Female patients with Lynch syndrome complicate with endometrial cancer at a high incidence. In the revised 1999 Amsterdam II Criteria (AC II), endometrial cancer was included as a cancer with similar features to colon, small intestine, ureteral and kidney cancers.[13] The prevalence of Lynch syndrome is 0.9–2.7%[14] and approximately 2.3% of cases of endometrial cancer occur due to Lynch syndrome.[15] The lifetime risk of endometrial cancer is 28–60% in women with aberrant genes associated with Lynch

syndrome.[16] hMLH1, hMSH2 and hMSH6 mutations are particularly EPZ015666 order important in families of patients with Lynch syndrome. Most mutations occur in hMLH1 and hMSH2, whereas hMHS6 mutations are important in tumorigenesis in patients with endometrial cancer.[17, 18] Kawaguchi et al.[19] proposed a possible new cascade in which hMSH6 mutation is induced by silencing of hMLH1 due to aberrant DNA hypermethylation in endometrial cancer. Westin et al.[20] showed that the incidence of Lynch syndrome was 1.8% in endometrial cancer in total and 9% in endometrial cancer in LDK378 women aged less than 50 years old, but 29% in cases with lower uterine

segment cancer (LUS) and germ cell mutation of hMSH2. These results suggest a correlation between endometrial cancer of the uterine isthmus and Lynch syndrome. Masuda et al.[21] also found germ cell mutations of hMLH1 in 1.4% of patients with LUS. Based on these findings, Lynch syndrome may be

clinically predictive of the onset site of endometrial cancer. Several gene mutations have emerged as candidates for roles in carcinogenesis of type I and II endometrial cancer (Fig. 2), based on observation of the mutation in endometrial hyperplasia and at least a similar incidence of mutation in endometrial cancer. Different genes are involved in carcinogenesis of the two types of endometrial cancer. Gene mutations found in type I endometrial cancer include those in PTEN, β-catenin and Adenosine K-ras. PTEN is a tumor suppressor gene on chromosome 10 and has been identified as a disease gene in three autosomal dominant disorders (Cowden disease, Lhermitte-Duclos disease and Bannayan-Zonana syndrome). PTEN inactivation is also found in malignant melanoma, brain tumors, and endometrial, ovarian, thyroid, breast and prostate cancers. PTEN protein induces apoptosis and carcinogenesis occurs in cells with PTEN mutation due to avoidance of apoptosis. PTEN mutations have been detected in 20–33% of cases of atypical endometrial hyperplasia and 33–50% of cases of endometrial cancer;[22-24] thus, PTEN appears to be involved in the early stage of carcinogenesis, which is a pattern that differs from that in late-onset cancer, including rectal cancer.

, 1998). Dimerization via the HisKA

domain of EnvZ is essential for its autophosphorylation and phosphotransfer functions. The HisKA domain comprises a four-helix bundle formed by two identical helix–turn–helix subunits, revealing the molecular assembly of two active sites within the dimeric kinase (Tomomori et al., 1999). KdpD functions as a homodimer (Heermann et al., 1998). Coproduction of two kinase inactive KdpD derivatives KdpD/His673Gln and KdpD/Asn788Asp resulted in a KdpD protein that regained kinase activity in vitro. This result suggested that the functional state of KdpD is at least a dimer and that Protease Inhibitor Library the kinase reaction occurs in trans, meaning that one subunit binds ATP in the HATPase_c domain and phosphorylates the other subunit in the HisKA domain. A similar mechanism of autophosphorylation has been observed for other histidine kinases (Yang & Inouye, 1991; Ninfa et al., 1993; Swanson et al., 1993; Wolfe & Stewart, 1993). To solve the question whether KdpD undergoes a monomer-to-dimer transition upon activation, the relative molecular masses of nonphosphorylated KdpD and phosphorylated KdpD were MG-132 supplier determined using several techniques. The molecular mass of native KdpD correlated with a KdpD dimer, and there was no difference between KdpD and phospho-KdpD. Cross-linking experiments with single Cys KdpD derivatives provided evidence for a close contact between

the monomers in the transmitter domain as well as in TM1, but the Cys residues did not play a role in the stabilization of the dimer (Heermann et al., 1998). Nevertheless, an intramolecular disulfide bridge formed between Cys852 and Cys874 was found to be next important for kinase activity (Jung et al., 1998). Each histidine kinase contains a highly specific stimulus-percepting

