graminearum homolog of A nidulansApsB The functions of FgApsB w

graminearum homolog of A. nidulansApsB. The functions of FgApsB were evaluated by constructing a deletion mutant of FgApsB, designated ΔFgApsB-28. Conidiation and mycelial growth rate are reduced in ΔFgApsB-28. The hyphae of ΔFgApsB-28 are thinner than those of the wild type and have a

different branching angle. ΔFgApsB-28 exhibited reduced aerial hyphae formation, but increased production of rubrofusarin. Whereas nuclei are evenly distributed in germ tubes and hyphae of the wild type, they are clustered and irregularly distributed in ΔFgApsB-28. The mutant exhibited increased resistance to cell wall-damaging agents, but reduced virulence on flowering wheat heads, which MK-2206 solubility dmso is consistent with its reduced production of the toxin deoxynivalenol. All of the defects in ΔFgApsB-28 were restored by genetic complementation with the parental FgApsB gene. Taken together, the results indicate

that FgApsB is important for vegetative differentiation, asexual development, nuclear migration, and virulence in F. graminearum. “
“The formation of nonspecific ion channels by small oligomeric amyloid intermediates is toxic to the host’s cellular membranes. Thermostable direct hemolysin (TDH) and TDH-related hemolysin (TRH) are major virulence factors of Vibrio parahaemolyticus. We have previously reported the MAPK inhibitor crystal structure of TDH tetramer with the central channel. We have also identified the molecular mechanism underlying the paradoxical responses to heat treatment of TDH, known as the Arrhenius PRKD3 effect, which is the reversible amyloidogenic property. In the present report, we describe the biophysical properties of TRH, which displays 67% amino acid similarity with TDH. Molecular modeling provided a good fit of the overall structure of TDH and TRH. Size-exclusion chromatography, ultracentrifugation, and transmission electron microscopy revealed that TRH formed tetramer in solution. These toxins showed similar hemolytic activity on red blood cells. However, TRH had less amyloid-like structure than TDH analyzed by thioflavin T-binding assay

and far-UV circular dichroism spectra. These data indicated that amyloidogenicity upon heating is not essential for the membrane disruption of erythrocytes, but the maintenance of tetrameric structure is indispensable for the hemolytic activity of the TDH and TRH. Vibrio parahaemolyticus is a gram-negative marine bacterium recognized as a major cause of seafood-borne gastroenteritis around the world. Wound infections, septicemia, and other infections are also caused occasionally by V. parahaemolyticus outbreaks (Blake et al., 1980; Daniels et al., 2000). Thermostable direct hemolysin (TDH) and its homolog TRH are the major virulence factors of this microorganism (Honda et al., 1980, 1988; Joseph et al., 1982; Shirai et al., 1990).

, 2007a, b) and compared to a larger

, 2007a, b) and compared to a larger Autophagy inhibitor published database of P. aeruginosa isolates from nonocular sources (Stewart et al., 2011). Various markers in the set of P. aeruginosa isolates associated with keratitis were discordant with the wider P. aeruginosa population. These included previously reported associations, such as carriage of exoU. It was also demonstrated that 17 of 63 (27%) keratitis isolates from 2003 to 2004 carried a distinctive allele of pilA, the gene that encodes the pilin of type IV pili. Thus, the keratitis isolates were associated

with specific characteristics, suggesting that a subpopulation of P. aeruginosa may be adapted to causing corneal infections (Stewart et al., 2011). However, we could not be sure whether these genetic features of keratitis-associated isolates would be consistent temporally or represented a feature of the particular time Ibrutinib period chosen

for sampling. To address this question, in this study, we report the analysis of a set of keratitis-associated P. aeruginosa isolates, collected by the MOG from patients in the UK, during a different time period, 5 years later. Sixty isolates (listed in Table 1) from corneal scrape samples were collected from patients with bacterial keratitis (2009–2010) from the six hospitals comprising the MOG. DNA was purified using the Wizard Genomic DNA purification kit (Promega, UK), as per the manufacturer’s instructions. A further 18 isolates of P. aeruginosa from bloodstream infections (collected and stored in Liverpool 2010–2011) Vasopressin Receptor were also used. All isolates tested positive for the oprL gene using a P. aeruginosa-specific PCR assay (De Vos et al., 1997). Genotyping of P. aeruginosa was conducted using the AT genotyping system (Wiehlmann et al., 2007a, b; Alere Technologies, Jena, Germany), as per the manufacturer’s instructions. Analysis of 13 single nucleotide polymorphisms (SNPs) based on the conserved genome, and three variable markers (flagellin types a or b and the mutually exclusive type III secretion exotoxin genes exoU or exoS),

