We conclude EPZ5676 chemical structure that Reelin-induced cofilin phosphorylation

is likely to play an important role in the assembly of SPNs in the IMLC. The present results confirm and extend previous studies that showed malpositioning of SPNs in the reeler mutant (Yip et al., 2000, 2009). In wild-type animals, Reelin is present between the central canal and the lateral margin of the spinal cord (Yip et al., 2009). This central location suggested a repulsive activity of Reelin as in the reeler mutant SPNs are not assembled in the IMLC but over-migrate towards the central canal. In line with such a function, ectopic expression of Reelin in neuronal progenitors near the central canal partially rescued the reeler phenotype (Yip et al., 2009). Although these studies pointed to a repulsive effect or stop signal function of Reelin in the migration of SPNs, the underlying molecular mechanisms remained elusive. In the present study, we provide evidence for Reelin terminating the migration process of SPNs by inducing the phosphorylation of cofilin. Cofilin is an actin-associated protein that depolymerizes F-actin Epigenetics inhibitor and thereby provides abundant G-actin molecules for reorganization of the cytoskeleton (Bamburg, 1999). Reorganization of the actin cytoskeleton is required in all processes that involve changes in cell shape. When phosphorylated at serine3,

cofilin is no longer able to depolymerize F-actin, thereby stabilizing the actin cytoskeleton (Arber et al., 1998). By using an antibody specifically raised against p-cofilin, we show in the present study that SPNs in wild-type animals are strongly immunoreactive, whereas they are virtually from unstained in reeler mutants, dab1 mutants and mutants lacking ApoER2. Mutants deficient in VLDLR showed a reduced but still recognizable staining for p-cofilin, similar to previous results in the neocortex (Chai et al.,

2009). We conclude from these data that the Reelin-induced phosphorylation of cofilin contributes to the stop signal function of Reelin on SPNs in the spinal cord. In support of this hypothesis, recombinant Reelin added to spinal cord tissue from reeler mutants significantly increased cofilin phosphorylation. In the absence of Reelin, cofilin in SPNs is less phosphorylated and hence the cytoskeleton less stabilized as cofilin continues to depolymerize F-actin, resulting in changes of cell shape and in increased cell motility. Compatible with this hypothesis, SPNs in the reeler mutant over-migrate and occupy territories close to the central canal; their normal assembly in the IMLC does not take place (Yip et al., 2000). Cofilin is a ubiquitous molecule present in many motile cells, and cofilin mutants show severe neuronal migration defects reminiscent of those in the reeler mutant (Bellenchi et al., 2007). We have previously shown that Reelin stabilizes the actin cytoskeleton of migrating neocortical neurons by inducing cofilin phosphorylation (Chai et al., 2009).

Cross-linked peptidoglycan synthesis has been monitored in Escherichia coli (Eco) membranes by incubation with the two sugar precursors UDP-N-acetyl-muramylpentapeptide [UDP-MurNAc(pp)] and UDP-GlcNAc, one of which is radiolabelled (Chandrakala et al., 2001). In the membranes, the disaccharide unit of peptidoglycan is synthesized on a lipid carrier by the MraY and MurG enzymes and subsequently polymerized by the transglycosylase and cross-linked to pre-existing peptidoglycan by the transpeptidase (Fig. 1). The radiolabelled,

newly synthesized cross-linked peptidoglycan formed can be monitored by paper selleck chemicals chromatography or a microplate scintillation proximity assay (SPA) using wheat germ agglutinin (WGA)-coated SPA beads (Chandrakala et al., 2001, 2004). To monitor MurG activity,

the pathway of reactions must be stopped at lipid II (Mengin-Lecreulx et al., 1991) (Fig. 1a) using an inhibitor of the transglycosylase (Ravishankar et al., 2005). Typically, in a first step, the MurG substrate is synthesized in situ; in a second step, transfer of radiolabelled GlcNAc by MurG occurs (Fig. 1b). The product lipid II can be separated from UDP-GlcNAc by paper chromatography (Mengin-Lecreulx et al., 1991) or by an SPA (Ravishankar et al., 2005) (Fig. 1b). We intended setting up an assay Venetoclax in vivo for Mycobacterium tuberculosis (Mtu) MurG by introducing it into an E. coli background, so that an established SPA (Ravishankar et al., 2005) could be used. Strain OV58 has an amber mutation in murG and a temperature-sensitive amber suppressor, so that practically no E. coli protein is made at 42 °C (Salmond et al., 1980; Mengin-Lecreulx et al., 1991). A key question was