domain, the so-called input domain. The input domain of KdpD comprises a large cytoplasmic N-terminal domain, four transmembrane domains (TM1–TM4), and a short part of the C-terminal cytoplasmic domain (Fig. 1). In the C-terminal part of the input domain, adjacent to TM4, a cluster of positively charged amino acids (Arg residues) was identified that is important for the ratio between kinase and phosphatase activities (Jung & Altendorf, 1998a). Replacement of these Arg residues by Gln resulted in KdpD derivatives with either an increased kinase and decreased phosphatase activity (Arg511Gln) or a decreased kinase and increased phosphatase activity (Arg503Gln, Arg506Gln, Arg508Gln). Because the removal of one positively charged amino acid residue was sufficient to perturb the ratio of the KdpD activities, it was proposed that electrostatic interactions within the protein affect the kinase to phosphatase equilibrium (Jung & Altendorf, 1998a). Earlier, the transmembrane domains of KdpD were thought to be essential for sensing.

, 2001). For

each transformant that disrupted a gene in the find more current library that had not been disrupted in the previous library, the genomic position of the transposon was confirmed by performing two sets of PCR amplifications, analyzed on agarose gels stained with ethidium bromide, as described (French et al., 2008). The first set used a transposon-specific primer paired with a gene-specific primer. The presence of a PCR product of the predicted size indicated that the transposon was at the expected location, provided that the same PCR product was absent when using the parental wild-type strain as template. For the second PCR amplification, two gene-specific primers were used that would flank the site of the transposon. If the expected product was obtained with wild-type DNA as template but no product was obtained with the transformant DNA as template, it was concluded that the gene was disrupted

and that the transformant lacked a second, intact copy of the gene. For some transformants, the PCR amplifications confirmed the location of the transposon but also detected the presence of an intact copy of the gene. In these cases, the transformant culture was subcloned and the two PCR reactions were performed again on each subclone. Before subcloning, cell aggregates were Proteasome inhibitor disrupted by sonicating in a sonifier (model Clomifene 250/450; Branson, Danbury, CT) at a power level of 5 and a duty cycle of 10% for 20 s. These conditions maximally increased the CFU of the cultures.

No gene was considered to be disrupted unless the PCR data indicated that at least one subclone had the transposon at the expected site with no intact copy of the gene. Rarely, the PCR data indicated that all subclones of a transformant had an intact copy of the gene that was disrupted by the transposon. The presence of both a disrupted and an intact copy of the gene suggested gene duplication. In these cases, the identity of the PCR products was confirmed by performing another PCR amplification. The products from the first amplification that had used primers that flanked the insertion site of the transposon were used as template, and an internal set of primers was used for amplification. In cases where there was doubt regarding the results, the PCR products were also sequenced. A total of 1210 different minitransposon insertion sites were mapped. Thus, the library is smaller than the original Tn4001T library for which 1856 different insertion sites were mapped (French et al., 2008). Combined, the libraries provide excellent coverage, with, on average, a transposon insertion site every 300 bp in the 960-kb genome of M. pulmonis.

“
“Lacticin 3147 is a two-peptide broad spectrum lantibiotic produced by Lactococcus lactis DPC3147 shown to inhibit a number of clinically relevant Gram-positive pathogens. Initially isolated from an Irish kefir grain, lacticin 3147 is one of the most extensively studied lantibiotics to date. In this study, the bacterial diversity of the Irish kefir

grain from which L. lactis DPC3147 was originally isolated was for the first time investigated using a high-throughput parallel sequencing strategy. A total of 17 416 unique V4 variable regions Selleckchem GPCR Compound Library of the 16S rRNA gene were analysed from both the kefir starter grain and its derivative kefir-fermented milk. Firmicutes (which includes the lactic acid bacteria) was the dominant phylum accounting for >92% of sequences. Within the Firmicutes, dramatic differences in abundance were observed when the starter grain and kefir milk fermentate were compared. The kefir grain-associated bacterial community was

largely composed of the Lactobacillaceae family while Streptococcaceae (primarily Lactococcus spp.) was the dominant family within the kefir milk fermentate. Sequencing data confirmed previous findings that the microbiota of kefir milk and the starter grain are quite different while at the same time, establishing that the microbial diversity of the starter grain is not uniform with a greater level of diversity associated with the interior kefir starter grain compared with the exterior. Kefir is a slightly

