The fourth type of replicon are the repABC-type operons, which are specifically found in Alphaproteobacteria and which can be differentiated from the three other groups as in this system the oriV is situated within the replicase gene (Petersen, Selleck Dabrafenib 2011). The comparison of the organization of the three relevant genes on the plasmids from sphingomonads demonstrated that the three groups of ‘megaplasmids’ identified in the course of the sequence comparisons of the individual rep and par genes also corresponded with the gene organization. Thus, in the group of plasmids consisting of pNL1,

pCAR3, pSWIT02 and Mpl (‘Mega-RepAC’), the repA genes are always transcribed in the opposite direction to the parAB genes (Fig. 3). For pNL1 and pCAR3, it has been previously shown that in the sequence space between the repA and parA genes, several 16–17 bp long repeats are present. This indicates that these repeats function as iterons

and thus are the DNA sequences to which the RepA proteins bind (Romine et al., 1999; Shintani et al., 2007). A search for similar iterons at the corresponding position of plasmid pSWIT02 (using the program repfind; Kinase Inhibitor Library http://zlab.bu.edu/repfind) identified three copies of a 14 bp DNA sequence, which was part of the 16 bp iteron found at the respective site in pCAR3. Thus, it can be concluded that the plasmids belonging to the ‘Mega-RepAC-family’ belong to the RepA-group of Alphaproteobacterial replicons as previously defined by Petersen (2011). The ‘Mega-RPA’ group (consisting of plasmids pNL2, pISP1 and Lpl) demonstrated the gene order parA, parB, repA (Fig. 3).

This MYO10 is the same gene order as found in the repABC operons. Unfortunately, the nomenclature of the genes participating in the repABC operons is different from the nomenclature used for the three other types of replicons. Thus, in the case of the repABC operons, RepA and RepB have sequence similarities to proteins involved in active segregation of plasmids – and thus are equivalent to ParA and ParB in the other systems – and RepC is the replication initiator protein – and thus is equivalent to RepA in the other systems (Cevallos et al., 2008). The repABC plasmids show in addition to the highly conserved gene order also further characteristics. Thus, it had been shown that in the large intergenic sequence between repB and repC, a gene is present which codes for a small antisense RNA which is involved in the control of plasmid replication (Cevallos et al., 2008). Therefore, the sequence space between the genes coding for the parB and repA genes of plasmids pNL2, pISP1 and Lpl were analysed and compared with the respective sequences encoding for the antisense RNAs from various plasmids belonging to the repABC family (Venkova-Canoca et al., 2004), but no significant sequence homologies were detected. This suggested that the plasmids of ‘Mega-RPA-group’ do not belong to the repABC plasmids.

(2003) with slight modifications. Cosmids of S. coelicolor containing the genes for replacement were introduced by transformation into E. coli BW25113 (pIJ790). Electrocompetent cells were prepared and electroporated with a PCR product (containing an aac(3)IV gene) using a GenePulser II (Bio-Rad Inc.). The PCR-targeted constructs were introduced by electroporation into E. coli ET12567 (pUZ8002) and then transferred by conjugation into S. coelicolor. Thiostrepton-resistant colonies were selected for single

crossing PF 01367338 over between the cosmid and the host chromosome. After sporulating on MS medium without antibiotic selection, thiostrepton-sensitive but apramycin-resistant colonies were screened to obtain double-crossover clones. To remove the aac(3)IV marker for the next round of gene disruption and replacement, cosmid with the aac(3)IV gene inserted in a FRT-aac(3)IV-FRT cassette was introduced by electroporation into E. coli BT340 containing a flp gene encoding Flp recombinase to remove the cassette. Clones containing a double-crossover allelic exchange in S. coelicolor were confirmed by PCR analysis and some clones (i.e. ZM4) by microarray hybridization analysis performed in the Shanghai Biochip Inc. To delete a large segment (e.g. > 40 kb)