whether the Mtu murG would functionally replace the E. coli homologue. Wheat germ agglutinin-coated (WGA) beads for the SPAs were from Amersham International plc. U.K. UDP-[3H]-N-acetyl glucosamine was from NEN Dupont, USA. Moenomycin was gifted by Hoechst India. Ni-NTA resin was from Qiagen, USA. Other chemicals were from Sigma-Aldrich. Thiamine-diphosphate kinase UDP-N-acetyl muramyl pentapeptide [UDP-MurNAc(pp)] was purified from Bacillus cereus 6A1 (Chandrakala et al., 2001) and radiolabelled by incubation with [3H]-NHS-propionate (Solapure et al., 2005). Escherichia coli murG(Ts) (Salmond et al., 1980) was a gift from W.D. Donachie. pRSETA and E. coli BL21(DE3) were from Novagen; pBAD/Myc-HisA and PMOSBlue were from Stratagene. L-broth (LB) was used for bacterial growth medium, and ampicillin was added at 50 or 100 μg mL−1 when required (LB-amp). The murG gene was PCR-amplified from Mtu genomic DNA with forward (5′- AAG GAC ACG GTC AGC CAG CC -3′) and reverse primers (5′- TCT AAA GCT TCG TCG TTG TCC TGG CAC CGG -3′) and cloned into pBAD/Myc-His A (Guzman et al., 1995) between the NcoI and HindIII sites. The resulting plasmid pAZI8952 has Mtu murG gene under the control of BAD promoter.

Moreover, it is unclear whether an initial assembly of various synaptic molecules located at the extrasomal regions (e.g. growth cones) can indeed result in fully

mature and consolidated synapses in the absence of somata signalling. Such evidence is difficult to obtain both in MAPK Inhibitor Library price vivo and in vitro because the extrasomal sites are often challenging, if not impossible, to access for electrophysiological analysis. Here we demonstrate a novel approach to precisely define various steps underlying synapse formation between the isolated growth cones of individually identifiable pre- and postsynaptic neurons from the mollusc Lymnaea stagnalis. We show for the first time that isolated growth cones transformed into ‘growth balls’ have an innate propensity to develop specific and multiple synapses within minutes of physical contact. We also demonstrate that a prior ‘synaptic history’ primes the presynaptic growth ball to form synapses quicker with subsequent partners. This is the first demonstration that isolated Lymnaea growth cones have the necessary machinery to form functional synapses. “
“CX 546, an allosteric positive modulator of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid-type ionotropic glutamate receptors (AMPARs), belongs to a drug class called ampakines. These compounds have been shown to enhance long-term

potentiation Buparlisib (LTP), a cellular model of learning and memory, and improve animal learning task performance,

and have augmented cognition in neurodegenerative patients. However, the chronic effect of CX546 on synaptic structures has not been examined. The structure and integrity of dendritic spines are thought to play a role in learning and memory, and their abnormalities have been implicated in cognitive disorders. In addition, their Anidulafungin (LY303366) structural plasticity has been shown to be important for cognitive function, such that dendritic spine remodeling has been proposed as the morphological correlate for LTP. Here, we tested the effect of CX546 on dendritic spine remodeling following long-term treatment. We found that, with prolonged CX546 treatment, organotypic hippocampal slice cultures showed a significant reduction in CA3–CA1 excitatory synapse and spine density. Electrophysiological approaches revealed that the CA3–CA1 circuitry compensates for this synapse loss by increasing synaptic efficacy through enhancement of presynaptic release probability. CX546-treated slices showed prolonged and enhanced potentiation upon LTP induction. Furthermore, structural plasticity, namely spine head enlargement, was also more pronounced after CX546 treatment. Our results suggest a concordance of functional and structural changes that is enhanced with prolonged CX546 exposure.

