With the washing times increased, the silver content slightly decreased from 98.65 see more to 81.65 mg/kg while the corresponding whiteness increased. It is surprising that the antibacterial rate is still more than 97.43% for S. aureus and 99.86% for E. coli after 50 washings. Table 3 The WI, silver content, and antibacterial rate of different washing times Silk samples Laundering cycles Silver content (mg/kg) WI Antibacterial activities   S. aureus E. coli   Surviving cells (CFU/ml) % reduction Surviving cells (CFU/ml) % reduction Untreated – - 90.79 2.28 × 106 – 4.37 × 106 – Silver-treated

fabrics – 98.65 86.32 1.16 × 103 99.49 8.74 × 102 99.98 5 95.02 86.43 3.44 × 103 98.49 1.74 × 103 99.96 10 88.85 87.13 1.28 × 103 99.49 6.11 × 103 99.86 20 87.14 87.58 2.53 × 103 SAHA HDAC order 98.89 1.48 × 103 99.96   50 81.65 87.71 5.86 × 103 97.43 6.11 × 103 99.86 The excellent laundering durability of the silver nanoparticle-treated silk fabrics may be caused by the following this website reasons. Firstly, some imino groups of RSD-NH2 form a silver ammonia complex with silver nanoparticles, which easily penetrate into the amorphous zone of silk fibers. Secondly, silk is a protein fiber and amino acid is its basic structural unit, which has a large number of amino and carboxyl groups on the surface. The van der Waals force between molecules, as well as the hydrogen bond, will enhance the bonding between silver particles

and silk fabrics [20]. The surface morphology of the original silk fabric and the silver nanoparticle-treated silk fabrics is compared in Figure  7. The synthesis condition of the silver nanoparticles is the mixture of 50 mg/l AgNO3 and 2 g/l RSD-NH2 solution. The scanning electron microscope images showed that silver nanoparticles

distributed evenly on the surface of the silver nanoparticle-treated fabric. As the silver nanoparticle-treated silk fabric has good washing properties, silver nanoparticles can be found on the surface of the treated fabric even after washing for 50 times. Also, the K/S value indicates the presence of silver on the silk fabric. As shown in Figure  8, the obvious absorption peaks between 400- and 420-nm wavelength appeared in curves, which is consistent Phosphatidylethanolamine N-methyltransferase with the absorption peak of the silver nanoparticle solution [21]. Thus, we can deduce that there are indeed nanosilver particles on the surface of the silver-treated silk fabrics. Figure 7 SEM images of the surface of the silk fabrics. (a) Original silk fabric. (b) Nanosilver-treated silk fabric. (c) Nanosilver-treated silk fabric after washing for 50 times. Figure 8 K/S spectrum of silver nanoparticle-treated silk fabrics. Conclusions A silver nanoparticle solution was prepared in one step by mixing AgNO3 and RSD-NH2 solution under vigorous stirring at room temperature. The multi-amino compound (RSD-NH2), which has abundant amino and imino groups, was synthesized by methacrylate and polyethylene polyamine in methanol.

Therefore, information regarding referral to adjunct services was not available for our study population. Our study focuses on access to GW4869 colonoscopic diagnosis of emergency CRC as a surrogate for multidisciplinary care. However, referral to other subspecialty services may potentially confound our analysis, especially if procedures are needed to optimize patients prior to surgery, such

as placement of inferior vena cava filters (as AMN-107 prophylaxis to prevent pulmonary emboli), or performance of angiograms to diagnose and treat cardiovascular disease. We were also unable to obtain information regarding the number and timing of outpatient colonoscopies in our study population, because the procedures were often performed in community hospitals or private endoscopy clinics outside of our institution. This data would provide a true reflection of overall

wait-times for surgical resection among emergency CRC patients, and could be addressed by a prospective analysis. While it is possible that patients who underwent colonoscopy may have presented to a peripheral facility for management of their emergency CRC (thereby underestimating estimates of the study population overall), we believe this is unlikely in most cases because these patients are typically transferred to LHSC, buy Gemcitabine which serves as the regional cancer centre, for surgical management. In conclusion, we demonstrate that the implementation of ACCESS expedites the treatment of emergency colorectal cancer patients by combining the diagnosis, workup, and surgical treatment within a single admission without delaying treatment. This study adds to the growing body of evidence that ACS programs effectively deliver surgical care, and can also potentially improve the quality of delivered care for patients who require more complex

care. Although the availability BCKDHB of colonoscopy resources for emergency CRC patients is only one of many equally valid outcomes for CRC, our experience demonstrates that the reorganization of resources can significantly improve access to emergency colonoscopies for a vulnerable population. Future multi-centre studies examining the impact of ACS services on emergency cancer care are needed to demonstrate differences in clinical outcomes among this population. Acknowledgements The authors would like to thank Ms. Lisa Creasor (Health Records, London Health Sciences Centre) and Ms. Frances Whiston (Clinical Research Unit, London Regional Cancer Program, London Health Sciences Centre).

