, 2003; Toledo-Arana et al., 2007; Fozo et al., 2010; Sridhar et al., 2010). Together with computational tools for the detection of sRNAs in completed genomes (Sridhar et al., 2010) such as B. proteoclasticus B316T, we believe that transposon mutants with Tn916 insertion into intergenic regions may prove to be useful Doxorubicin mouse tools for studying the transcription and/or the translation of adjacent genes regulated by sRNAs and are currently investigating the transcription/translation characteristics of several intergenic mutants obtained from this study. We thank Peter Janssen for critically reviewing this manuscript. This work was funded under the Rumen Microbial

Functional Genomics Programme (FRST C10X0314) by the New Zealand Foundation for

Research, Science and Technology as part of the New Economy Research Fund. “
“The long polar fimbriae (Lpf) is one of few adhesive factors of Shiga toxin-producing Escherichia coli (STEC) and it is associated with colonization of the intestine. Studies have demonstrated the presence of lpf genes in several pathogenic E. coli strains, and classification of variants based on polymorphisms in the lpfA1 and lpfA2 genes has been adopted. Using a collection of Argentinean locus of enterocyte effacement (LEE)-negative STEC strains, we determined that the different lpfA types were present in a wide variety Dabrafenib clinical trial of serotypes with no apparent association between the types of lpfA1 or lpfA2 genes and the severity of human disease. The lpfA2-1 was the most prevalent variant identified, which was present in 95.8% of the isolates, and lpfA1-3 and

lpfA2-2, proposed as specific biomarkers of E. coli O157:H7, were not found in any of the serotypes studied. The prevalence of lpf genes in a large number of strains is useful to understand the genetic diversity of LEE-negative STEC and to define the association of some of these isolates carrying specific lpf-variants with disease. Shiga toxin-producing Escherichia coli (STEC) strains are foodborne enteric pathogens associated with different Cediranib (AZD2171) clinical manifestations such as nonbloody diarrhea, hemorrhagic colitis (HC) and hemolytic uremic syndrome (HUS) (reviewed in Nataro & Kaper, 1998). Although E. coli O157:H7 is the most prevalent serotype associated with sporadic cases and large outbreaks of HC and HUS, there is growing concern about the emergence of highly virulent STEC non-O157 serotypes that become globally distributed and associated with outbreaks and/or severe human illness (Coombes et al., 2008). Ruminants, particularly cattle, are recognized as the main natural reservoir for STEC and cattle-derived food products have been implicated in many outbreaks (Caprioli et al., 2005).

aureus is able to import heme, when supplied as either hemin or hemoglobin, in the absence of isdE and htsA. Thus, the lipoprotein-encoding

genes isdE and htsA are dispensable for heme ROCK inhibitor acquisition by S. aureus. This precludes the use of the ΔhemBΔisdEΔhtsA strain to definitively study the role of heme acquisition in heme-auxotrophic SCVs in an in vivo model. It also indicates that the reduced virulence of the ΔisdEΔhtsA in a murine systemic infection model cannot be explained by an inability to import heme (Mason & Skaar, 2009). These data lend further weight to the already strong body of evidence that HtsA is solely involved in transport of the siderophore staphyloferrin A (Beasley et al., 2009; Grigg et al., 2010). Furthermore, these experiments contradict the suggestion that IsdE may transfer heme to the HtsBC transporter, as heme import is still functional in the absence of both htsA and isdE (Hammer & Skaar, 2011). The proposed transport pathway from hemoglobin, bound by IsdB and IsdH, via IsdA and IsdC to IsdE (Muryoi et al., 2008; Zhu et al., 2008; Hammer & Skaar, 2011) also cannot be fully dependent on IsdE, given the continued function of heme import from hemoglobin in the ΔhemBΔisdEΔhtsA strain. This strongly suggests that additional components,

which have yet to be identified, are involved in the transport of heme into the S. aureus cytoplasm. To examine the role of heme import in heme-auxotrophic SCVs, identification of these heme transport components is required. This research was supported by Arthritis Research UK project

