lu Y, Engelke K (2006) Quality and performance measures in bone densitometry. Part 2: fracture risk. Osteoporos Int 17:1449–1458PubMedCrossRef 20. Ranjanomennahary P, Ghalila SS, Malouche D, Marchadier A, Rachidi M, Benhamou C, Chappard C (2011) Comparison of radiograph-based texture analysis and bone mineral density with three-dimensional microarchitecture ALK cancer GW-572016 chemical structure of trabecular bone. Med Phys 38:420–428PubMedCrossRef 21. Fouque-Aubert A, Boutroy S, Marotte H, Vilayphiou N, Lespessailles E, Benhamou CL, Miossec P, Chapurlat R (2011) Assessment of hand trabecular bone texture with high resolution direct digital radiograph in rheumatoid arthritis: a case control study. Joint Bone Spine 79:379–383PubMedCrossRef 22. Hans D, Goertzen AL, Krieg MA, Leslie

WD (2011) Bone microarchitecture assessed by TBS predicts osteoporotic fractures independent of bone density: the Manitoba study. J Bone Miner Res 26:2762–2769PubMedCrossRef 23. Hans D, Barthe N, Boutroy S, Pothuaud L, Winzenrieth R, Krieg MA (2011) Correlations between trabecular bone score, measured using anteroposterior dual-energy X-ray absorptiometry acquisition, and 3-dimensional parameters of bone microarchitecture: an experimental study on human cadaver vertebrae. J Clin Densitom 14:302–312PubMedCrossRef

24. Genant HK, Lang TF, Engelke K, Clomifene Fuerst T, Gluer C, Majumdar S, Jergas M (1996) Advances in the noninvasive assessment of bone density, quality, and structure. Calcif Tissue Int 59(Suppl 1):S10–S15PubMedCrossRef 25. Mazess RB, Collick B, Trempe J, Barden H, Hanson J (1998) Performance evaluation of a dual energy x-ray bone densitometer. Calcif Tissue Int 44:228–232CrossRef 26. Schousboe JT, Ensrud KE, Nyman JA, Kane RL, Melton LJ 3rd (2005) Potential cost-effective use of spine radiographs to detect vertebral deformity and select osteopenic post-menopausal women for amino-bisphosphonate therapy. Osteoporos Int 16:1883–1893PubMedCrossRef 27. Schousboe JT, Ensrud KE, Nyman JA, Kane RL, Melton LJ 3rd (2006) Cost-effectiveness of vertebral fracture assessment to detect prevalent vertebral deformity and select postmenopausal women with a femoral neck T-score >-2.5 for alendronate therapy: a modeling study. J Clin Densitom 9:133–143PubMedCrossRef 28.

B: The minimum spanning tree was

constructed with a categorical coefficient. Each circle represents a different MLST type (ST). The colour of a circle and the line clustering the MT with the same colour are corresponding to identical sequence type (ST). Same colours design STs in Figure 1A. Size of the circle reflects the number of isolates designed in italic numbers within parenthesis, while the width of the line reflects the genetic distance between MT (heavy short lines connect SLVs, thin longer lines connect DLVs, and dotted lines indicate the most likely connection between 2 STs differing by more than 2 loci). The number of loci that differ between two MTs is indicated on the lines connecting the MTs. Clonal learn more complexes (CC) were defined as MTs having a maximum distance of changes at 2 loci and a minimum cluster size of 2 types. Each CC as a cluster is shaded in a different colour. Knowing selleck compound the MLVA type it is possible to deduce not only the ST but also the associated serotype depending on the clonality of the serotypes. It is the case for serotype 1 because of its strong clonality, whereas it is not possible for the serotype 19F. Moreover, the carriage is more frequent for certain serotypes, particularly serotype 19F, meaning that isolates belonging to those serotypes often exchange DNA with other carried. So the