on the S. coelicolor chromosome, two fragments (e.g. > 5 kb) from different cosmids of the ordered library plus a kanamycin resistance gene (kan) were cleaved and cloned in the polylinker of pHAQ31 or pHY642. The

resulting plasmid was introduced by electroporation into E. coli ET12567 (pUZ8002) and see more then http://www.selleckchem.com/products/apo866-fk866.html transferred by conjugation into S. coelicolor. Thiostrepton-resistant colonies were selected for single crossing over, and thiostrepton-sensitive but kanamycin-resistant colonies for double crossing over. Clones containing a double-crossover allelic exchange in S. coelicolor were further confirmed by PCR analysis. A 2.6-kb fragment (digested with XbaI and NheI) containing a phiC31 integrase gene was cloned in a pHAQ31-derived cosmid containing the entire actinorhodin biosynthetic gene cluster. The resulting plasmid, pCWH74, was introduced by conjugation into Streptomyces strains. To quantitate the production of actinorhodin, strains were inoculated into R2YE (lacking CaCl2, KH2PO4, and L-proline) liquid medium, 1 mL culture was harvested, and spun at 15 294 g for 1 min to collect the supernatant, which was further treated with KOH and scanned at 640 nm. Measurements of actinorhodin production were carried out by the method of Kieser et al. (2000). PCR-targeting of cosmids is a precise and efficient method for gene disruption and replacement in Streptomyces. Because two long segments (e.g. > 5 kb) on a suicide plasmid are employed for homologous recombination with chromosomal sequences, high frequencies of single- and double-crossover events can usually be obtained by screening a few clones (Gust et al., 2003).

002; Fig. 1b). In addition – and as previously demonstrated [6, 23] – the

pretreatment set-point viral load correlated significantly with the post-STI viral load (P < 0.001). The duration of STI and viral load at pretreatment set point were therefore included in multivariable analyses. Alectinib research buy Eighty-nine patients (68%) carried at least one HLA-B Bw4 allele. Bw4 alleles can be further separated into those carrying isoleucine or threonine at position 80 (Bw4-80Ile and Bw4-80Thr, respectively). Functionally, alleles with isoleucine act as strong ligands, whereas alleles carrying a threonine act as weak ligands of KIR3DL1 [24]. The former were detected in 52 patients (40%) and the latter in 37 patients (28%), whereas 41 patients carried no Bw4 alleles (32%). Patients not carrying a Bw4 allele showed a median post-STI viral load of 3.24 log copies/ml (IQR 2.21–4.29 log copies/ml), whereas the median post-STI viral load was 2.39 log copies/ml (IQR 0–3.62 log copies/ml) in Bw4-positive patients (P = 0.003; Fig. 2a). No difference was found between carriers of 80Thr and 80Ile subgroups of the Bw4 (median increase 2.40 and 2.39 log copies/ml, respectively; P = 0.66; Fig. 2b). We next analysed the impact of allelic diversity within the KIR3DL1 locus in Bw4-positive patients. Of 125 KIR3DL1-positive patients, 84 tested Selleck UK-371804 positive for at least one Bw4

antigen. We found no difference between patients carrying KIR3DL1 alleles with high (*h/*x) and low (*l/*l) surface expression (median increase 2.91 and 2.71 log copies/ml, respectively; P = 0.57; Fig. 2c). Equally, the presence of the KIR3DL1*004 allele DCLK1 – which in conjunction with Bw4 has been shown to delay the progression to AIDS – had no significant impact on post-STI viral loads (median increase 2.65 vs. 2.91 log copies/ml, respectively; P = 0.58; Fig. 2d). The activating receptor KIR3DS1 – which segregates as an allele of KIR3DL1 – was contained in 45 patients’ genotypes (35%), of which 13 also carried Bw4Ile. The presence of KIR3DS1 with Bw4Ile has been shown to delay progression