For perforated giant duodenal ulcers, the defect is often too large to perform a primary repair. Leak rates of up to 12% have been reported from attempted closure with an omental patch procedure [74]. The proximity of the defect and its relation to the common bile duct and ampulla of Vater must also be thoroughly investigated. Intraoperative cholangiography may even be necessary to verify

common bile duct anatomy. There are several different procedures that have been described for duodenal defects such as a jejunal serosal patch, tube duodenostomy, and several variations of omental plugs antrectomy with diversion is the classic and most commonly described intervention, if the Erastin mouse ampullary region is not involved. Affected patients are often in extremis at the time of presentation, and therefore a damage control procedure will likely be the safest and most appropriate see more operation

for the patient. An antrectomy, with resection of the duodenal defect for duodenal ulcers proximal to the ampulla, will allow a definitive control of the spillage. Depending upon the location of the duodenal defect, closure and diversion via antrectomy may be the safest method for damage control. The proximal gastric remnant should be decompressed with a nasogastric tube placed intraoperatively with verification of its correct position. Anastomoses should be GANT61 chemical structure avoided in presence of hypotension or hemodynamic instability, especially if the patient requires vasopressors. After copious abdominal irrigation, a temporary abdominal closure device can be placed. The patient can then be resuscitated appropriately in the ICU. The surgeon can return to the OR for re-exploration, restoration of continuity, possible vagotomy, and closure of the abdomen once the patient is hemodynamically stable [75]. We suggest resectional surgery in case of perforated peptic ulcer larger than 2 cm (Additional file 4 : Video 4) We suggest resectional surgery in presence of malignant perforated ulcers or high risk of malignancy

(e.g. large ulcers, endoscopic features of malignancy, presence of secondary lesions or suspected metastases, etc.) (Additional Epothilone B (EPO906, Patupilone) file 4 : Video 4). We suggest resectional surgery in presence of concomitant significant bleeding or stricture. We suggest use of techniques such as jejunal serosal patch or Roux en-Y duodenojejunostomy or pyloric exclusion to protect the duodenal suture line, in case of large post-bulbar duodenal defects not amenable to resection (i.e. close to or below the ampulla). Whenever possible (i.e. stable patient), in case of repair of large duodenal ulcer, we suggest to perform a cholecistectomy for external bile drainage (e.g. via trans-cystic tube). We suggest duodenostomy (e.g.

In the present study, by cell biological analysis we demonstrated that inhibition of CCI-779 miR-125b promoted the migration and invasion of NSCLC cells, providing some evidence that miR-125b could serve as a tumor suppressor in the metastasis of NSCLC in vitro. The upstream regulators of miR-125b expression remain to be identified. Recently Liu et al. reported that STAT3 could promote the transcription of miR-125b in human osteosarcoma cells [24]. In addition, CDX2,

a homeobox transcription factor, has been recently shown to bind to the promoter region of miR-125b and activate its transcription in malignant myeloid selleck screening library cells [25]. By microarray analysis, we previously found that miR-125b was significantly upregulated in MTA1 knockdown NSCLC cells [6]. In this study, we verified that endogenous expression of miR-125b increased after the depletion of MTA1 in two NSCLC

cell lines, suggesting that miR-125b is regulated by MTA1 at the level of transcription. Furthermore, we found that the inhibition of miR-125b could rescue the suppressive effects of MTA1 silencing on NSCLC cell migration selleck inhibitor and invasion. These results demonstrate for the first time that miR-125b is a functional target of MTA1 in lung cancer cells and suggest that ectopic expression of miR-125b is a promising strategy to counteract the promotion of tumor progression by MTA1. It is known that MTA1, which is an integral part of nucleosome remodeling and deacetylation (NuRD) complexes, represses the Resveratrol transcription of target genes by recruiting histone deacetylases onto the promoter regions of target genes and inducing histone deacetylation [25]. Further studies are needed to elucidate the mechanism by which MTA1 downregulates the transcription of miR-125b in lung cancer cells. Conclusions In summary, we found that the expression of MTA1 and miR-125b is negatively