serotype of a pneumococcus strain can change but not

its other genetic characteristics’. Indeed, carriage serotypes are distributed along the dendrogram and can belong to very different genotypes. However, in order to compare identical number of MLST and MLVA markers, a set of seven MLVA markers was considered. The set includes three markers with the highest discriminatory power (DI > 0.8), one marker with a low discriminatory power acting as an anchor for the dendrogram, and three others, selected for a low IMD and for their ability to distinguish ST 227 and ST 306, and based on previous data [19]. The composition of the MLVA set was adapted as follows: ms17, ms19, ms25, ms27, ms33, ms37, ms39 . The comparison between Lepirudin MLST and MLVA using seven markers was obtained by construction of a minimum spanning tree (Figure 2A). Congruence MLST/MLVA was 47.2%. Figure 2 Minimum spanning tree constructed from 7 MLVA markers for 331 pneumococcal isolates from this study. A: ms17, ms19, ms25, ms27, ms33, ms37, ms39 markers used for this study; B: ms17 ms19, ms25, ms34, ms37, ms39 markers [25]; C: ms15, ms25, ms32 ms33, ms37, ms38, ms40 [26]. Clusters were defined as MTs having a maximum distance of changes at 1 loci and a minimum cluster size of 1 type. The minimum spanning tree was constructed with a categorical coefficient. Each circle represents a different MLVA type (MT). The colour of a circle indicates the number of the corresponding sequence type (ST).

0,

P < 0.001) but not day (df = 4, F = 0.2, P = 0.91). However a Tukey-Kramer post-hoc test revealed that only the DMSO-treated cells, which were expected to show reduced viability, differed significantly from control cells (P < 0.05), while none of the dsRNA/siRNA treated cells differed from controls (P > 0.05). Figure 4 Proportion of viable cells (absorbance of individual wells divided by mean absorbance of control wells) in cells treated with media only (cells), 8% DMSO, or dsRNA/siRNAs targeting Ago-1, Ago-2, Dcr-1 or Dcr-2. Only DMSO significantly affected cell viability. DENV replication following knockdown of RNAi genes To test whether the RNAi response has an effect on DENV replication in S2 cells, four components of the RNAi pathway (Dcr-1, Dcr-2, Ago-1 and Ago-2) were individually depleted via knockdown with an appropriate dsRNA or siRNA. The efficacy of depletion Inflammation inhibitor of each enzyme was confirmed Poziotinib cell line using Western blot analysis (Figure 5). Dcr-1 levels were depleted for six days following treatment, but unlike the other three treatments there were no days on which Dcr-1 expression was undetectable. Dcr-2 expression was undetectable until day three post-treatment

and showed steady recuperation thereafter. Ago-1 expression was undetectable through day five post-treatment. Ago-2 expression was undetectable until day three post-treatment and rebounded on day four. To prevent recovery of expression,

all infected cell knockdowns were re-fed dsRNA/siRNA on day three post initial dsRNA/siRNA treatment. Figure 5 Knock down of specific enzymes of the RNAi pathway. Immunoblot of: A- Dcr-1 dsRNA-treated S2 cells detected with Dcr-1 antibody. B- Dcr-2 dsRNA-treated Abiraterone cell line S2 cells detected with Dcr-2 antibody. C- Ago-1 dsRNA-treated S2 cells detected with Ago-1 antibody. D- Ago-2 siRNA treated-S2 cells detected with Ago-2 antibody. E – H: Actin expression for samples of A, B, C and D as an equal loading control. As shown in Figure 6, all 12 DENV strains tested achieved significantly higher titers (usually a 100-fold increase) in cells depleted of Dcr-2 relative to control cells (paired t-test, df = 11, P < 0.0001). The 12 DENV strains attained similar titers in cells treated with a control dsRNA treatment as compared to untreated cells. Moreover, there was no significant difference among serotypes in the impact of Dcr-2 knockdown, measured as the difference in titer for a particular replicate virus in knockdown cells versus control cells (ANOVA, df = 3, F = 1.04, P = 0.41). In contrast, variation in the impact of RNAi knockdown on the three DENV strains within serotypes was detected using factorial ANOVAs for each serotype; when significant differences were detected, a Tukey-Kramer post-hoc test was used to determine which strains showed significant differences in response to knockdown.