grant funding RGFP966 (grant number 18294). “
“Neisseria gonorrhoeae is a strict human pathogen that causes the sexually transmitted infection termed gonorrhea. Recent reports indicate that gonococci can form a biofilm in vivo and under 17-DMAG (Alvespimycin) HCl laboratory conditions. It is unclear, however, if formation of such biofilms or their dispersal are influenced by host factors that would be encountered during infection. In this respect, physiological levels of polyamines have been reported to influence biofilm structures formed by other Gram-negative bacteria as well those formed by Gram-positive bacteria and can cause dispersal of a biofilm formed by Bacillus subtilis. Based on these reports, we examined the influence of polyamines on gonococcal biofilm formation and their dispersal. We now report that physiological levels of certain polyamines, notably spermine, can significantly decrease the capacity of gonococci to form a biofilm, but do not cause dispersal of a preformed biofilm. In the context of natural gonococcal infection, the presence of physiological levels of spermine may be antagonistic for gonococci to form a biofilm and this may be of importance in the spread of the pathogen from a localized region. “
“Although it is known that Escherichia coli O157 is capable of long-term soil survival, little is known about the mechanisms involved.

44; 95% selleck screening library confidence interval (CI) 1.24−9.57; P < 0.05] and ‘other’ Black (born outside sub-Saharan Africa) ethnicity (AOR 4.63; 95% CI 1.06–20.11; P < 0.05). We also found an association between older age and decreased likelihood of lifetime IPV (AOR 0.92; 95% CI 0.86–0.97;

P < 0.05). Over half of the women in this study reported lifetime experience of IPV. We found associations between IPV and mental health problems, younger age and other Black ethnicity. In view of its high prevalence, we advocate greater awareness of IPV among HIV healthcare professionals and recommend universal screening. Intimate partner violence (IPV) is defined as physical, sexual or psychological harm by a current or former partner or spouse [1]. The World Health Organization's multi-country study found that lifetime prevalence of physical and/or sexual partner violence was between 15 and 71% [2]. IPV is estimated to affect 28% of women living in the UK in their lifetime [3]. The social, psychological and physical consequences of IPV are considerable and it has been shown to Erlotinib have adverse effects on health in both the short and long term [4]. Women experiencing IPV are more likely to be in regular contact with healthcare professionals than

women who are not experiencing IPV, providing important opportunities to identify women and offer support [5]. This has led to the UK’s Department of Health recommending that all National Health Service (NHS) trusts work towards routinely asking women about their experiences of IPV in clinical

settings [6]. Women living with HIV are more likely to experience IPV than HIV-negative women [7-10]. IPV may predate the HIV diagnosis or follow as a consequence of it [11]. IPV is a risk factor for HIV acquisition, possibly as a result of nonconsensual sex or difficulties negotiating safer sex [12-15]. Furthermore, male perpetrators of IPV are more likely to have HIV or other sexually transmitted infections (STIs) than nonperpetrators [16, 17]. IPV is also a predictor of worse HIV outcomes [18]. It may impair a woman’s ability to disclose her HIV status to her partner [19, 20], and to make appropriate decisions about health, including attendance at clinic appointments [21, 22], adherence to medication [23], and abstaining from breastfeeding to prevent mother-to-child transmission [9]. Calpain In view of the recognized paucity of data on IPV in women living with HIV in the UK [24], we conducted a study of women attending the HIV out-patient department at the Homerton University Hospital. The hospital is in Hackney in East London, an area with significant socioeconomic deprivation [25] and where local lifetime prevalence of physical IPV is as high as 41% in women attending primary care [26]. Within our HIV clinic population there are high levels of social vulnerability [27] and a higher proportion of female patients than in many other UK centres.

Analysis of growth of the parental strain, Ev1 and their respective cg2937 disruptions in CGXII Neu5Ac

medium, revealed that disruption of cg2937 results in a complete loss of growth (Fig. 3a and b). The same phenotype was observed on solid media (Fig. 3d). We examined [14C]-Neu5Ac uptake using Ev1 and Ev1 cg2937::pDRIVE where uptake was also completely abolished in the strain disrupted in cg2937 (Fig. 3c). Hence, we conclude that the cg2937-40 genes encode the sole sialic acid transporter in C. glutamicum. Given the clear demonstration that the soil bacterium C. glutamicum has the ability to grow on sialic acid, we examined the distribution of the sialic acid transport and utilization genes within the genus Corynebacterium (Fig. 4). It is clear that the sialic