correlated in lung cancer cells and they have antagonistic effects on the migration and invasion of NSCLC cells. The newly identified MTA1-miR-125b axis will help further elucidate the molecular mechanism of NSCLC progression and suggest that ectopic expression of miR-125b is a potentially new therapeutic regimen against NSCLC metastasis. Acknowledgement This study was supported by grants from National Natural Science Foundation of China (No. 81001047/H1615), Educational Commission of Guangdong Province (No. LYM09037), Science and technology projects in Guangdong Province (No. 2012B031800127), and Natural Science Foundation of Guangdong Province (No. 9151051501000035). References 1. Jiang Q, Zhang H, Zhang P: ShRNA-mediated gene silencing of MTA1 influenced on protein expression of ER alpha, MMP-9, CyclinD1 and invasiveness, proliferation in breast cancer cell lines MDA-MB-231 and MCF-7 in vitro. J Exp Clin Cancer Res 2011, 30:60.PubMedCrossRef 2.

Conclusions In this work, PLMA thin film doped with Mn:ZnSe QDs was spin-deposited on the front surface of Si solar cell in order to improve the solar cell efficiency via PL conversion. Significant efficiency enhancements (approximately 5% to 10%) were achieved indeed under AM0 conditions. Both the effects of AR and PL conversion contributed to the solar cell efficiency enhancements but that of PL took a small portion. A precise assessment of PL contribution to the efficiency enhancement was made by investigating the PV responses of Si solar cells coated with QD-doped PLMA to monochromatic and AM0 light sources as functions of QD concentration,

combined with reflectance and EQE measurements. Our work shows that the

real PL contribution might not RAD001 purchase be all that as reflected by the apparent efficiency enhancement, and cautions are to be taken when applying the PL conversion in this aspect. On the other hand, it indicates Quisinostat in vivo again that for practical use of PL conversion, high altitude or/and outer space environments are preferred where the UV proportion is high, and continuing to search for high PL efficiency materials and design efficient optical-coupling structures is still necessary. Acknowledgments This work was supported by the National Basic Research Program of China (973 Program) under Farnesyltransferase the grant number 2012CB934303

and by the National Natural Science Foundation of China under the grant numbers 61275178, 10974034, and 60878044. Experimental assistances from Professors J. D. Wu, N. Xu, and J. Shen are gratefully acknowledged. References 1. Goetzberger A, Hebling C, Schock HW: Photovoltaic materials, history, status and outlook. Mater Sci Eng R-Rep 2003, 40:1.CrossRef 2. Strumpel C, McCann C, Beaucarne G, Arkhipov V, Slaoui A, Svrcek V, del Canizo C, Tobias I: Modifying the solar spectrum to enhance silicon solar cell efficiency – an overview of available materials. Sol Energ Mat Sol C 2007, 91:238.CrossRef 3. Trupke T, Green MA, Wurfel P: Improving solar cell efficiencies by down-conversion of high-energy photons. J Appl Phys 2002, 92:1668.CrossRef 4. Trupke T, Green MA, Wurfel P: Improving solar cell efficiencies by selleck screening library up-conversion of sub-band-gap light. J Appl Phys 2002, 92:4117.CrossRef 5. Van Sark WGJHM, de Wild J, Rath JK, Meijerink A, Schropp REI: Upconversion in solar cells. Nanoscale Res Lett 2013, 8:81.CrossRef 6. Svrcek V, Slaoui A, Muller JC: Silicon nanocrystals as light converter for solar cells. Thin Solid Films 2004, 451:384.CrossRef 7. Stupca M, Alsalhi M, Al Saud T, Almuhanna A, Nayfeh MH: Enhancement of polycrystalline silicon solar cells using ultrathin films of silicon nanoparticle. Appl Phys Lett 2007, 91:063107.CrossRef 8.