carbonated fermented beverage manufactured through the fermentation of milk with kefir starter grains. These grains are unique dairy starters that contain a symbiotic AT9283 purchase consortium of microorganisms strongly influenced by grain origin and culture conditions (Garrote et al., 2010). Although the total number of microorganisms and their relative composition in grains is variable and ill-defined, kefir grains have been shown to contain lactic acid bacteria (LAB; primarily lactobacilli and lactococci), yeasts, and occasionally acetic acid bacteria, within a protein–lipid–polysaccharide solid matrix (Lopitz-Otsoa et al., 2006). The starter grains are vital components for the kefir fermentation as the finished product does not possess the same number or complexity of microorganisms and therefore cannot be used to reinitiate further MTMR9 kefir fermentations (Simova et al., 2002; Farnworth, 2005). Following the fermentation process the kefir grains can be recovered, reused, and grown, often over periods of several decades. In addition to the value of the kefir-associated microbial community as a whole, specific strains isolated from kefir may have value as probiotics (Golowczyc et al., 2008) or as producers of antimicrobial compounds (Ryan et al., 1996; Rodrigues et al., 2005). However, the symbiotic nature of the kefir microbiota can make the identification of such strains and their subsequent investigation more complicated.

The relative contributions of variables that were highly correlated [i.e. gender and height; body mass index (BMI) and height] were evaluated in nested models. To examine the incremental Galunisertib mw effect of OXPHOS CI and CIV enzyme activity as well as that of mt 8-oxo-dG levels, each was then introduced individually into the previously constructed model. Model selection was based on adjusted R-square and Akaike’s information criterion (AIC). Of the 152 subjects enrolled in SEARCH 003, skin punch biopsies were obtained from 132 subjects who agreed to participate in the neuropathy substudy. All

of these 132 ENFD specimens were judged by the Johns Hopkins Cutaneous Nerve Laboratory as evaluable, and are the focus of this report. All subjects were Thai, with 56.1% recruited from the Thai Red Cross AIDS Research Centre and 43.9% from Queen Savang Vadhana Hospital (Table 1). The gender distribution of 44.7% male is consistent with the gender distribution of the HIV/AIDS epidemic in Thailand. Only a small percentage

of subjects had other common aetiologies for neuropathy (history of isoniazid use, concomitant infection with hepatitis MG-132 solubility dmso C or the presence of diabetes). The median (interquartile range) ENFD (fibres/mm) values prior to initiation of ARV therapy were 21.0 (16.2–26.6) for the distal leg and 31.7 (26.2–40.0) for the proximal thigh. Distal leg ENFD correlated positively with CD4 cell count, and negatively with age, height, log10 plasma HIV RNA, and OXPHOS CI and CIV activity levels (Table 2). The relationships between distal leg ENFD and height, CD4 cell count and OXPHOS CIV are shown graphically in Figure 2. No significant correlations were found with BMI, homeostatic model assessment for insulin resistance (HOMA-IR), fasting glucose, PBMC mtDNA or mt-specific 8-oxo-dG. Women had significantly higher distal

leg natural log (ln) ENFD than men (mean ENFD: women, 24.2 fibres/mm; men, 19.5 fibres/mm; P < 0.01). Proximal thigh ENFD correlated positively with distal leg ENFD. Similar to distal leg ENFD, proximal thigh ENFD correlated positively with CD4 cell count and negatively with height, with no correlations with HOMA-IR, fasting glucose, PBMC mtDNA or mt-specific 8-oxo-dG. Proximal thigh ENFD, however, differed from distal leg ENFD in Demeclocycline showing significant negative correlations with BMI and no correlations with PBMC OXPHOS CI or CIV activity levels. Women had slightly higher proximal thigh ln ENFD than men (mean ENFD: women, 36.0 fibres/mm; men, 31.6 fibres/mm; P = 0.03). Neither distal leg nor proximal thigh ENFD correlated with history of previous ARV medication use during pregnancy or with history of neurotoxic medical comorbidity/medication use (data not shown). The results of the multiple linear regression analyses are shown in Table 3. Simple linear regression analysis showed age, height, CD4 cell count and HIV RNA to each be significantly associated with distal leg ENFD (all P-values < 0.01).