acid genes are not unique to C. glutamicum, but are present in a number of other members of the genus Corynebacterium Belinostat particularly in organisms that cause diseases in human and animals where genome BMN 673 price sequences are available such as Corynebacterium diphtheriae (Cerdeno-Tarraga et al., 2003), Corynebacterium ulcerans (Trost et al., 2011) and Corynebacterium pseudotuberculosis (Trost et al., 2010). In every case, they have a SatABCD-like sialic acid transporter and the full set of genes needed for catabolism, namely nanA, nanE, nanK, nagA and nagB. While C. glutamicum, C. diphtheriae, C. pseudotuberculosis and C. ulcerans all encode a sialidase on their genome, the predicted sialidase in C. glutamicum (cg2935) is the only one encoded within the main nan-cluster and is not a clear orthologue of the nanH sialidase seen in the other three organisms (marked as nanH in Fig. 4). Sialic acid utilization has been well studied in a range of pathogens, and in this work, we demonstrate clearly that the soil bacterium C. glutamicum can transport and utilize Neu5Ac as a sole carbon source. Examination of the genome reveals what appears to be

a fairly canonical sialic acid cluster containing a full set of genes including an ABC transporter that we have demonstrated is essential for uptake (Fig. 4). It is not clear why the presence of sialic acid utilization genes was not recognized in a previous study (Almagro-Moreno & Boyd, 2009), looking at the distribution of the nanAEK genes in bacteria. The only ID-8 member of the genus Corynebacterium, where sialic acid biology has been previously studied, is in C. diphtheriae. A sialidase was first isolated from this pathogen in 1963 (Warren & Spearing, 1963; Moriyama & Barksdale, 1967) and, remarkably, NanA activity was also identified shortly afterwards (Arden et al., 1972). Interestingly, the same study demonstrated that both sialidase and NanA (N-acetylneuraminate lyase) activities were also observed in C. ulcerans and Corynebacterium ovis (now C. pseudotuberculosis; Arden et al., 1972), which agrees with the presence of both nanH and nanA genes in all of these sequenced genomes (Fig. 4).

Agrobacterium tumefaciens C58C1 strains carrying the vector pBin-Hyg-Tx, pBin::nopT1, and pBIN::nopT2 were infiltrated into N. tabacum cv. Xanthi and N. benthamiana leaves. NopT1 elicited localized cell death in both Nicotiana species (Fig. 4b). By contrast, leaves infiltrated with A. tumefaciens carrying pBin::nopT2 did

not show any visible symptoms (Fig. 4c). No visible symptoms of cell death were observed when Agrobacterium with an empty vector was infiltrated (Fig. 4a). In light of these results, further studies focused on the analysis of NopT1 function. To determine whether the putative catalytic triad (C/H/D) of NopT1 is required for the HR-like cell death in tobacco, we constructed substitutions at positions 100 (C100S), 213 (H213A), and 228 (D228A) with Ala (Fig. 2d). Metformin solubility dmso this website The coding regions of the site-directed mutants were subcloned into a binary Agrobacterium vector and tested for ability to elicit the HR in N. tabacum and N. benthamiana when overexpressed directly within the plant cells via the Agrobacterium-transient expression system. None of the mutants elicited cell death (Fig. 4e–g), whereas the wild-type NopT1 elicited a strong HR (Fig. 4b). We also

examined whether the site-directed mutants retained enzymatic activity. As shown in Fig 2b, all site-directed mutants had lost the NopT1 processing in E. coli, although not completely and their in vitro enzymatic activity selleck inhibitor was significantly reduced in comparison with wild-type protein (Fig. 3c). These results corroborate further the prediction that that NopT1 is a cysteine protease and requires an intact catalytic triad for both enzymatic and HR-eliciting activity. Previous studies have shown

that all YopT/AvrPphB family members identified so far contain an embedded consensus site for eukaryotic fatty acylation which may be exposed following autoproteolytic processing of these effectors (Puri et al., 1997; Nimchuk et al., 2000; Dowen et al., 2009). Similarly, NopT1 possesses putative sites (Fig. 1b) for both N-myristoylation (G50) and S-palmitoylation (C52 and C53) that lack experimental validation. To investigate whether these acylations play a role in cell death elicitation by NopT1, we made deletion and site-directed mutants affecting either one or both sites. Initially, we made a deletion mutant, Δ50N, in which an ATG codon was introduced just before the A51 codon by replacing the glycine (G) residue at position 50 by a methionine (M) residue. Transient expression via agroinfiltration of this mutant displayed identical necrotic phenotype to that elicited by the full-length protein, in terms of both timing and intensity of the necrotic response (Fig. 4d). Although myristoylation of NopT1 has not been demonstrated biochemically, it is tempting to speculate that an intact myristoylation motif may not be required for HR elicitation by NopT1 at least in plants tested.