was used to generate a four character hexadecimal code as described previously (Wiehlmann et al., 2007a, b; Stewart et al., 2011). This hexadecimal code was used to assign specific clone types. The genotypic relationships between keratitis isolates of P. aeruginosa and nonocular isolates were assessed by analysing each strain for 14 binary markers as described previously (Stewart et al., 2011). Presence or absence of exoS or exoU was not included in this analysis. The wider population was represented by a database of 322 nonkeratitis P. aeruginosa isolates, representing 128 clones, taken from various sources (Wiehlmann et al.,2007a, b; Mainz et al., 2009; Rakhimova et al., 2009). The analysis was undertaken using the eBURST(v3) algorithm (Feil et al., 2004; Spratt et al., 2004).


a result the changes observed here are not associated


a result the changes observed here are not associated with the early stages of goal–reward associations, but rather the changes that occur following repeated drug use. Following cocaine self-administration, we observe functional reductions in activity in brain regions involved with drug-induced reward learning mechanisms. Specifically, the reductions in the prefrontal cortex and nucleus accumbens activity suggest that there may be suppression SB203580 manufacturer of cortico-striatal loops. Goal-directed learning is reliant on the dorsomedial striatum through loops that project from the cortex to the striatum (Alexander et al., 1986; Lawrence et al., 1998; McFarland & Haber, 2002; Haber & Calzavara, 2009). Here we show reductions in functional activity in these areas, implying that this type of learning may also be impaired. These data suggest that (1) individuals may be less able to learn new goal-directed behaviors, and (2) they also may be less able to

GDC-0068 molecular weight replace already formed associations. Replacing associations that occurred during the development of drug addiction is a process that is essential for continued abstinence and the prevention of relapse in abstinent individuals. In addition, the motivational loop, comprising the ventral striatum, orbitofrontal and anterior cingulate cortex, hippocampus, and amygdala (Lawrence et al., 1998), seemed to be particularly affected. These Protein kinase N1 reductions in regional functional activity may also potentially lead to drug-taking in order to restore these brain areas to the functional state that was present before the drug-taking was initiated (Koob & Le Moal, 1997). In addition to reductions in areas involved in reward learning and motivational behaviors, there were also reductions in regions involved in learning and memory. Reductions in functional activity were observed in the hippocampus, medial thalamus and basolateral amygdala. Reduced activity in these regions has important implications for normal functioning and the learning capacity

at baseline after the cessation of drug consumption. Even more important for cocaine users is the role that learning plays in cue–reinforcement pairings during drug misuse. It is well established that cue conditioning plays a role in the effects of drugs and on relapse, where cues alone are sufficient to reinstate drug taking/seeking after periods of prolonged abstinence (Shaham et al., 2003; Lu et al., 2004; Schmidt & Pierce, 2010). The basolateral amygdala has also been shown to be a major modulator of the extinction of conditioned place preference, further suggesting that the reductions in functional activity, and perhaps learning, may lead to a decreased ability to replace associations between drugs and cues (Schroeder & Packard, 2003, 2004).