As the isolated DENV-3 strain possesses high sequence similarity to DENV-3 strains in neighboring regions, the data suggests local transmission of the virus in the African continent. However, further epidemiological studies would be needed to identify DENV outbreaks and ascertain the virus strains causing local outbreaks. Although close monitoring of febrile travelers provides data on DENV outbreaks in endemic regions, improved disease

surveillance and a higher priority in dengue laboratory diagnosis in Africa is vital to reflect the true incidence of the disease. Identification of genotypes and strains along with disease prevalence in endemic areas is of importance because some DENV strains have been associated with increased disease severity and may possess higher epidemic potential.[3, 4] Currently, there are no effective drugs or vaccines against DENV infection. Transmission selleck screening library of DENV within Africa presents challenges for diagnosis and effective disease management of febrile travelers returning from the continent. Additionally, there is a need for higher awareness toward the increasing risk of DENV infection

in travelers among health care personnel in both endemic and non-endemic regions. Thus, rapid and accurate diagnosis of DENV is particularly important for travelers returning from West Africa in which other viral hemorrhagic fevers, including yellow fever and Lassa fever are endemic. This work was supported by funding from Research on Emerging and Re-emerging Infectious Diseases by the Ministry of Health, Labor, and Welfare, Japan (H21-shinkou-ippan-005, Selinexor cell line H23-shinkou-ippan-006, and H23-shinkou-ippan-010). The authors state that they have no

conflicts of interest. “
“There has been a great increase of Plasmodium vivax incidences in the Republic of Korea and the genetic diversity of the parasite became more complex with the rapid dissemination of newly introduced genotypes. Surveillance of imported malaria is very important, but there is no good way to determine imported vs. internal cases. In this study, we characterized imported vivax cases, analyzed the genetic sequence of three imported vivax malaria cases for the merozoite surface protein-1 FER (MSP-1) and circumsporozoite protein (CSP) genes, and clearly discriminated an imported vivax case that was misdiagnosed as indigenous by genetic analysis. PCR reaction for the merozoite surface protein-1 (MSP-1) and circumsporozoite protein (CSP) genes from three imported vivax cases were amplified and sequenced. The genetic variations were compared with a previously constructed database of South Korean isolates. The imported vivax cases showed various patterns on incubation period before onset. Most cases were from other parts of Asia. The MSP-1 gene sequence analysis of three imported cases showed that the imported cases had completely different sequences from any subtypes from Korean isolates.

S9). It is further confirmed by the coverage estimators of Chao1, which showed a high value of the hzsB clone library than that of the 16S rRNA gene (16.9 vs. 5). The Shannon (2.2 vs. 1.35) and Simpson (0.14 vs. 0.27) indices also implied a higher buy AZD6244 diversity of

anammox bacteria by amplifying the hzsB gene. Compared with primers targeting the hzsA subunits, similarly high specificities were observed that no false positives were detected in 92 (hzsB) and 46 (hzsA) clones. The primer pair of hzsB_396F and hzsB_742R was applied for the quantification of anammox bacterial abundance in the soil core. The copy number measured in the surface sample (0–10 cm) was 7.0 ± 0.3 × 105 copies g−1 dry soil and decreased slightly to 2.0 ± 0.9 × 105 copies g−1 dry soil at 20–30 cm depth as shown in Fig. 2a. Below this depth, hzsB gene copy numbers increased and peaked at 40–50 cm depth of 2.7 ± 1.3 × 106 copies g−1 dry soil,

which accounts for about 2.3% of total bacterial cells (Fig. 2c) assuming that the anammox bacteria contained one copy of the hzsCBA gene cluster (Strous et al., 2006; Kartal et al., 2011) and 3.8 copies of the 16S rRNA gene for all bacteria (Fogel et al., 1999). For the samples below 60 cm, the copy numbers decreased below the detection limit of the qPCR assay. The variety in anammox bacterial abundance in the soil core was more or less similar to the result based on 16S rRNA gene from the same site (Zhu et al., 2011b). Little significant correlation was observed between the abundance of anammox bacteria and see more environmental factors (Table 2). Similar to the anammox in stratified water columns and sediments where active anammox was restricted to specific layers (Dalsgaard et al., 2003, 2005), anammox bacteria seemed to prefer

selective niches at particular depths in soil (Humbert et al., 2010). Owing to the high interfering background in soil samples, only the primers targeting the 16S rRNA gene were capable for the in situ quantification of soil sample until now (Hamersley et al., 2007; Hu Lepirudin et al., 2011; Zhu et al., 2011b). As the specificity and sensitivity of 16S rRNA gene detection are highly dependent on the abundance of anammox bacteria in environmental samples (Song & Tobias, 2011), the hzsB gene would be a more precise biomarker for the quantification of anammox in soil. To analyze the community structure of n-damo bacteria on a functional level, primers targeting the pmoA gene were used in samples from representative depths (0–10, 20–30, 40–50, and 60–70 cm). The n-damo-specific pmoA primer A189_b was combined with the widely applied cmo682 primer (Holmes et al., 1995; Luesken et al., 2011c). Following by a nested PCR approach (cmo182-cmo568) (Luesken et al., 2011c), sequences clustering with the pmoA sequence present in the genome of M.