Compared with late starters, late presenters (adjusted OR 1.30; 95% CI 1.02, 1.67; P=0.04) and ideal starters (adjusted OR 1.57; 95% CI 1.23, 2.02; MAPK Inhibitor Library mouse P=0.0004) were both more likely to experience clinical progression at week 48 (the latter finding was mainly

attributable to the higher rate of loss to follow-up among ideal starters); differences were, however, reduced and nonsignificant at week 96. Finally, when we reanalysed our data using a threshold of <500 copies/mL to define virological suppression, we found high rates of viral suppression in all groups. At week 48, rates of virological suppression among those remaining under follow-up and on treatment were 92.7, 92.9 and 94.3% in late presenters, late starters and ideal starters, respectively. Rates of virological suppression were not significantly different among late presenters (adjusted OR 1.34; 95% CI 0.90, 1.98; P=0.15), ideal starters (adjusted OR 1.26; 95% CI 0.82, 1.94; P=0.29) and late starters in multivariable analyses. By week 96,

virological suppression rates among those remaining under follow-up and on treatment were 93.3, 96.3 and 94.9% in late presenters, ideal starters and late starters, respectively, with no significant differences among late find more presenters (adjusted OR 1.49; 95% CI 0.91, 2.45; P=0.12), ideal starters (adjusted OR 1.36; 95% CI 0.76, 2.43; P=0.30) and late starters. We demonstrated that, among patients who remained under follow-up and on treatment, virological responses at 48 or 96 weeks did not differ substantially (-)-p-Bromotetramisole Oxalate between late starters and late presenters; similar conclusions were reached when additionally controlling for the actual CD4 cell count and viral load at the time of HAART initiation, and in several sensitivity analyses designed to assess the robustness

of the findings to missing data and changes in the viral load assay over time. Despite these similar virological responses, late presenters did experience blunted immunological responses at both 48 and 96 weeks compared with late starters, although the difference between the two groups reduced over time. Of note, there was a smaller, although also statistically significant, numerical difference between late starters and ideal starters in terms of CD4 cell count increase at 48 weeks, which is consistent with a prior analysis of this cohort showing smaller CD4 cell count gains in patients with higher baseline CD4 cell counts [15]; there was no significant difference by week 96. The early difference in CD4 cell count response between late starters and late presenters may be secondary to increased comorbidities or use of concomitant medications in the late presenters (supported by the higher frequency of new AIDS events in this group).

Compared with late starters, late presenters (adjusted OR 1.30; 95% CI 1.02, 1.67; P=0.04) and ideal starters (adjusted OR 1.57; 95% CI 1.23, 2.02; MLN8237 price P=0.0004) were both more likely to experience clinical progression at week 48 (the latter finding was mainly

attributable to the higher rate of loss to follow-up among ideal starters); differences were, however, reduced and nonsignificant at week 96. Finally, when we reanalysed our data using a threshold of <500 copies/mL to define virological suppression, we found high rates of viral suppression in all groups. At week 48, rates of virological suppression among those remaining under follow-up and on treatment were 92.7, 92.9 and 94.3% in late presenters, late starters and ideal starters, respectively. Rates of virological suppression were not significantly different among late presenters (adjusted OR 1.34; 95% CI 0.90, 1.98; P=0.15), ideal starters (adjusted OR 1.26; 95% CI 0.82, 1.94; P=0.29) and late starters in multivariable analyses. By week 96,

virological suppression rates among those remaining under follow-up and on treatment were 93.3, 96.3 and 94.9% in late presenters, ideal starters and late starters, respectively, with no significant differences among late selleck compound presenters (adjusted OR 1.49; 95% CI 0.91, 2.45; P=0.12), ideal starters (adjusted OR 1.36; 95% CI 0.76, 2.43; P=0.30) and late starters. We demonstrated that, among patients who remained under follow-up and on treatment, virological responses at 48 or 96 weeks did not differ substantially Nintedanib (BIBF 1120) between late starters and late presenters; similar conclusions were reached when additionally controlling for the actual CD4 cell count and viral load at the time of HAART initiation, and in several sensitivity analyses designed to assess the robustness

of the findings to missing data and changes in the viral load assay over time. Despite these similar virological responses, late presenters did experience blunted immunological responses at both 48 and 96 weeks compared with late starters, although the difference between the two groups reduced over time. Of note, there was a smaller, although also statistically significant, numerical difference between late starters and ideal starters in terms of CD4 cell count increase at 48 weeks, which is consistent with a prior analysis of this cohort showing smaller CD4 cell count gains in patients with higher baseline CD4 cell counts [15]; there was no significant difference by week 96. The early difference in CD4 cell count response between late starters and late presenters may be secondary to increased comorbidities or use of concomitant medications in the late presenters (supported by the higher frequency of new AIDS events in this group).