Upstream of the ply gene cluster, three genes, orf03394 (orf1), orf03396 and orf03399, encoding proteins with similarities to 3-dehydroquinate synthase,

sugar kinase and nucleotidyl transferase respectively, seemingly have no relationship with the biosynthesis of PLYA. orf03392 (orf2), adjacent to orf1, is predicted to encode a protein with similarity to a transcriptional regulator, which may be involved in the biosynthesis of PLYs. Downstream of the ply gene cluster, three genes, orf14746 (plyZ), orf14744 Emricasan order (orf11) and orf14742 encode proteins with similarities to LysR family transcriptional regulator, hypothetical protein ROP_29250 and hypothetical protein ROP_03220. To prove that the genes beyond this cluster are not related to PLY biosynthesis, we inactivated orf1 and orf11. The resulting mutants have no effect on the PLYA production (Figure  3, trace ii and iii), indicating that the 37 ORFs-contained ply gene cluster is responsible for the PLYs biosynthesis. Assembly of the C15 acyl side chain by PKSs Within the ply cluster, 4 modular type I PKS genes (plyTUVW) encode four PKS modules, the organization of which

is accordant with the assembly of the C15 acyl side chain of PLYA via three steps of elongation from the propionate starter unit (Figure  2B). Both PlyT and PlyW consist of ketosynthase AP26113 price Rebamipide (KS), acyltransferase (AT), and acyl carrier protein (ACP). However, the active site Cys (for transthioesterification) of the PlyT-KS is replaced with Gln (Additional file 1: Figure S1), so it belongs to the so called “KSQ” that often occurs in the

loading module of PKS system [24]. Therefore, PlyT acts as a loading module for formation of the propionate starter unit by catalyzing decarboxylation of methylmalonyl group after tethering onto ACP (Figure  2B). The conserved regions of AT domain including the active site motif GHSQG [25] in both PlyT and PlyW (Additional file 1: Figure S2), along with substrate specificity code (YASH) [26] indicate that both ATs are specific for methylmalonyl-CoA, consistent with the structure of the side chain of PLYA (Figure  2B). In PlyU, in addition to KS, AT, and ACP domains, a dehydratase (DH) domain and a ketoreductase (KR) domain are present. However, the DH domain here is believed to be nonfunctional because the key amino acid residue H of the conserved motif HxxxGxxxxP [27] is replaced by Gln (Additional file 1: Figure S3).

The difference in local control times can be ascribed

to the decision to enroll in the intraoperative group cats with rapidly growing neoplasms, leading to greater electroporation fields. One critical advantage Lazertinib concentration of this technique is the possibility to repeat the treatment in selected patients experiencing local recurrence without the side effects of re-irradiated tissues [26]. A similar study in 22 dogs with soft tissue sarcomas, preferentially treated with a postoperative protocol, yielded a median time to recurrence of 730 days with a 95% response rate, and again hemangiopericytoma showed to be extremely sensitive to ECT, data confirmed by results obtained in cats as well [27, 39]. The side effects of veterinary patients

treated with adjuvant ECT were confined to local inflammation and occasional wound dehiscence [26, 27]. Concurrently, adjuvant ECT has been tested in a cohort of 28 dogs with mast cell sarcomas, resulting in a response rate of 85% and a mean time to recurrence of 52.7 https://www.selleckchem.com/products/ON-01910.html ± 6.5 months, moreover the authors reported that at the time of writing the median time to recurrence was not reached yet, since 24 of the patients were still disease free [28]. Two patients experiencing marginal recurrence were successfully treated with a minor surgery combined with a single application of electrochemotherapy [28]. The use of ECT is not strictly limited to superficial neoplasms: there is also some evidence that trains of biphasic pulses can improve the local control of incompletely excised however deep perianal tumors, with preservation of organ function [35, 36, 40]. Caution

should be exerted when adopting ECT as a rescue in patients that failed radiation therapy. A case report describes a severe radiation recall in a cat treated with adjuvant radiation therapy for a recurring fibrosarcoma [41]. Interestingly, this cat has been locally treated with cisplatin rather than bleomycin and perhaps the reaction has been triggered by the local administration of a platinum compound, since it is among the drugs linked with this type of complication [42]. Table 1 summarizes the results obtained in companion animals carrying spontaneous tumors that have been so far treated with electrochemotherapy.