When these genes were deleted, the number of transconjugants decreased in the same fashion as when the cells were treated with kanamycin and streptomycin. These results indicate that the process of E. coli conjugation may be promoted by combination treatment with kanamycin and streptomycin and that two proteins potentially participated in this process. “
“CheY, the response regulator of the chemotaxis system in Escherichia coli, can be regulated by two covalent modifications

– phosphorylation and acetylation. Both covalent modifications are involved in chemotaxis, but the mechanism and role of the acetylation are still obscure. While acetylation was shown to repress the binding of CheY to its target proteins, check details the effect of acetylation on the ability of CheY to undergo autophosphorylate with AcP is not fully investigated. To obtain more information on the function of this acetylation, we successfully expressed and purified CheY protein with a 6 × His-tag on the C-terminus. Subsequently, acetylated CheY (AcCheY) was obtained with AcCoA as the acetyl donor, and the acetylation level of AcCheY was confirmed by Western blotting and then mass spectrometry. Using tryptophan fluorescence intensity measurements as

a monitor Selleck YAP-TEAD Inhibitor 1 of phosphorylation, we showed that acetylation reduces the ability of CheY to undergo autophosphorylation. “
“The surface adhesin P97 mediates the adherence of Mycoplasma hyopneumoniae to swine cilia. Two reiterated repeats R1 and R2 are located at the C-terminus of P97. The purpose of this study was to evaluate the immunogenicity of Montanide adjuvant IMS 1113 plus soluble subunit proteins rR1, rR1R2 and their chimeric forms coupled with B subunit of the heat-labile enterotoxin of Escherichia coli (LTB). Each recombinant protein in this study was capable of eliciting anti-R1 specific humoral antibodies (IgG), mucosal antibodies (IgG and IgA) and IFN-γ production. The chimeric protein rLTBR1R2 elicited the quickest humoral antibody response

among the recombinant proteins. Serum and bronchoalveolar lavage analysis revealed that each recombinant protein was capable of inducing both Th1 and Th2 responses. Importantly, all of the proteins induced an anti-R1-specific Th2-biased response in both humoral and mucosal compartments, similar to the response observed in a natural infection Non-specific serine/threonine protein kinase or vaccination process. These observations indicate that rR1, rR1R2, rLTBR1 and rLTBR1R2 with IMS 1113 might represent a promising subunit vaccine strategy against porcine enzootic pneumonia in pigs. “
“Pseudomonas aeruginosa has emerged as a major pathogen in nosocomial infections. Biofilm formation allows the microorganism to persist in hospital water systems for extended periods, which have been associated with nosocomial infections. The aim of this study was to evaluate the frequency of P. aeruginosa colonization of hospital tap waters by nested PCR assay.

The backward inner primer (BIP) consists of the B1c sequence (complementary to B1), TTTT and B2 sequence. LAMP was performed in a total 25-μL reaction

mixture containing 1.6 μM of each inner primer (FIP and BIP), 0.2 μM of each outer primer (F3 and B3), 1.4 μM dNTPs and 1 M betaine (Sigma). Each LAMP reaction also included 20 mM Tris-HCl (pH 8.8), 10 mM KCl, 10 mM (NH4)2SO4, 6 mM MgSO4, 0.1% Tween 20, 1.0 μL (8 U) Bst DNA polymerase large fragment (New England BioLabs) and 1 μL of template DNA. The mixture was incubated at 61 °C for 60 min in a water bath and then heated at 80 °C for an additional 10 min to terminate the reaction. The LAMP products GDC-0068 clinical trial were subjected to 2% agarose gel electrophoresis, stained with ethidium bromide and visualized under UV light. On the basis of the restriction maps of the target sequences of LAMP product, AluI was selected for use for restriction analysis. Following overnight digestion