to AIDS [25]. In our setting, we found no difference in the rise in viral load between KIR3DS1+/Bw4-80Ile+ patients (median increase 2.65 log copies/ml) and patients who did not carry either KIR3DS1 or Bw4-80Ile or both (median increase 2.91 log copies/ml; P = 0.81; Fig. 2e). Finally, we analysed the impact of the SNPs in HCP5 and in HLA-C −35. Nine patients (7%) carried one G allele in the HCP5 locus, and all remaining patients were homozygous for the wild-type T-allele. The median viral load was lower in patients with HCP5-G (median 2.76 log copies/ml) compared with HCP5-TT homozygous patients (median 2.85 log copies/ml). This difference was, however, not statistically significant (P = 0.90; Fig. 2f). At the HLA-C −35 locus, 79 patients (61%) were homozygous for the major T-allele and seven patients (5%) were homozygous carriers of the protective C allele, whereas the remaining 44 patients (34%) carried one copy of each allele.

The outer membrane profile was reorganized, anabolic pathways and core as well as energy metabolism were repressed and the alginate regulon and sugar catabolism were activated. At the investigated early time point of cold adaptation, the transcriptome was reprogrammed in almost all functional categories, but the protein profile had still not adapted to the change of living conditions in the cold. Free-living bacteria are frequently exposed

to temperatshifts and nonoptimal growth temperatures. In order to grow at low temperatures, the organism must overcome the growth-diminishing effects of this stress condition, such as Dabrafenib price decreased membrane fluidity, altered redox status, increased stability of RNA and DNA secondary structures and thus a reduced Selleckchem MS-275 efficiency of replication, transcription

and translation (Phadtare, 2004). Cold shock response and adaptation have been studied extensively in bacterial model organisms such as Escherichia coli (Phadtare et al., 1999; Gualerzi et al., 2003; Inouye & Phadtare, 2004) and Bacillus subtilis (Graumann & Marahiel, 1999; Beckering et al., 2002; Weber & Marahiel, 2002; Mansilla & de Mendoza, 2005; Budde et al., 2006; El-Sharoud & Graumann, 2007). Pseudomonas putida strain KT2440 (Bagdasarian et al., 1981; Regenhardt et al., 2002) is another bacterial model organism particularly for environmental microbiology. We recently screened a transposon library for genes that are essential for the survival of P. putida KT2440 at low temperatures (Reva et al., 2006). Life at lower temperature was hampered when the transposon had inactivated key genes that are necessary these for the maintenance of (1) transcription, translation and ribosomal activity, (2) membrane integrity and fluidity and (3) redox status of the cell. Here, we report on the global genomewide response of P. putida KT2440 to a downshift of temperature from 30 to 10 °C at both the mRNA

transcript and the protein level. Transcriptome and proteome analyses were accomplished using deep cDNA sequencing and a gel-free, MS-centered proteomics approach. Pseudomonas putida KT2440 (strain DSM6125) (Bagdasarian et al., 1981) was obtained from DSMZ (Braunschweig, Germany). Bacterial cultures were inoculated from a frozen stock culture and incubated at 30 °C for 8 h at 250 r.p.m. in Luria–Bertani medium. An aliquot of 0.2 mL was added to 20 mL M9 medium (Na2HPO4 33.9 g L−1, KH2PO4 15.0 g L−1, NaCl 2.5 g L−1, NH4Cl 5.0 g L−1, MgSO4 2 mM, CaCl2 0.1 mM, FeSO4·7H2O 0.01 mM, pH 6.8) supplemented with 15 mM succinate as the sole carbon source in a 100-mL flask and incubated overnight at 30 °C. Bacteria were then grown in a 1.5-L batch culture (M9+15 mM succinate) using the BioFlo 110 Fermenter (New Brunswick Scientific Co., Edison, NJ) to ensure constant pH, aeration and agitation. When cultures reached the mid-exponential phase (OD600 nm∼0.8), the temperature was decreased from 30 to 10 °C.