AP was known to be synthesized initially in the cytoplasm and then translocated out through the inner membrane to be finally localized as dimeric, active form at the periplasm [32, 33]. As the dimerization of AP, through the disulfide bond, could not take

GSK690693 nmr place in the reducing milieu of the cytoplasmic environment, the cytosolic pool of the nontranslocated AP in the CCCP-treated cells had shown no activity [34, 35]. Figure 4 A. L evel of active AP in E. coli MPh42 cells grown in the presence of different concentrations of CCCP. Cells were initially grown to log phase (~1.5 × 108 cells/ml) at 30°C in complete MOPS medium and were then transferred to phosphate-less MOPS medium. The re-suspended cells were divided in different parts to treat with the different concentrations of CCCP (0, 10, 30 and 50 μM). The divided

cell cultures were then allowed to grow further at 30°C for induction of AP. At different intervals of time, a 1.0 ml cell aliquot was withdrawn from each culture to assay the active AP level. B. Western blot of the different fractions (periplasmic, cytoplasmic and membrane) PF-6463922 datasheet of E. coli MPh42 cells grown in the presence of CCCP (50 μM). After allowing induction of AP for 30 min, the periplasmic, cytoplasmic and membrane fractions were isolated from equal number of each of the CCCP-treated and the control cells and the western blotting experiment was subsequently performed using anti-AP antibody. Lanes (a, b, c) and (e, f, g) represent the membrane, periplasmic and cytoplasmic fractions of control and CCCP-treated cells respectively; lane d represents purified AP. To investigate whether the non-translocated AP in cell cytosol could have been transported out to the periplasm on withdrawal of CCCP from the growth medium, pulse-chase and immunoprecipitation experiment was performed. Cells, grown in phosphate-free (required for the induction of AP) and

methionine-free MOPS medium in the presence of 50 μM CCCP, were radio-labeled with 35S-methionine for 30 min; the CCCP was then removed IMP dehydrogenase by centrifugation and the cells were resuspended in the phosphate-less MOPS medium. Finally the chasing with cold methionine was allowed for 1 hr. The periplasmic fractions of the chased cells were isolated, immunoprecipitated with anti-AP antibody, the immunoprecipitates were run in 12% SDS-polyacrylamide gel, western blotting with anti-AP antibody was done and the blotted membrane was finally autoradiographed [36]. The autoradiograph (Fig. 5A) showed that the periplasmic fraction of the CCCP-treated cells had contained no trace of AP (lane b), whereas that of the control cells contained it (lane a). This signified that the AP, synthesized during the presence of CCCP (i.e., for the labeling period of 30 min), could not be translocated out to the periplasm, even after 60 min of chasing in the absence of CCCP. The western blot result (Fig.

Critically reviewed the manuscript: MNBM. Both authors read and approved the final manuscript.”
“Background Bacterial persistence is a form of phenotypic heterogeneity in which a subset of cells within an isogenic

population is able to survive challenges with antibiotics or other stressors better than the bulk of the population [1]. The persistence phenotype is transient and non-genetic, in contrast to antibiotic resistance, which is due to genetic changes. However, the ability to form persister cells, or the fraction of persister cells that are present in a culture, can be genetically controlled (see below). KPT-8602 nmr The phenomenon of persistence has significant clinical relevance [2], and it may be a primary factor as to why many infections require long-course antibiotic treatment for successful resolution [3]. Indeed, many patients with chronic infections harbor pathogens with increased rates of persister formation [4]. Thus, one of the most important questions concerning persister formation is determining the mechanisms that allow cells to become physiologically recalcitrant to treatment with antibiotics or other stressors. Recent work has suggested that persisters become drug tolerant because they enter a dormant or slow-growing state [5–9]. This

dormant state is thought to protect them from the lethal action of antimicrobials, since many antibiotics interfere with proliferative processes, such as cell wall assembly, DNA replication, INK1197 or protein synthesis [7, 10]. Genetic studies in E. coli K12 have implicated several genes that play a role in the rate of formation of both dormant and persister cells. Many of these genes Tryptophan synthase encode

toxin-antitoxin (TA) modules [7, 8, 11]. One example is hipA (high persistence). One allele of this gene (hipA7) causes a 100 to 1000-fold increase in persister levels [12], and over-expression of hipA leads to growth arrest and a persistence phenotype [13]. Several other loci have also been associated. Maisonneuve et al. [11] recently showed that overexpression of any one of five toxins from mRNase TA pairs resulted in higher fractions of persisters for both ciprofloxacin and ampicillin. In addition, by serially deleting up to ten TA loci, the authors showed that decreasing the number of TA loci decreased the fraction of persisters. Deleting ten TA loci decreased the persister fraction by 100-fold, from approximately 1% to 0.01% after five hours of antibiotic treatment, and this decrease occurred for both ciprofloxacin and ampicillin. The authors proposed a model in which mRNase toxins inhibit global translation, cells become dormant, and thus persist. These data suggest that in E. coli K12, a substantial fraction of persisters arise through mechanisms involving mRNase TA loci (deleting all ten loci results in a 99% reduction in persister frequency; deleting any one locus results in only an approximately 10% reduction in persister frequency). It is unknown whether similar mechanisms are important in other bacteria.