Many of the secreted

proteins were found to have predicted hydrolytic activities: two genes (PPA0644 and PPA2106) are predicted endo-glycoceramidases, sharing 42% identity on the protein level. Although their substrate specificities are unknown, PPA0644 and PPA2106 share 27% and 30% protein identity, respectively, with the characterized and structurally analyzed endo-glycoceramidase II from Rhodococcus sp., which hydrolyzes glycosidic linkages between the oligosaccharide and ceramide moieties of gangliosides [29]. Another secreted protein, PPA2164, a glycoside hydrolase family 3 protein, shares 31% identity on the protein level with NagZ (formerly YbbD) of B. subtilis. Mdivi1 purchase NagZ is a β-N-acetylglucosaminidase involved in the peptidoglycan recycling pathway; it cleaves the terminal non-reducing N-acetylglucosamine of muropeptides

[30]. P. acnes also secreted a putative lysozyme (PPA1662) which is 47% identical on the protein level to the muramidase from Streptomyces coelicolor. This muramidase not only cleaves the β-1,4-glycosidic bond between N-acetylmuramic acid and N-acetylglucosamine units, but also exhibits β-1,4-N,6-O-diacetylmuramidase activity, enabling this S63845 enzyme to degrade Staphylococcus aureus cell walls [31]. Whether PPA1662 is an autolytic lysozyme involved in cell wall turnover has still to be elucidated. However, the peptidoglycan of P. acnes contains non-N-acetylated glucosamine residues and is therefore resistant to lysozyme [32]. We speculate that PPA1662 has a different substrate specificity, acting on non-N-acetylated peptidoglycan, or, alternatively, it acts as a defense system against competing bacteria on the skin. Two strains, KPA and 329, secreted a hyalorunate lyase (PPA0380), confirming previous PCI-34051 price investigations on a P. acnes protein with hyalorunate lyase activity [33, 34]. Preliminary the functional characterization revealed that

the enzyme exerted activity against chondroitin 4- and 6-sulphates but not against dermatan sulphate [33]. In accordance, the closest characterized homolog, the chondroitin lyase of Arthrobacter aurescens (37% protein identity to PPA0380) acts on chondroitin sulfate but not on dermatan sulfate [35]. Similar to other chondroitin lyases, it is capable of cleaving hyaluronan, a non-sulfated glycosaminoglycan and a major component of the extracellular matrix of connective tissues. Consistent with the known lipolytic activity of P. acnes [36], we identified lipolytic enzymes in the secretory fraction, including the previously characterized triacylglycerol lipase, designated glycerol-ester hydrolase A (GehA; PPA2105).

ZH and YH performed the strain selection and identification experiments. LS and MS carried out the purification and identification of lipopeptide antibiotics. All authors read and approved the final manuscript.”
“Background A rapid dissemination of Escherichia coli and others enterobacteria producing extended-spectrum

beta-lactamases (ESBLs) has been reported in many European countries, including Spain, and is a matter of major concern [1, 2]. The bla CTX-M genes are becoming the most prevalent ESBLs encountered in Enterobacteriaceae[2]. The prevalent bla CTX-M-type genes in Europe have been identified as bla CTX-M-1, bla CTX-M-3, bla CTX-M-9, bla CTX-M-14 and KU55933 research buy bla CTX-M-15[2]. Infections GSK461364 research buy caused by enterobacteria producing ESBL are associated with increased morbidity, mortality, and health-care associated costs [3]. During recent years, extensive characterization of plasmid families (usually by replicon typing [4, 5] or, more recently, by relaxase identification [6]) has provided

additional information on epidemiological aspects of transmissible antimicrobial resistance [7]. Many of these studies have focused on E. coli producing ESBL [8, 9]. From these studies, some plasmid families were demonstrated to be largely prevalent in Enterobacteriaceae, emerging in association with specific ESBL genes. For instance, the bla CTX-M-15 and bla CHIR98014 CTX-M-3 genes have often been located on plasmids belonging to the IncF group [10] and IncL/M family Acyl CoA dehydrogenase [11] respectively, in different countries [12–16]. It would be interesting to know if in a specific geographical area, plasmid-mediated antimicrobial resistance in multiresistant E. coli producing ESBL is due to plasmids of the same incompatibility group(s) as those present in other multirresistant isolates not producing ESBL. The objective of this study was to determine whether the clonal variability and content of plasmids, resistance genes and integrons of clinical isolates of E. coli producing

ESBL (Ec-ESBL) were similar or not to those of E. coli isolates lacking ESBL (Ec-MRnoB) isolated in the same geographical area and period. Results Phenotype of resistance and clonal relationship MIC50 and MIC90 values of the different agents against the two groups of multiresistant E. coli are presented in Table 1. All Ec-ESBL were susceptible to cefotetan, imipenem, meropenem, amikacin and tigecycline. According to the EUCAST [17], all Ec-ESBL isolates were resistant to cefotaxime, 96% to cefepime, 96% to aztreonam and 23% to ceftazidime (Table 1). Moreover, 39% of the isolates belonging to the Ec-ESBL collection were co-resistant to quinolones, tetracycline and trimethoprim-sulfamethoxazole.