Among these compounds, 2,4-diacetylphloroglucinol (2,4-DAPG) produced by some Pseudomonas spp. is of particular significance for the suppression of root diseases (Keel et al., 1996; Haas & Defago, 2005). The antibiotic 2,4-DAPG is a polyketide compound with antifungal, antibacterial, antihelminthic and phytotoxic activities (Keel et al., 1992; Dowling Osimertinib clinical trial & O’gara, 1994). The genes involved in the biosynthesis of this antibiotic cloned from several Pseudomonas strains include four structural

genes, phlA, phlC, phlB and phlD, which are transcribed as a single operon (phlACBD) (Fenton et al., 1992; Bangera & Thomashow, 1996, 1999; Wei et al., 2004a). A specific transcriptional regulator gene, phlF, is localized upstream of the phlACBD operon and transcribed in the opposite direction (Abbas et al., 2002). Intensive

studies on the regulation of 2,4-DAPG production in recent years have revealed a number of transcriptional and post-transcriptional elements. Besides PhlF, other identified regulatory elements include the two-component system GacS/GacA (Haas & Keel, 2003), sigma factors RpoS (Sarniguet et al., 1995), RpoD and RpoN (Schnider et al., 1995; Péchy-Tarr et al., 2005), the H-NS family regulators MvaT and MvaV (Baehler et al., 2006), the translational repressor proteins RsmA and RsmE (Heeb et al., 2002; Reimmann et al., 2005), the oxidoreductase DsbA (Mavrodi et al., 2006) and the resistance-nodulation-division efflux pump EmhABC (Tian et al., 2010). Quorum RG7420 molecular weight sensing (QS)

is a process of cell-to-cell communication that enables bacterial populations to collectively control gene expression and thus coordinate group behaviors (Miller & Bassler, 2001). In many Gram-negative bacteria, Janus kinase (JAK) the QS system is based on the function of two proteins that belong to the LuxI-LuxR family of transcriptional regulators. The LuxI protein synthesizes N-acyl-homoserine lactone (AHL) signaling molecules that can diffuse through the cell envelope. AHLs bind to the transcriptional regulator LuxR, forming a complex that plays an important regulatory role in a diverse array of physiological activities (González & Keshavan, 2006; Keller & Surette, 2006). QS has also been implicated in the interaction between plants and plant growth-promoting rhizobacteria. For example, the PhzI–PhzR QS system regulates the biosynthesis of the phenazine antibiotic in the plant-beneficial bacterial strains Pseudomonas aureofaciens 30-84 (Pierson et al., 1994) and Pseudomonas chlororaphis PCL1391 (Chin-A-Woeng et al., 2001). A second QS system in strain 30-84, CsaI-CsaR, which does not influence phenazine production, is involved in rhizosphere competitiveness and biosynthesis of cell-surface components (Zhang & Pierson, 2001).

[43] While a number of pharmacists

expressed negative personal attitudes towards CPD, the majority of the research participants within the various studies seemed beset by the compound interaction of barriers apparently outside of their control, such as time and resource issues. A number of theories have been developed to examine the process by which people attribute behaviour (including their own) to internal or external causes and there is now a large body of Cyclopamine mouse evidence showing that people’s judgements about the causes of behaviour are not completely rational but biased.[44] A common observation is that people attribute successes internally, as within their control, whereas failures are attributed externally to others or to the circumstances, Fulvestrant ic50 a concept captured by the term ‘self-serving attribution bias’.[44] A self-serving bias is therefore said to exist where an individual’s assignment of responsibility affects his or her beliefs in an optimistic way, a way that