Biotinylated RNA approximately 21–23 nucleotides in length accumulated in

mock- and TE/3’2J/GFP virus-infected cell lysates, whereas little biotinylated RNA was detected in the expected size range at any time points tested in TE/3’2J/B2 virus-infected cell lysates (Figure 2). Figure 2 Accumulation of Dicer cleavage products in cells infected with TE/3’2J/GFP or TE/3’2J/B2 virus. Cell lysates were generated from Aag2 cells 36 hours post mock-, TE/3’2J/GFP, or TE/3’2J/B2 virus-infection (MOI = 0.01) (indicated to left of each panel). A synthetic 500 bp biotinylated dsRNA product was introduced into the lysates and, at indicated time points, samples were taken and the presence of small RNAs was determined by Northern blot analysis. Ethidium bromide-stained ribosomal RNAs located below each blot serve as loading controls. Arrows indicate position of 25 and selleck kinase inhibitor 19 nucleotide markers. After determining that B2 protein could inhibit the accumulation of siRNAs derived from a synthetic dsRNA in cell culture-derived lysates, we investigated the ability of the protein to inhibit virus-specific siRNA accumulation during virus replication in mosquito cells. The accumulation of SINV E1 gene-derived antisense small RNAs was examined in infected Aag2 cells over a 72-hour time course. Beginning

at 24 hours and continuing to 72 hours post-infection, SINV-specific RNAs 21–23 nucleotides in size were detected in Aag2 cells infected with TE/3’2J and TE/3’2J/GFP viruses. The size of the small RNAs is consistent with previous reports of virus-derived click here siRNAs detected in mosquito PFT�� datasheet cells [6, 17–21]. Few RNAs of this size were detected at any time in mock-infected cells or cells infected with TE/3’2J/B2, suggesting that B2

protein can function to inhibit virus-specific RNAi in mosquito cell culture (Figure 3A). Figure 3 Detection of virus-specific siRNAs in Aag2 cells (A) and Ae. aegypti (Higgs White Eyes) mosquitoes (B). Monolayers of Aag2 cells were mock infected or infected with TE/3’2J, TE/3’2J/GFP, or TE/3’2J/B2 virus at MOI = 0.01. Mosquitoes were intrathoracically inoculated with cell culture medium from TE/3’2J, TE/3’2J/GFP, or TE/3’2J/B2 virus. At indicated times post infection, total RNA was isolated and probed using an E1-specific riboprobe for virus-derived siRNA. Ethidium bromide-stained ribosomal RNA below each blot serves as a loading control. Time in hours post infection is noted below ribosomal RNA controls. Arrows indicate position of 25 and 19 nucleotide markers. The same methodologies were used to detect virus-derived siRNAs in intrathoracically-injected Ae. aegypti mosquitoes. Similar to cell culture, small RNAs 21–23 nucleotides in size were detected in TE/3’2J- and TE/3’2J/GFP-infected mosquitoes at 48 hours post-infection (Figure 3B).

Biotic interaction between protists and viruses are also known and have been shown [64]. Viruses specifically infect protists, e.g. the Coccolithovirus and it’s host, the calicifying haptophyte Emiliania huxleyi[65]. Additionally, viruses can also have

an an indirect influence on protists by infecting the bacteria on which the protistan grazers feed or protistan grazers can even feed directly on viruses even though the carbon transfer to the higher trophic level is of minor importance [66]. Furthermore, different bacterioplankton communities can produce a bottom-up control on grazing Talazoparib concentration protists. Namely, the growth efficiency of protists can relate strongly to the available bacterial prey [63, 67]. This is highly likely because differences in bacterial community composition in DHABs have been shown before [68, 69]. That leads to the assumption that different bacterial communities support different phagotrophic protists that show strong preferences for particular prey species [63, 67, 70, 71] or morphotypes [72, 73]. Other possible