ϕE202 B. thailandensis E202 spontaneously produced a bacteriophage,

designated ϕE202, which formed turbid plaques on B. mallei ATCC 23344. No other plaque types were identified. ϕE202 production was increased 55-fold by brief exposure to UV light (data not shown). Based on its morphotype (Fig. 1A), ϕE202 can be classified as a member of the order Caudovirales and the family Myoviridae [38]. We examined the host range of ϕE202 using 17 Burkholderia species (Additional file 1, Table S1). Bacteriophage ϕE202 formed plaques on 9 of 10 natural B. mallei strains. It also formed plaques on a capsule-deficient Blasticidin S clinical trial mutant derived from ATCC 23344, DD3008 [39], suggesting that this website the capsular polysaccharide is not required for ϕE202 attachment. In contrast, two B. mallei strains that do not produce lipopolysaccharide (LPS) were resistant to plaque

formation by ϕE202; NCTC 120 and DD110795 (a laboratory-passaged derivative of ATCC 15310), which suggests that LPS is a receptor, or co-receptor, for ϕE202. Given the >90% nucleotide identity of the tail assembly genes of the Burkholderia Myoviridae, it is likely that they all share the same receptor(s). Unlike other characterized Burkholderia Myoviridae (ϕE125, ϕ1026b), ϕE202 forms plaques on a species other than B. mallei (Additional file 1, Table S1), namely 3 strains of B. pseudomallei; NCTC 4845, STW 199-2, and STW 115-2. It is currently buy AG-881 unknown why these B. pseudomallei strains exhibit plaque formation with ϕE202 while others do

not. No other Burkholderia species examined formed plaques with ϕE202 (Additional file 1, Table S1). Genomic analysis of the Burkholderia phages I. Myoviridae subgroup A and B Based on sequence similarity, ϕ52237, ϕE202, and ϕK96243 belong to subgroup A of the Myoviridae and ϕE12-2, GI15, and PI-E264-2 to subgroup B (Fig. 2). Furthermore, the genomic structure of each of these are arranged in multigene “”modules”" that encode proteins involved in a common function, such as DNA packaging, head biosynthesis, tail biosynthesis, host lysis, lysogeny or DNA replication [40, 41] (Fig. 1B). The relative order of these modules in ϕ52237, ϕE202, and ϕE12-2 is similar to that of bacteriophages P2 and ϕK96243 [42]. The order is also conserved in bioinformatically-identified Sclareol prophage-like elements GI15 of B. pseudomallei K96243 and PI-E264-2 of B. thailandensis E264 (see below). Figure 2 Unrooted radial phylogenetic tree of the Burkholderia bacteriophages, putative prophages, and prophage-like regions analyzed in this study. The tree was constructed from BLASTP distance matrix (cutoff E-10) using FITCH with the global and jumble options. The modules for tail assembly, lysis, and head assembly of all Myoviridiae phages were highly conserved (Fig. 1B). However, the region encoding for lysogeny and DNA replication contained abundant genetic variability.

A bioassay was performed using the Agrobacterium tumefaciens reporter strain KYC55/pJZ410/pJZ384/pJZ372 [46] in plate and spectrophotometric tests to determine whether this molecule is present in ZFF. LacZ activity was detected in all four positive control plates at nM concentrations of AHL but not in this website ZFFnic or ZFFsoj prepared

from zoospore suspensions at > 104 spores ml-1 nor in concentrated extracts from them obtained with ethyl acetate. These results indicate that zoospores from these oomycete species do not produce AHLs which therefore cannot be responsible for any ZFF activity. Temperature sensitivity of ZFF activities To begin to characterize the signal molecules in ZFF we tested their temperature sensitivity. ZFFnic did not stimulate zoospore aggregation after a freeze-thaw or heat treatment, suggesting that the molecule promoting 3-MA ic50 this behavior may be a protein or lipoprotein that is sensitive to heat and freezing. On the other hand, freeze-thaw did not affect the activity