Phanerochaete sordida YK-624 (ATCC 90872) from rotten wood (Hirai et al., 1994) was used in this study. The fungus was maintained on potato dextrose agar slants at 4 °C. AFB1 was purchased from Wako Pure Chemical Industries (Japan). The umu test with umulac AT (Protein

Purify Ltd, Japan) was used to assay mutagenic activity. All other chemicals were extra-pure grade Fulvestrant in vivo and were used without further purification. MnP from P. sordida YK-624 was prepared and purified using the modified method described by Kondo et al. (1994). The MnP solution did not contain LiP activity, and has been purified to homogeneity in sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis. The purified MnP on isoelectric focusing showed one isoform (data not shown). MnP activity

was measured by monitoring the oxidation of 2,6-dimethoxyphenol to coerulignone (ɛ470=49.6 mM−1 cm−1) (Pèriè & Gold, 1991). The reaction mixture (1 mL) contained 2,6-dimethoxyphenol (1 mM), MnSO4 (1 mM), and H2O2 (0.2 mM) in 50 mM malonate, pH 4.5. One katal (kat) was defined as the amount of enzyme producing 1 mol product s−1. MnP reactions were performed in 1 mL of reaction mixture containing 5 nkat MnP, 10 μL of 1 mM AFB1 in 10% dimethylsulfoxide, 1 mM MnSO4, 0.1% Tween 80, 4 nkat glucose oxidase, and 2.5 mM glucose in 50 mM MI-503 purchase malonate, pH 4.5. Reactions were performed in triplicate for 24 h at 30 °C and mixing at 150 r.p.m. In some experiments, the amount of MnP (1–20 nkat) and the reaction time (1–48 h) were changed, and Tween 80 was excluded. The amount of AFB1 was determined by HPLC under the following conditions: column, Wakosil-II 5C18HG (4.6 mm × 150 mm, Wako Pure Chemical Industries); mobile phase, 40% aqueous methanol; flow rate, 0.5 mL min−1; and detection wavelength, 365 nm. The umu test with umulac AT was used to assay the mutagenic activity of AFB1 (Oda et al., 1995). The test was performed with Salmonella typhimurium TA1535 and S9 liver homogenate. The TA1535 strain was constructed by subcloning the bacterial O-acetyltransferase gene into a plasmid vector pACYC184 and introducing the plasmid into the original S. typhimurium TA1535/pSK1002 strain harboring

an umuC‘–’lacZ fusion gene. Assays were tuclazepam carried out in triplicate using 10 μL of test sample, 10 μL of S9mix (a metabolic activation system based on S9 liver homogenate), and 100 μL of bacterial culture. After incubation for 2 h at 37 °C, 100 μL of X-Gal solution was added to each well, and after 1 h at 37 °C, the reaction was stopped by the addition of SDS/dimethylsulfoxide solution. The absorbance of the mixture was read at 600 nm. The relative mutagenic activity (%) was defined as the percentage of β-galactosidase activity of the AFB1-containing reaction mixture (with 5, 10, or 20 nkat MnP) divided by the activity of the AFB1-containing reaction mixture without MnP. AFB1 (final concentration 160 μM) was incubated at 30 °C for 48 h in a 100-mL reaction mixture containing 750 nkat MnP, 1 mM MnSO4, 0.

In the natural environments, most bacteria can form biofilms, embedded within a self-produced extracellular polymeric matrix consisting mainly of polysaccharide groups (Flemming & Wingender, 2010). The biofilm formation as a bacterial survival strategy leads to increased resistance to heat, acid, preservatives, and antibiotics (Stewart & William Costerton, 2001; Chmielewski & Frank, 2003; Van Houdt & Michiels, 2010). Bacterial infections can mainly occur after consumption of contaminated foods. The

ingested bacteria are exposed to acidic stress and bile Navitoclax order salt under oxygen-limited conditions during transit through the stomach, the small intestine, and the colon. These stress conditions can influence antibiotic resistance patterns, biofilm-forming abilities,

and virulence properties (Riesenberg-Wilmes et al., 1996; Gahan & Hill, 1999; Schobert & Tielen, 2010). Moreover, antibiotic-resistant bacteria can possibly reside in biofilms and lead to enhanced tolerance to adverse environmental conditions, causing serious infectious learn more diseases (Gustafson et al., 2001; Langsrud et al., 2004; Ngwai et al., 2006; Kim & Wei, 2007). However, there is a lack of information on the biofilm-associated infections involved in altered virulence properties of antibiotic-resistant bacteria. Therefore, the objective of this study was to evaluate the gene expression patterns of biofilm and planktonic cells of antibiotic- resistant foodborne pathogens, Salmonella Typhimurium and Staphylococcus aureus, when exposed to acidic stress under anaerobic condition. Strains of S. aureus KACC13236 and S. Typhimurium KCCM 40253 were obtained from the Korean