at 37 °C, the digested products (2 μL) were analyzed by electrophoresis in 3% agarose gels stained with ethidium bromide. The LAMP products were also detected by adding 1.0 μL of original SYBR Green I diluted 1000-fold to the tube. The color of the solution was then observed. www.selleckchem.com/products/PD-0332991.html The PCR of Angen et al. (2007) was used as the first round of nested PCR. Briefly, 2 μL of template DNA was added to a 48-μL PCR mixture, containing 5 μL of 10 × PCR buffer, 0.15 mM of dNTPs, 65 ng each of the oligonucleotide primers HP1F3 and HP2F2, 130 ng of primer HP-Revx and 1.0 U Tag polymerase (Fermentas Inc.). In the second round of nested PCR, 2 μL of undiluted first-round PCR

product was added to a 48-μL PCR mixture, similar to the first-round PCR, but containing 130 ng of F3 and B3 primers. Both rounds were run under the following conditions: 35 cycles of denaturation at 94 °C for 1 min, annealing at 56 °C for 45 s, extension at 72 °C for 1 min and a final extension at 72 °C for 7 min. PCR reactions were performed using the GeneAmp PCR System 9700 (Applied Biosystems). The sensitivity of the LAMP and nested PCR tests was compared using a pure culture of H. parasuis serovar 5 Nagasaki strain, pericardial fluid (PF) spiked with the same strain and lung tissue homogenate spiked with the same strain, respectively. A suspension of the pure culture of H. parasuis serovar 5 Nagasaki strain was adjusted to 8 × 109 CFU mL−1 as measured Pregnenolone by triplicate plate counts. The suspension was then diluted in a 10-fold series in PBS to give dilutions containing 8 × 100–8 × 108 CFU mL−1 and 0.3 mL of each dilution was added to 2.7 mL sterile water, PF or lung tissue homogenate, respectively. Then the cells were heat treated in a boiling water bath for 10 min and centrifuged at 13 400 g for 10 min. As the template for the LAMP and nested PCR, 1 and 2 μL of the resulting supernatant containing extracted DNA was used, respectively. Sensitivity was also tested for H. parasuis serovar 5 Nagasaki strain.

The estimated half-life of σS changed from 0.7 min in pgsA+ (JU01) cells to 8.5 min in pgsA3 (JU02) cells (Fig. 3). This result indicates that degradation of σS in the mutant cells is indeed retarded, and this is likely due to the presumably reduced content of ClpXP protease, although the involvement of other factor(s) in the degradation cannot be completely ruled out. In order to further assess the contribution of clpPX repression to the extended half-life U0126 of σS in pgsA3 cells, we examined the effect of the introduction

of a clpPX plasmid (pHR718-clpPX). The highly increased content (7.9-fold over wild type) of σS in the pgsA3 cells (strain ST002) decreased to almost the level found in ST001 (pgsA+) cells after the introduction of the clpPX plasmid (Fig. 2c). This result reconfirms the conclusion that the pgsA3 mutation represses the expression of clpPX (as shown in Fig. 2a and b) Belnacasan concentration and may also indicate that other factors participating in the regulation of the activity of ClpXP protease

(Hengge-Aronis, 2002) are not involved in, or contribute less to, the long half-life of σS. These other conceivably involved factors include Rsd, which is believed to affect σS association with core RNA polymerase by a putative action as anti-σD (Jishage & Ishihama, 1999), and Crl, which is assumed to act by modulating the association with the RNA polymerase core (Pratt & Silhavy, 1998); however, neither rsd nor crl expression is reduced in the pgsA mutant cells as evidenced by microarray analysis (Nagahama et al., 2007). The activity of σS in the mutant cells is therefore not

affected by these regulatory factors. The repression of clpPX may PRKACG thus very well be the main defect in the ClpXP degradation pathway of σS in cells with acidic phospholipid deficiency. We have arrived at the conclusion that the slower degradation of σS in the mutant cells contributes considerably to the accumulation of σS and that this is caused by the repression of clpPX. However, how does the acidic phospholipid deficiency trigger the repression of clpPX in pgsA3 mutant cells? It is known that the expression of the clpPX operon involves promoters under the control of σE, σH, and σD (Li et al., 2000; Phodius et al., 2006; Regulon DB ver. 6.4, http://regulondb.ccg.unam.mx/index.jsp). The expression of rpoE, which codes for σE, is negatively regulated by the Cpx two-component signal transduction system (De Wulf et al., 2002). The expression of rpoH, which codes for σH, is controlled by σE in addition to σD. The Cpx system is activated in mutant cells lacking the zwitterionic phospholipid phosphatidylethanolamine, the third major phospholipid in E. coli membranes (Mileykovskaya & Dowhan, 1997). We observed a significant activation (8.