explanations are founder effects, which describe a genetic deviation of an isolated find more population or founder population (on an island for example) compared to the original population based on a low number of alleles within the founders individuals [74], random effects or genetic drift is the change in the frequency of a gene in a population due to random sampling [75] and random extinctions that describe when a gene causes its carriers to have a deviating fitness from unity, its frequency will be determined by selection [76] in different basins. For protists in particular there is no literature available on this topic to our knowledge. At last, the Monoplization Hypothesis by De Meester et al. [77] could be relevant to protist biogeography Chlormezanone stating that a fast population growth and local adaptation

and colonization of a new habitat result in the monopolization of resources, which yields a strong priority effect. The effect is even enhanced when a locally adapted population can provide a ‘large resting propagule bank’ as a strong buffer against new genotypes invading. This holds true especially for species that reproduce asexually and form resting stages. Even though mass effect and dispersal [78] cannot be ruled out, these are unlikely alternatives to explain the observed community patterns. The habitats of the water column above the DHABs represent a potential source habitat with ‘high quality’. In comparison, the narrow interphase and the brine show ‘low quality’ conditions because these habitats harbor high gradients of change, anoxia, high salt concentration up to saturation and therefore require a high degree of physiological adaptation for microbial colonization. Chances for highly specialized organisms to cross environmental barriers outside their habitat and to disperse beyond their specific habitat are very low.

Cells were dark acclimated for 15 min and gently

filtered onto 13-mm diameter Millipore AP20 glass fiber filters. These filters were placed into the manufacturer’s leaf clip Entospletinib in vitro and an actinic light intensity of 217 μmol photons m−2 s−1 was used to probe the photo-physiology of the algal cells. Chlorophyll a fluorescence parameters were assayed and calculated according to the definitions of Baker (2008). Results Growth of photoheterotrophic versus phototrophic Chlamydomonas To determine the impact of photoheterotrophic versus phototrophic conditions on the growth of Chlamydomonas, wild-type cells were grown in various concentrations of iron with either acetate or CO2 supplied as a carbon source. Within carbon source treatments, iron-replete (20-μM Fe) and iron-deficient (1-μM Fe) cultures grew at the same rate, while iron-limited (≤0.2-μM Fe) cultures grew at a slower rate. The difference in growth rate as a function of iron nutrition was more pronounced in photoheterotrophic conditions where the growth rate in iron limitation was about half (57%) of the rate in the replete situation when compared to phototrophic conditions where the rate in iron limitation was 75% of that in the replete situation (Table 1). In the presence of acetate, iron-replete and -deficient cultures reached a final density of 1.5 × 107 cells/ml

after CHIR98014 6 days of growth, while iron-limited cultures reached stationary phase in 8 days, achieving a final density of only 5–9 × 106 cells/ml (Fig. 1). In contrast,

phototrophic iron-replete and -deficient phototrophic cultures reached a density of only 9 × 106 cells/ml, comparable to the final cell density of iron-limited photoheterotrophic cultures (Fig. 1). Table 1 Growth rate of photoheterotrophic versus phototrophic cells in response to iron nutrition Fe (μM) Acetate μ (day−1) CO2 μ (day−1) 0.1 0.96 ± 0.12 0.56 ± 0.04 0.2 0.90 ± 0.04 0.59 ± 0.07 1 1.44 ± 0.15 0.68 ± 0.11 20 1.68 ± 0.08 0.74 ± 0.06 Osimertinib Standard deviation based on biological triplicates Fig. 1 Growth in photoheterotrophic versus phototrophic growth conditions in response to iron nutrition. Cells were grown in the presence (A) and absence (B) of acetate in various concentrations of iron. Cultures lacking acetate were bubbled with air. Various concentrations of iron represented by empty triangles (0.1-μM Fe), filled triangles (0.2-μM Fe), empty circles (1-μM Fe), and filled circles (20-μM Fe). Standard deviation based on biological triplicates. Dotted line indicates cell density at which cells were collected for analysis Phototrophic cells accumulate more Fe than photoheterotrophic cells In order to relate the growth rate to iron nutrition, the iron content of cells in the presence and in the absence of acetate was determined by inductively coupled plasma-mass spectroscopy.