HCV antiviral recipients, diabetics and those on lipid-lowering drugs at baseline were excluded from the study. Factors associated with a decreased risk of grade 3 or 4 hyperlipidaemia or lipid-lowering drug use were assessed by multivariate logistic regression. A total of 1587 HIV-monoinfected, 190 HIV/HBV-coinfected and 255 HIV/HCV-coinfected patients were evaluated. Most were male (85–92% for the 3 groups evaluated: HIV, HIV/HBV, HIV/HCV). The median

[interquartile range (IQR)] age at HAART initiation was 48 (44–56) years and was similar between groups. The median (IQR) CD4 count at HAART initiation was 245 (120–370) cells/μL in HIV-monoinfected participants, 195 (110–330) cells/μL in HIV/HBV-coinfected participants and 268 (140–409) Selleckchem EPZ015666 cells/μL in HIV/HCV-coinfected participants. Factors associated with a decreased risk of grade 3 or 4 hyperlipidaemia or lipid-lowering drug use included HIV/HCV coinfection [odds ratio (OR) 0.46; 95% confidence interval (CI) 0.34, 0.61; P<0.0001], HIV/HBV coinfection (OR

0.74; 95% CI 0.55, 0.99; P=0.04), year of starting HAART after 2004 vs. 1997 or earlier (OR 0.37; 95% CI 0.29, 0.48; P<0.0001) and year of starting HAART between 1998 and 2003 vs. 1997 or earlier (OR 0.75; 95% CI 0.61, 0.92; P<0.01). Factors Selleckchem Roscovitine associated with increased risk included age (OR 1.55; 95% CI 1.39, 1.72; per 10 years, P<0.0001) and male gender (OR 1.84; 95% CI 1.36, 2.48; P<0.0001). HIV/HCV and Liothyronine Sodium to a lesser extent HIV/HBV coinfections are protective against HAART-related hyperlipidaemia. HIV, hepatitis B virus (HBV) and/or hepatitis C virus (HCV) infections frequently co-exist because of common risk factors for exposure

[1,2]. A negative interaction results in many instances. On average, HCV viral loads are increased and liver fibrosis rates are accelerated in the presence of HIV [3,4] and mortality rates are increased [5]. CD4 T-lymphocyte recovery following the initiation of combination antiretroviral therapy is blunted in HIV/HCV coinfection, although the causative role of HCV remains debatable [3]. Also, the occurrence of liver-specific adverse events related to antiretroviral therapy is increased and the efficacy of HBV and HCV antiviral therapy is diminished [4–6]. In contrast to the prevailing negative relationship between HIV and HCV infections in terms of the effect on the coinfected individual, there is evidence that the abnormal lipid profile observed in many patients following the initiation of highly active antiretroviral therapy (HAART) may be less pronounced in those with HIV/HCV coinfection [7]. Lower total cholesterol and low-density lipoprotein (LDL) cholesterol levels have been reported in those with HCV infection, with and without advanced liver disease [8–13].

HCV antiviral recipients, diabetics and those on lipid-lowering drugs at baseline were excluded from the study. Factors associated with a decreased risk of grade 3 or 4 hyperlipidaemia or lipid-lowering drug use were assessed by multivariate logistic regression. A total of 1587 HIV-monoinfected, 190 HIV/HBV-coinfected and 255 HIV/HCV-coinfected patients were evaluated. Most were male (85–92% for the 3 groups evaluated: HIV, HIV/HBV, HIV/HCV). The median

[interquartile range (IQR)] age at HAART initiation was 48 (44–56) years and was similar between groups. The median (IQR) CD4 count at HAART initiation was 245 (120–370) cells/μL in HIV-monoinfected participants, 195 (110–330) cells/μL in HIV/HBV-coinfected participants and 268 (140–409) RG7422 chemical structure cells/μL in HIV/HCV-coinfected participants. Factors associated with a decreased risk of grade 3 or 4 hyperlipidaemia or lipid-lowering drug use included HIV/HCV coinfection [odds ratio (OR) 0.46; 95% confidence interval (CI) 0.34, 0.61; P<0.0001], HIV/HBV coinfection (OR

0.74; 95% CI 0.55, 0.99; P=0.04), year of starting HAART after 2004 vs. 1997 or earlier (OR 0.37; 95% CI 0.29, 0.48; P<0.0001) and year of starting HAART between 1998 and 2003 vs. 1997 or earlier (OR 0.75; 95% CI 0.61, 0.92; P<0.01). Factors see more associated with increased risk included age (OR 1.55; 95% CI 1.39, 1.72; per 10 years, P<0.0001) and male gender (OR 1.84; 95% CI 1.36, 2.48; P<0.0001). HIV/HCV and Megestrol Acetate to a lesser extent HIV/HBV coinfections are protective against HAART-related hyperlipidaemia. HIV, hepatitis B virus (HBV) and/or hepatitis C virus (HCV) infections frequently co-exist because of common risk factors for exposure