From the 12-month time-point, 36 of 2052 patients died (5566 pers

From the 12-month time-point, 36 of 2052 patients died (5566 person-years). Overall, 52.0% of deaths after 8 months (26 of 50) and 50.0% of deaths after 12 months (18 of 36) were

in discordant responders. In an unadjusted analysis, the risk of an AIDS event after either 8 or 12 months was not significantly different for discordant and concordant responders. CT99021 chemical structure However, the risk of death was higher for discordant responders at both 8 months (IRR 2.27, 95% CI 1.30–3.95, P=0.004) and 12 months (IRR 3.19, 95% CI 1.66–6.14, P<0.001). After adjusting for age, baseline viral load and CD4 cell count, and having an AIDS event prior to the follow-up at 8 and 12 months, the risk of death was still higher for discordant responders at 8 months (IRR 2.08, 95% CI 1.19–3.64, P=0.01) and 12 months (IRR 3.35, 95% CI 1.73–6.47, P<0.001) (Table 6). At 8 months, the

risk of death was also slightly higher in those who were older (IRR 1.03 per additional year, 95% CI 1.00–1.06, P=0.048); however, baseline viral load, CD4 cell count and having had an AIDS event prior to the point of determining discordancy were not significantly associated with death. At 12 months, older age was again associated with an increased risk of death (IRR 1.03, 95% CI 1.00–1.07, P=0.050), with a higher baseline CD4 count being associated with a reduced risk (IRR 0.63 per 100 cells/μL increase, 95% CI 0.44–0.90, P=0.012). The risk of an AIDS event in the adjusted analysis was only significantly Wnt inhibitor associated with baseline viral load when discordancy was categorized at 8 months (IRR 1.82, 95% CI 1.14–2.88, P=0.011). Despite the efficacy of HAART in suppressing HIV viral replication, a rather large proportion however of individuals experienced a limited increase in CD4 cell count, or no increase, by around 8 or 12 months. Such responses, assessed at 12 months and, to a lesser extent, at 8 months, were associated with poorer outcome. In many patients (35% of those evaluable)

the discordant response was transient, on the definition used here, with a >100 cells/μL increase by 12 months, even though this was not achieved earlier. Changing treatment was not associated with a change in status between 8 and 12 months. This suggests that the later improvement in CD4 cell count seen in some patients categorized early as having a suboptimal CD4 response was a consequence of a continued, albeit slow, recovery of immune function on HAART, rather than a result of a change of regimen to one with greater potency with respect to restoration of immune function. The incidence of a discordant response in this study was 32% at 8 months and 24% at 12 months. These rates need to be seen in the particular context of the inclusion criteria for the study, which were intended to select a homogeneous group of patients with respect to an early virological response, and to ensure the availability of follow-up data.

This alkane-induced protein would thus be a prime candidate poten

This alkane-induced protein would thus be a prime candidate potentially mediating alkane transport. Using a transcriptomics approach, a number of additional alkane-induced regulatory systems have been detected (Table 1), as compared with our previous proteomics study (Sabirova et al., 2006). A transcriptional regulator of the GntR family, Wee1 inhibitor encoded by ABO_0121, is located next to the ABO_0122 encoding the alkB2 monooxygenase, suggesting that the ABO_0121-encoded gene product might regulate the expression of the adjacent monooxygenase. Another regulatory system consisting of ABO_1708 and

ABO_1709, adjacent to each other and likely to be operon-arranged, encodes a pair of sensor histidine kinase and DNA-binding response regulator that are also upregulated on alkanes. Their close proximity to the gene of fatty acid degradation (fadH dienoyl-CoA reductase) may indicate that this regulatory system controls the oxidation of fatty acids in Alcanivorax. Our transcriptome data also hint towards quorum sensing playing a role in biofilm formation of Alcanivorax on alkanes, as the major transcriptional

regulator QseB encoded by ABO_0031 was found to be upregulated on hexadecane (Table 1). Quorum sensing has indeed been reported to trigger biofilm formation via the biosynthesis of extracellular exopolysaccharides (EPS) (Sauer et al., 2002), also visible on our EM pictures. We did not detect increased expression