of ZFFnic in promoting plant infection by zoospores (data not shown). AZD1152 purchase In addition, ZFFnic boiled for 5 minutes remained as active as the untreated in promoting infection (Figure 4), indicating that the molecule which stimulates plant infection is temperature insensitive and different from that involved in aggregation. Figure 4 Zoospore-free fluid (ZFF) stimulation of Phytophthora infection is unaffected by heat treatment. Each leaf of Catharanthus roseus cv. Little Bright Eye was inoculated with twelve 10-μl drops of inoculum of P. nicotianae at approximately one zoospore per drop. Zoospores were suspended in (A) sterile distilled water, (B) untreated ZFF from the same species at 5 × 105 zoospores ml-1 and (C) heat-treated ZFF. Disease symptoms were photographed

after 3-day incubation at 23°C. Conclusion This study demonstrated inter-specific activities of zoospore extracellular products in promoting zoospore aggregation and plant infection by Phytophthora. Zoosporic oomycetes contain hundreds of species and are widespread in irrigation water and plant production fields. However, specific populations detected in primary inoculum sources are not in sufficient numbers Ixazomib to produce signals that could promote plant infection. Inter-specific chemical communication (probably self-interested) as a strategy used by zoosporic pathogens for effective plant infection provides insights into the destructiveness of these pathogens and the importance of the microbial community and the environment in the infection process. AI-2 was excluded as a signal for communal behavior in zoosporic oomycetes, despite its detection in ZFF and widespread presence in the environment. AI-2 synthase RPI and purified AI-2 both were not required for regulation of zoospore aggregation and infection.

Indeed, when divIB mutant cells were shifted to the higher temperature, cells elongated markedly (compare Figure 1G and 1I), which was also true for dynA divIB double mutant cells, whose length could not easily be distinguished by eye from the divIB single mutant strain, neither at 30°C (Figure 1H) nor at click here 42°C (Figure 1J). We measured average cell length for 140 to 150 cells for each strain and for each growth temperature, from 3 independent experiments. The average cell length of divIB mutant cells was 4.03 μm (1.4 μm standard deviation, SD) at 30°C and 5.15 μm (4.9 μm SD) at 42°C, while that of dynA divIB mutant

cells was 3.9 μm (1.2 μm SD) at 30°C and 6.18 μm (5.15 μm SD) at 42°C. Average cell length of dynA mutant cells at 42°C was 3.75 μm FK506 concentration (1.1 μm SD). The high standard deviation at 42°C stems from the fact that a considerable number of cells were extremely long (up to 25 μm), while most cells had a size below 5 μm. To account for this, we grouped cells into three categories: cells below 5.5 μm, cells between 5.5 and 10 μm, and cells above 10 μm. For divIB single mutant cells, 6.3% of the cells were above 5.5 μm long, and 0.7% above 10 μm at 30°C, while at 42°C, 19% were above 5.5 μm and 8% above 10 μm. At 30°C, 8.5% of double mutant cells were above 5.5 μm and 1.5% above 10 μm, and at 42°C, 34% were above 5.5 μm

and 12% above 10 μm (Table 1). Thus, the fraction of double mutant cells was higher in each of the “large cell” categories compared with the single divIB mutant cells. Single and double mutant cells contained normally segregated nucleoids (Figure 1G-J), showing

that cell elongation is not an effect of delayed or blocked chromosome segregation. These data show that the deletion of a late cell division gene also exacerbates the dynA phenotype, showing that DynA does not only affect a step in cell division that is specific to the activity of EzrA. Table 1 Distribution of cell length in single and double mutant cells   <5.5 μm >5.5 μm <10 μm >10 μm ΔdivIB 30°C 93% 6.3% 0.7% ΔdynA ΔdivIB 30°C 90% 8.5% 1.5% ΔdivIB 42°C 73% 19% 8% ΔdynA ΔdivIB 42°C 64% 34% 12% DynA co-localizes Clomifene with FtsZ and affects the formation of the Z ring We generated a dynA(ypbR)-yfp fusion that was integrated into the original gene locus. Cells expressing DynA-YFP did not show any double septa, or highly elongated cells, indicating that the fusion can functionally replace the wild type protein and/or any of the possible post-translationally modified versions of DynA. Western blot analysis showed that full length DynA-YFP is expressed at extremely low levels, as well as a C-terminal fragment of 27 kDa and several smaller fragments (Figure 2, note that YFP is 28 kDa, giving rise to a band of 55 kDa). The 27 kDa band appeared at JSH-23 concentration roughly the same level as full length protein.