[1,2]. A negative interaction results in many instances. On average, HCV viral loads are increased and liver fibrosis rates are accelerated in the presence of HIV [3,4] and mortality rates are increased [5]. CD4 T-lymphocyte recovery following the initiation of combination antiretroviral therapy is blunted in HIV/HCV coinfection, although the causative role of HCV remains debatable [3]. Also, the occurrence of liver-specific adverse events related to antiretroviral therapy is increased and the efficacy of HBV and HCV antiviral therapy is diminished [4–6]. In contrast to the prevailing negative relationship between HIV and HCV infections in terms of the effect on the coinfected individual, there is evidence that the abnormal lipid profile observed in many patients following the initiation of highly active antiretroviral therapy (HAART) may be less pronounced in those with HIV/HCV coinfection [7]. Lower total cholesterol and low-density lipoprotein (LDL) cholesterol levels have been reported in those with HCV infection, with and without advanced liver disease [8–13].

coli ArgDC mutant in an acid shock assay. MK2206 Active AaxB was detected in four additional species: Chlamydia caviae, Chlamydia pecorum, Chlamydia psittaci, and Chlamydia muridarum. Of the C. trachomatis

serovars, only E appears to encode active enzyme. To determine when functional enzyme is present during the chlamydial developmental cycle, we utilized an anti-AaxB antibody to detect both uncleaved and cleaved enzyme throughout infection. Uncleaved enzyme production peaked around 20 h postinfection, with optimal cleavage around 44 h. While the role ArgDC plays in Chlamydia survival or virulence is unclear, our data suggest a niche-specific function. Infection with Chlamydia, a genus of Gram-negative obligate intracellular

bacteria, may result in ocular, genital, or pneumonic disease, depending on the route of entry and bacterial species/serovar. While the majority of Chlamydia species are zoonotic, infecting a wide range of mammalian and avian hosts, the Chlamydia trachomatis serovars are human-specific pathogens (Carlson et al., 2005; Rohde et al., 2010). All species undergo a unique biphasic developmental cycle transitioning between the extracellular, infectious elementary body (EB) and the intracellular, replicative form known as the reticulate body (RB; AbdelRahman & Belland, 2005). Arginine decarboxylases PD0332991 order (ArgDCs), which catalyze the conversion of arginine into agmatine, are conserved in bacteria and play dual roles in acid resistance and the metabolism of polyamines such as putrescine (Tabor & Tabor, 1984; Lin et al., 1995). In bacteria such as Yersinia, functional ArgDC is required to produce biofilms, making this enzyme essential for virulence (Patel et al., 2006). Two ArgDC are encoded by Escherichia coli: the acid-inducible adiA and a constitutive speA that functions in polyamine biosynthesis (Stim & Bennett, 1993). In Chlamydia, the only known ArgDC is encoded by aaxB, which resides in an operon between the putative porin aaxA and the characterized arginine–agmatine antiporter, aaxC (Giles & Graham,

2007; Fig. 1a). Although AaxB is Edoxaban functionally equivalent to E. coli AdiA, the enzyme itself is actually a member of the pyruvoyl-dependent ArgDC (PvlArgDC) and shares more similarities with ArgDC from organisms such as Methanococcus jannaschii (Graham et al., 2002). The AaxB proteins of Chlamydia pneumoniae and C. trachomatis serovars D and L2 were previously characterized (Giles & Graham, 2007; Giles et al., 2009). All sequenced C. pneumoniae encode a 25 kDa proenzyme, which requires autocleavage between the conserved Thr52Ser53residues to produce 16 kDa α and 9 kDa β subunits. The cleaved subunits are then free to assemble into the active (αβ)3 complex. In contrast, C. trachomatis serovars D and L2 have inactivated AaxB through one of two independent mutations (Giles et al., 2009).

1D Strong recommendation. Very low-quality evidence. Benefits appear to outweigh risk and burdens, or vice versa. Evidence limited to case studies. Strong recommendation based mainly on case studies and expert judgment. 2A Weak recommendation. High-quality evidence. Benefits Z-VAD-FMK ic50 closely balanced with risks and burdens. Consistent evidence from well-performed randomized, controlled trials or overwhelming

evidence of some other form. Further research is unlikely to change our confidence in the estimate of benefit and risk. Weak recommendation, best action may differ depending on circumstances or patients or societal values. 2B Weak recommendation. Moderate-quality evidence. Benefits closely balanced with risks