of the cognate histidine kinase, QseC, encoded by ABO_0030. This finding indicates that for initial signal reception and transduction constant levels of sensor Selleck Staurosporine protein suffice, while the subsequent coordinated regulation of the expanded quorum-sensing regulon qse does require increased titers of Qse regulator protein. Finally, an HD-GYP domain protein encoded by ABO_2132 and mentioned earlier in ‘Alkane-induced biofilm formation and adhesion to hydrocarbons’ is also upregulated on alkanes and hence represents eltoprazine another worthy target for regulatory studies of growth on alkanes. To conclude, our transcriptomics analysis of A. borkumensis responses to alkane exposure adds a complementary view on alkane metabolism by this bacterium, in addition to our previous proteomics study, and reveals a number of novel observations, for instance concerning the molecular mechanisms of alkane transport across the cytoplasmic membrane, and pointing to a diverse set of enzymes for the degradation of alkanes. Alcanivorax SK2 seems to respond to growth on alkanes by forming cell aggregates, probably supported by enhanced synthesis of EPS and probably following in a quorum-sensing-mediated aggregation process. Finally, the study has also revealed many transcriptional regulators to be differentially expressed, indicating a complex regulatory interplay of alkane degradation with other metabolic functions in this marine organism.

The mothers of untested children ≤18 years old were more likely t

The mothers of untested children ≤18 years old were more likely to be recently diagnosed with HIV infection compared with the overall clinic cohort of women with children. The reason for this is not clear. It may be that this group of women had less time to engage with health services to have their children tested, or had younger children with more recent and asymptomatic vertical infection. The most common

reason given for not testing was a perceived ‘unlikely risk’. This is similar to the experience of other UK centres [7,8]. Two hundred RG7420 concentration and forty-six untested children resident in the UK were identified through this study, all potentially at risk of vertically transmitted HIV infection, of whom only 49 were ≤18 years old. The mothers have been made aware that vertically acquired HIV infection can present late and can be potentially life threatening. A multidisciplinary team involving adult and paediatric HIV healthcare professionals has been set up to negotiate

and facilitate testing of the untested children ≤18 years old resident in the UK, within a timescale agreed with the parents. The safety of the children remains the priority and a clear threshold Dasatinib has been set for referral to child-safeguarding services. Further qualitative studies are planned to explore the reasons behind mothers’ decision-making around child HIV testing, comparing those with tested and untested children. “
“In high-income countries, late presentation to care can impair reductions in morbidity and mortality risks, increase the risk of HIV transmission at the population level, and prevent Mannose-binding protein-associated serine protease patients from experiencing the full benefits of advances in HIV treatment. Most relevant studies do not distinguish between late HIV diagnosis and delayed entry into care. Factors associated with the latter should be characterized to improve HIV care interventions at individual and public health levels. Estimates of the time from ‘diagnosis to

care’ in the payable HIV care context vary considerably. Bamford et al. [1] reported a median time of 8 months in Philadelphia (2005–2006). Hospital in-patient/public clinic diagnosis, age >40 years and injecting drug use (IDU) were associated with delayed access [1]. Torian et al. reported that the first HIV care visits occurred >3 months after diagnosis for 19.1% of patients diagnosed in 2003 in New York City, while 17.2% of patients never initiated care. Factors associated with delayed access were diagnosis at centres without in situ care facilities, non-White race/ethnicity, IDU and non-USA birth [2]. Hamers and Phillips [3] estimated that 30% of HIV-infected individuals in Europe are undiagnosed. In France, HIV testing is routinely performed during pregnancy, following voluntary patient request, and for prisoners and patients with sexually transmitted infections or tuberculosis.


“Motor buy ABT-199 stereotypy is a key symptom of various neurological or neuropsychiatric disorders. Neuroleptics or the promising treatment using deep brain stimulation stops stereotypies but the mechanisms underlying their actions are unclear. In rat, motor stereotypies are linked to an imbalance between prefrontal and sensorimotor cortico-basal ganglia circuits. Indeed, cortico-nigral transmission was reduced in the prefrontal but not sensorimotor basal ganglia circuits and dopamine and acetylcholine release was altered in the prefrontal but not sensorimotor territory of the dorsal striatum. Furthermore, cholinergic transmission in the prefrontal territory of the dorsal striatum plays a crucial

role in the arrest of motor stereotypy. Selleck Selumetinib Here we found that, as previously observed for raclopride, high-frequency stimulation of the subthalamic nucleus (HFS STN) rapidly stopped cocaine-induced motor stereotypies in rat. Importantly, raclopride and HFS STN exerted a strong effect on cocaine-induced alterations