makes things appear better than they are from the individual’s point of view. We believe there may be an element of self-serving attribution bias at play in terms of pharmacy professionals’ stated barriers to CPD. That is, pharmacy professionals’ own explanations for lack of participation in CPD could stem from their erroneous perception that it is mainly factors external to their control that pose the real barriers, and that ultimately external factors are helping to drive participation in CPD. This would indicate that making CPD a statutory requirement could compel pharmacy professionals to engage with the process at some level, and indeed the personal correspondence referred to above seems to indicate the same. Nonetheless, if CPD is to Cyclin-dependent kinase 3 be truly successful and useful for revalidation, it seems that people’s beliefs and attitudes must be addressed through the modification

of the various other external barriers perceived to be impacting on CPD behaviour. The implications of the current findings can be considered as follows. If CPD is to succeed and be useful as part of revalidation, pharmacy professionals’ beliefs and attitudes must be addressed by recognising and modifying barriers through a combination of four main categories of regulatory, professional, work-related and personal channels (see Figure 2). We believe it is possible to draw on the current findings to suggest a number of remedial steps in relation to these categories so as to ultimately impact on pharmacy professionals’ personal motivations and therefore participation in CPD.

007, Fig. 5). The loss of CinA, therefore, enhances the mutant’s sensitivity to killing by MMS, which is likely caused by diminished expression of recA in our SmuCinA mutant or due to a possible interaction with RecA at the DNA replication fork. However, our ability to partially restore viable CFUs by using the CinA complemented strain clearly suggests an important role for CinA in contending with MMS-induced stress in S. mutans. Here we have demonstrated that cinA is transcriptionally regulated by ComX, which in Obeticholic Acid price turn,

modulates genetic competence and cell death in S. mutans. Although, we only investigated CSP’s effects on cinA upregulation, it is likely that cinA also transcriptionally responds to XIP, which was shown to activate ComX (Mashburn-Warren et al., 2010; Lemme et al., 2011). In addition to ComDE, we know that other signaling systems also modulate ComX activity (e.g. ComRS, LiaRS, signaling pathway VicRK) (Mashburn-Warren

et al., 2010; unpublished data). Hence, it stands to reason that ComX-dependent transcription of cinA relies on multiple signaling inputs for optimal activity. Further, our results support the findings of Lemme et al., who showed that ComX can modulate cell death vs. competence depending on its activity (Mashburn-Warren et al., 2010; Lemme et al., 2011). Here, we have further shown that these ComX-regulated phenotypes are, at least in part, regulated via CinA. In this report, we also showed that S. mutans’ ability to withstand DNA damage induced by MMS was also dependent

on CinA. Taken together, we have demonstrated novel roles for the CinA in S. mutans in modulating genetic transformation, cell viability and tolerance to MMS. We would like to thank Martha Cordova for assistance with Northern blots. D.G.C. is a recipient of NIH grant R01DE013230-03 and CIHR-MT15431. “
“The atuR-atuABCDEFGH gene cluster is essential for acyclic terpene utilization (Atu) Dipeptidyl peptidase in Pseudomonas aeruginosa and Pseudomonas citronellolis. The cluster encodes most proteins of the Atu pathway including the key enzyme, geranyl-CoA carboxylase. AtuR was identified as a repressor of the atu gene cluster expression by (1) amino acid similarity to TetR repressor family members, (2) constitutive expression of Atu proteins in the atuR insertion mutant and (3) specific binding of purified AtuR homodimers to the atuR-atuA intergenic region in electrophoretic mobility shift assay (EMSA). Two 13 bp inverted repeat sequences separated by 40 bp in the atuA operator/promoter region were identified to represent two sites of AtuR binding by EMSA. Changing of two or more bases within the inverted repeat sequences abolished the ability of AtuR to bind to its target. All EMSA experiments were sufficiently sensitive with ethidium bromide-stained DNA fragments after polyacrylamide gel electrophoresis.