and burdens, some uncertainly in the estimates of benefits, risks and burdens. Evidence from randomized, controlled trials with important limitations (inconsistent results, methods flaws, indirect or imprecise). Further research may change the estimate of benefit and risk. Weak recommendation, alternative approaches likely to be better for some patients under some circumstances. 2C Weak recommendation. Low-quality evidence. Uncertainty in the estimates of benefits, risks, and burdens; benefits may be closely balanced with risks and burdens. Evidence from observational studies, unsystematic clinical experience, or from randomized, controlled trials with serious flaws. Any estimate of effect is uncertain. Weak recommendation; other alternatives may be reasonable. 2D Weak recommendation. Selleckchem PF-562271 Very low-quality evidence. Uncertainty in the estimates of benefits, risks, and burdens; benefits may be closely balanced with risks and burdens. Evidence limited to case studies and expert judgment. Very weak recommendation; other alternatives may be equally Thymidylate synthase reasonable. Databases: Medline, Embase, Cochrane Library Conference

abstracts: -  IAS Conference on HIV Pathogenesis and Treatment Date parameters: -  Databases: July 2013 Five systemic literature searches were undertaken from published work and conference abstracts up until July 2011 as described in the BHIVA guidelines development manual. The population was defined as HIV-positive women covering five areas. Search questions were set by the Writing Group within each search as listed below Study design: Systematic reviews (SRs), randomized control trials (RCTs), observational, risk, economic Population: HIV-positive women Intervention: starting antiretroviral therapy during pregnancy Comparator: none Outcomes: death, AIDS, non-AIDS co-morbidities, maternal obstetric morbidity, infant mortality and morbidity, mother-to-child HIV transmission, drug resistance.

However, for the convenience of the reader, these aspects and corresponding references are summarized in Tables 2 and 3, respectively. Auxins are a major class of phytohormones that are involved in the coordination of plant PF-01367338 in vitro growth and development. The effects of azospirilla on plant root morphology (e.g.

elongation of primary roots and increase of the number and length of lateral roots) have been shown to correlate with exogenous levels of the auxin indole-3-acetate (IAA), evidencing that positive effects on roots upon inoculation with azospirilla are mainly owing to the production and secretion of IAA by these bacteria (Dobbelaere & Okon, 2007; Spaepen et al., 2007, 2009). In A. brasilense, 90% of IAA is produced by the indole-3-pyruvate (IPA) pathway in the presence of tryptophan (Vande Broek et al., 1999; Spaepen et al., 2007, 2009). In this bacterium, the rate-limiting step in IAA synthesis is catalyzed by the enzyme IPA decarboxylase, which catalyzes the conversion of IPA

into IAA, and is encoded by the ipdC gene. Transcription of the ipdC gene is positively regulated by its end product IAA, which constitutes a positive feedback loop regulation (Spaepen et al., 2007). Dual inoculation of several legumes with rhizobia and azospirilla significantly http://www.selleckchem.com/products/gsk1120212-jtp-74057.html increases nodulation, nitrogen fixation, accumulation of macro- and microelements, and biomass as compared to inoculation with rhizobia alone Montelukast Sodium (Helman et al., 2011; Table 2). An A. brasilense ipdC mutant was partially defective in nodulation and nitrogen fixation of common bean roots co-inoculated with rhizobia, in comparison with co-inoculation with the parental type Sp245. This indicates that there is a differential response of the plant roots to the auxin produced by bacteria (Remans et al., 2008). In agreement, recent experiments with vetch showed that the ipdC mutant induced

less root hair formation and induction of secretion of nod gene inducers by roots, relative to the wild type (Star et al., 2011). Moreover, comparison between the ipdC mutant and the wild type in inoculation experiments with wheat plants demonstrated a direct link between IAA production and effects on root morphology (Spaepen et al., 2008). When the native ipdC promoter was replaced by a constitutive or a plant-inducible promoter in strain Sp245, effects on root morphology were similar as those observed with the wild type, but at lower inoculum concentrations (Spaepen et al., 2008). The transcriptome of the ipdC mutant and the wild type were recently compared in absence or presence of exogenously added IAA by microarrays (Van Puyvelde et al., 2011). Inactivation of ipdC or addition of IAA resulted in broad transcriptional changes, leading to the conclusion that IAA is a signaling molecule in A. brasilense.