Agricultural Culture Collection (KACC, Suwon, Korea) and the Korean Culture Center of Microorganisms (KCCM, Seoul, Korea), respectively. Strains of S. aureus CCARM 3080 and S. Typhimurium CCARM 8009 were purchased from the Culture Collection of Antibiotic Resistant Microbes (CCARM, Seoul, Korea). All strains were cultured in trypticase soy broth (TSB; BD, Becton, Dickinson and Co., Sparks, MD) at 37 °C for 20 h. The cultured cells were collected by centrifuged at 3000 g for 20 min at Orotidine 5′-phosphate decarboxylase 4 °C, washed twice with 0.1% sterile buffered peptone water (BPW), and then used to prepare biofilm cells for assays. The biofilm formation was evaluated based on the ability of strains to adhere to the surface of polystyrene Petri dishes. The strains of S. aureus KACC13236, S. Typhimurium KCCM 40253, S. aureus CCARM 3080, and S. Typhimurium CCARM 8009 were inoculated at approximately 106 CFU mL−1 in TSB adjusted to a sub-lethal pH of 5.5 using 1 M HCl and TSB at pH 7.3 as the control. The inoculated strains were anaerobically cultured without mechanical agitation at 37 °C for 48 h in a GasPak anaerobic system (BBL, Cockeysville, MD) with AnaeroGen (Oxoid Ltd, Hampshire, UK).

, 2010) may vary in individual strains depending on differences in the level of P2 prophage tail synthesis gene expression. In addition, the efficiency of cell lysis and the range of tail fiber specificity may also determine the contribution of xenorhabdicin to interspecies competition. Xenorhabdus bovienii-SF43 contains a remnant P2-type prophage (xbp1) that is strongly similar to the xnp1 locus of X. nematophila and is located at the same position in the genome. Together, these findings suggest that remnant

P2-type prophages are conserved in Xenorhabdus spp. and that ancestral acquisition of a P2-type prophage conferred the ability to produce xenorhabdicin. In addition, recombination events with truncated fiber genes located within a variable region of the remnant prophage may expand the host range specificity of xenorhabdicin. Please note: Wiley-Blackwell is signaling pathway 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. “
“The complete mitochondrial genome of Penicillium digitatum (Pers.:Fr) Sacc is reported, the first time in a phytopathogenic click here Penicillium species. Comparative analysis revealed its close relationship to mitochondrial genomes of other Penicillium and Aspergillus species, both in gene content and in arrangement. The intron content of protein coding

genes revealed several differences. The different exon–intron organization of CytochromeOxidaseSubunit 1 genes indicated their common origin before the divergence of Penicillium and Aspergillus, and that, Endonuclease largely, their introns were transmitted vertically. Penicillium digitatum (Pers.:Fr) Sacc, the causative agent of green mould decay, is the most devastating pathogen of postharvest citrus fruits. It contributes up to 90% of total losses during postharvest citrus packing, storing, transportation and marketing (Kanetis et al., 2007; Macarisin et al., 2007). Penicillium digitatum is ubiquitous. It is able to produce saprophytes on any organic substrate in orchards, fruit storage rooms, dump-tanks and flotation-tank water,

and in packing facilities when citrus fruits are absent, and to maintain a high level of inoculum in citrus orchards and packing-houses (Forster et al., 2004). Virtually the entire surface of every citrus fruit is contaminated by its conidia at harvest (Kanetis et al., 2007). Penicillium digitatum initiates inversions in injuries that inevitably occur during harvesting, transportation, packing and marketing. Despite the application of fungicides (Kanetis et al., 2007; Zhang et al., 2009) and biological agents (Droby et al., 1998; El-Ghaouth et al., 2000), as well as postharvest sanitation and storing conditions that are nonconducive to disease, green mould continues to exhibit a high loss pressure on stored citrus commodities worldwide (Forster et al., 2004; Wang & Li, 2008).