, 2008). To date the target of MMP9 proteolysis within the ECM that induces integrin signaling remains unknown. Another matrix metalloprotease, MMP3, is able to process agrin at the basal lamina of the neuromuscular junction in an activity-dependent manner (Werle & VanSaun, 2003). It has been suggested that this process is responsible for fast removal of agrin from the neuromuscular junction, where it induces acetycholine receptor clustering and is indispensible for normal neuromuscular junction development (Sanes & Lichtman, 2001). In line with this view, MMP3-knockout mice exhibit Ganetespib molecular weight abnormal neuromuscular junction morphology and

acetylcholine receptor distribution (VanSaun et al., 2003). Another protease that has recently been found to act on agrin as its main substrate

is the brain-specific serine protease neurotrypsin (Reif et al., 2008). Neurotrypsin can be released at synapses in an activity-dependent manner where it locally see more processes agrin into distinct fragments (Frischknecht et al., 2008; Stephan et al., 2008). Interestingly, neurotrypsin has been identified as essential for cognitive function in the human brain (Molinari et al., 2002). In an elegant series of experiments it was demonstrated that the proteolytic fragment of 22 kDa acquired signaling properties that induced filopodia in hippocampal slice cultures after induction of synaptic long-term potentiation (Matsumoto-Miyai et al., 2009). Thus, similar to MMP9, proteolytic cleavage of ECM components unmasked a signaling molecule, Pyruvate dehydrogenase which in turn led to an altered spine morphology and even to the generation of new synapses. Hence, these examples demonstrate that the ECM contains a variety of hidden instructive signals that can be revealed by specific proteolysis. Finally, it has been demonstrated that, similar to chondroitinase ABC treatment, the topical application of the serine protease tissue-type

plasminogen activator (tPA) can prolong the so-called critical period in the visual cortex (Mataga et al., 2004; Oray et al., 2004). It was shown that tPA induces activity-dependent pruning of dendritic spines in the visual cortex. However, it is currently unclear whether pruning after tPA treatment depends on a newly generated signaling molecule, similar to the mode of action of neurotrypsin or MMP9, or whether the effect is based on the removal of the PNN-like structures as a general barrier for filopodial outgrowth (Berardi et al., 2004). The ECM protein reelin has also been discussed as a serine protease (Quattrocchi et al., 2002). In the adult CNS it mediates its function via binding to its cell surface receptors very-low-density lipoprotein receptor (VLDLR) and ApoE2 receptor (APOE2R) and the downstream adaptor protein Dab1.

Typhimurium compared with the DMSO-treated control (47 genes upregulated; 66 genes downregulated; Fig. 1 and Supporting Information, Tables S1 and S2). The key findings were as follows. Transcription of genes encoding the T3SS-1 structural apparatus, regulators and check details chaperones was reduced by INP0403 treatment. For example, invC encoding the T3SS-1 ATPase was reduced 23.8-fold and hilD encoding a regulator of SPI-1 gene expression was reduced 9.7-fold (Table S2). Our data were largely in agreement with those obtained using SPI-1 chromosomal lacZ transcriptional fusions (Negrea et al., 2007), but no T3SS-1 translocators or effectors shared statistically

significant changes in transcription (Table S1). When examining the unfiltered Metformin chemical structure data, transcription of sipA, -B, -C and -D, encoding effector/translocator proteins, was reduced four- to fivefold and other T3SS-1 effector genes, including sopA, sopB, sopD and sopE2, were reduced by 1.5–2.5-fold (Table S1). Although transcription of these genes was reduced upon INP0403 treatment they did not meet the stringent filtering criteria. hilA similarly did not show statistically significant regulation by INP0403 (Table S1) for the same reason. HilA is encoded within SPI-1 and is a key transcriptional regulator of SPI-1 genes, non-SPI-1 encoded T3SS-1 effectors and SPI-4 genes (Bajaj et