Serological tests are not helpful in the diagnosis of cutaneous leishmaniasis. Therapy for leishmaniasis should see more be co-ordinated with the local tropical medicine service (category IV recommendation). 10.4.4.1 Visceral leishmaniasis. The treatment of choice for visceral leishmaniasis in an HIV-seropositive person is liposomal amphotericin B 4 mg/kg for 10 doses given on days 1–5, 10, 17, 24, 31 and 38 [35]. Although liposomal amphotericin

B is the lipid formulation available in the UK in some European countries alternative lipid formulations may be used; amphotericin B lipid complex has also been used for treatment of visceral leishmaniasis [36]. Review of clinical studies has suggested that treatment

with liposomal amphotericin B is as efficacious but less toxic than treatment with pentavalent antimonials [37]. HIV-seropositive individuals have a high relapse rate after treatment for leishmaniasis [36]. Secondary prophylaxis of visceral leishmaniasis is the standard of care in Europe because in the pre-ART era, relapse after treatment was almost inevitable [37,39]. Pentamidine (4mg/kg every 2 weeks intravenously) [40] or liposomal amphotericin B (5 mg/kg every 3 weeks intravenously) may be used, while amphotericin B lipid complex has also been used for secondary prophylaxis of visceral leishmaniasis [41,42]. There Isotretinoin is insufficient evidence to support the use of one specific regimen over another and this is best discussed with the MAPK inhibitor local tropical disease service. Case series describe the use of oral miltefosine treatment when standard treatment fails [43,44]. Case reports, however, describe the failure of this approach when miltefosine is used alone [45]. The use of pentavalent antimonials in combination with or followed by oral miltefosine, may be a better option when standard treatment fails but more data are needed

before firm recommendations can be made [46,47]. Complex cases should be discussed with the local tropical medicine service. 10.4.4.2 Cutaneous leishmaniasis. Cutaneous leishmaniasis can be treated with local infiltration of sodium stibogluconate or systemic treatment, depending on the species [48], although there is limited experience of local therapy in individuals with HIV infection. This is best discussed with the local tropical disease service. Primary prophylaxis of leishmaniasis is not recommended. For patients not taking HAART at the time of diagnosis, there is no specific evidence to guide when HAART should be started but expert opinion suggests this should be as soon as the patient is stable on antileishmanial therapy. There are few data to guide whether and when to stop secondary prophylaxis of visceral leishmaniasis.

Table S1. Primers used in this study. Please note: Wiley-Blackwell is not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article. “
“Heterotrophic bacteria

are key players in the biogeochemical cycle of iron (Fe) in the ocean, but the capability of different bacterial groups to access this micronutrient is ignored thus far. The aim of our study was to develop a protocol for the combined application of microautoradiography (MICRO) and catalyzed reporter Quizartinib molecular weight deposition–fluorescence in situ hybridization (CARD-FISH) using the radioisotope 55Fe. Among the different washing solutions tested, Ti-citrate-EDTA was the most efficient for the removal of extracellular 55Fe providing sufficiently low background values. We further demonstrate that the washing Angiogenesis inhibitor of cells with Ti-citrate-EDTA and the fixation with paraformaldehyde or formaldehyde do not induce leakage of intracellular 55Fe. Incubating natural bacterial communities collected from contrasting environments, the NW Mediterranean Sea and the Southern Ocean, with 55Fe revealed that 3–29% of bacterial cells were associated with silver grains. Combining microautoradiography with CARD-FISH, we demonstrate that the contribution of different bacterial

groups to total 55Fe-incorporating cells was overall reflected by their relative contribution to abundance. An exception to this pattern was the proportionally higher

contribution of Gammaproteobacteria, SAR86 and Alteromonas. Our study demonstrates the feasibility of MICRO-CARD-FISH using the radiotracer 55Fe and provides the first description of marine bacterial assemblages actively incorporating Fe. second Iron is a rare resource for microorganisms in the ocean. In surface waters, the iron demand of heterotrophic bacteria can be as high as that of phytoplankton, leading to a strong competition among microorganisms (Tortell et al., 1996). Concurrently, heterotrophic bacteria are key players in the remineralization of particulate biogenic and lithogenic iron, thereby contributing to the production of regenerated bioavailable iron (Tortell et al., 1999; Poorvin et al., 2004). Our understanding of the role of heterotrophic bacteria in iron cycling relies mainly on bulk measurements, such as the contribution of bacterial biomass to the biogenic iron stock and bacterial iron uptake rates (Strzepek et al., 2005). By contrast, links between bacterial diversity and biogeochemical functions involving iron are still lacking. Single-cell approaches were proven a powerful tool to study the role of bacterial groups in biogeochemical cycles of the major elements carbon, phosphorus, and sulfur.