al., 1995, 1996; De Keersmaecker et al., 2005; Morgan et al., 2007; Thijs et al., 2007). Few T3SS-2 genes were significantly repressed by INP0403 (sseE twofold, ssaL 3.2-fold), likely because the experiments were performed under T3SS-1-inducing conditions, rather than those that induce T3SS-2 (magnesium limitation and phosphate starvation; Deiwick et al., 1999). A quarter of all genes upregulated by more than twofold upon INP0403 treatment were involved in iron acquisition and transport, including feoA encoding ferrous second iron transport protein A, exbB and exbD involved in uptake

of the siderophore enterochelin and fhuA, B, C and D involved in hydroxymate-dependent iron transport. A cluster of genes encoding 50S and 30S ribosomal subunits were repressed 2.3–4.5-fold by INP0403, including rplO encoding the 50S ribosomal subunit L15 and rpsB encoding the 30S ribosomal subunit protein S2. It is possible that this may be associated with effects on iron availability, as downregulation of ribosomal proteins in response to iron limitation has been observed in both transcriptome and proteome studies of Francisella tularensis (Deng et al., 2006; Lenco et al., 2007). Genes encoding various transporters or drug resistance genes were activated, for example nanT encoding sialic acid transport protein and ybhF encoding a putative ABC-type multidrug transport system. Selected changes in transcript levels were validated using S. Typhimurium SL1344 strains containing single-copy gfp+ transcriptional fusions to promoters of the T3SS-1 gene prgH, the T3SS-2 gene ssaG, the housekeeping gene rpsM and a promoterless gfp+.

Table S3. Gene expression changes for healthy control cattle group (n=5) at 3 h between stimulated and nonstimulated MDMs in real-time quantitative PCR. 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. “
“Infected yellow catfish (Pelteobagrus fulvidraco) were sent from Niushan Lake Fishery, Hubei Province, China, to our laboratory for diagnosis. Macroscopic daffodil yellow mold was observed on the heads and fins of the fish and one Mucor species was isolated. Based on Selleckchem C225 the morphological and molecular analysis, the species was identified as Mucor circinelloides. Its optimum growth temperature was 30 °C and it could not grow at 40 °C. The infectivity results showed wound infection could cause 100% cumulative mortalities at all experimental CFU (106, 107 and 108). The cumulative mortalities of the intraperitoneal infection increased along with the sporangiospore concentrations; the highest mortality was 90% with 108 CFU. Histopathological studies showed M. circinelloides could cause

a series of pathological changes in the host tissues and they disseminated in different viscera, DAPT chemical structure perhaps by the blood. This is the first report of M. circinelloides infection in yellow catfish. Mucor are opportunistic fungi belonging to the family Mucoraceae of the class Zygomycetes. They are ubiquitous in the environment HA-1077 cost and have been reported

to be pathogenic in birds, animals and humans (Lie & Njo-Injo, 1956; Sugar, 1992, 2005). Mucormycosis is usually associated with immunosuppression, trauma and subsequent surgery in the human host (Lehrer et al., 1980; Sugar, 1992, 2005; Kontoyiannis et al., 2000, 2005; Gonzalez et al., 2002; Almyroudis et al., 2006) and generally causes localized cutaneous infection with high morbidity and even high mortality when disseminated (Ribes et al., 2000; Lenane et al., 2003; Almyroudis et al., 2006). It is characterized by the formation of sexual spores (zygospores) and vegetative mycelium that lack septa, except to delimit old or injured hyphae or reproductive structures in Mucorales. Asexual reproduction occurs most commonly by the formation of nonmotile, unicelled sporangiospores in uni- or multispored sporangia or merosporangia. Although the infectivity and nosogenesis involved with human mucormycosis are well documented, the only report to date describing it as a pathogen for fish is that of Yang et al. (2006), who isolated a Mucor sp. from Takifugu obscurus in Jiangsu province, China. However, their identification results were inconclusive because they identified it by phenotype only to genus level. If a case report of mucormycosis does not identify the species, it may be difficult to associate a disease specifically with a species (Kontoyiannis et al.