in prefrontal basal ganglia circuits. Raclopride restored the cholinergic transmission in the prefrontal territory of the dorsal striatum and the cortico-nigral information transmissions in the prefrontal basal ganglia circuits. HFS STN also restored the N-methyl-d-aspartic-acid-evoked release of acetylcholine and dopamine in the prefrontal territory of the dorsal striatum. However, in contrast to raclopride, HFS STN did not restore the cortico-substantia nigra pars reticulata transmissions but exerted strong Liothyronine Sodium inhibitory and excitatory effects on neuronal activity in the prefrontal subdivision of the substantia nigra pars reticulata. Thus, both raclopride and HFS STN stop cocaine-induced motor stereotypy, but exert different effects on the related alterations in the prefrontal basal ganglia circuits. “
“Observing a speaker’s articulations substantially improves the intelligibility of spoken speech, especially under noisy listening conditions. This multisensory integration of speech inputs is crucial to effective communication. Appropriate

development of this ability has major implications for children in classroom and social settings, and deficits in it have been linked to a number of neurodevelopmental disorders, especially autism. It is clear from structural imaging studies that there is a prolonged maturational course within regions of the perisylvian cortex that persists into late childhood, and these regions have been firmly established as being crucial to speech and language functions. Given this protracted maturational timeframe, we reasoned that multisensory speech processing might well show a similarly protracted developmental course. Previous work in adults has shown that audiovisual enhancement in word recognition is most apparent within a restricted range of signal-to-noise ratios (SNRs).

, 2011) The isobaric tag for relative and absolute quantitation

, 2011). The isobaric tag for relative and absolute quantitation (iTRAQ) Poziotinib and liquid chromatography tandem mass spectrometry (LC-MS/MS) assays were performed by Beijing Protein Innovation (BPI) using previously described methods (Chao et al., 2010). Differentially expressed genes were identified based on at least a twofold expression change and a P-value < 0.05 relative to the WT control. The identified proteins were assigned the appropriate gene numbers by reference to the S. suis strain 05ZYH33 genome (Chen et al., 2007). Where appropriate, the data were analysed using Student's t-test, and a value of P < 0.05 was considered significant. Via genome analysis

of S. suis 05ZYH33, we found that peptides encoded by 05SSU2148 and 05SSU2149 find protocol exhibit 25% and 30% amino acid sequence identity with the VirR and VirS proteins of C. perfringens strain 13 (Shimizu et al., 2002), respectively, forming a TCS belonging to the widespread LytR/AlgR family. 05SSU2148 and 05SSU2149

were accordingly renamed virR and virS. Sequence analysis of the virRS locus suggested that these overlapping genes are co-transcribed. Like most bacterial response regulators, VirR (237 aa) has a C-terminal helix-turn-helix DNA-binding domain for promoter recognition and transcriptional control of target genes. In its N-terminal region, VirR contains a typical receiver domain that receives the signal from its sensor partner. virS encodes a 435-aa protein with seven N-terminal transmembrane domains (predicted by tmhmm server v. 2.0 software) and a C-terminal Anacetrapib transmitter domain that includes a classical histidine kinase and an ATPase motif. A survey of the publicly available complete genome sequences of S. suis revealed the presence of a VirR/VirS homologue in other S. suis isolates, including

the European strain P1/7, the Vietnamese strain BM407 and 7 Chinese strains (98HAH12, SC84, GZ1, A7, ST1, JS14 and SS12). This suggests a wide distribution of the VirR/VirS system among S. suis isolates. Despite the well-characterized function of the VirR/VirS system in C. perfringens infection, the role of this TCS in S. suis remained unclear. To address this issue, an isogenic virRS knockout mutant (ΔvirRS) was constructed in strain 05ZYH33 by allelic replacement with a constitutive spc cassette (Supporting information, Fig. S1). The growth curves of WT and ΔvirRS cultured in THY medium at 37 °C were compared, and no significant difference was observed (Fig. 1). When streaked on THY plates supplemented with 5% sheep blood, ΔvirRS and WT colonies displayed a similar haemolytic phenotype. However, observation with a light microscope revealed that the mean chain length of the ΔvirRS mutant was much shorter than that of WT under the same growth conditions (Fig. 2a).

Continuous-time, multi-state Markov models

Continuous-time, multi-state Markov models Ulixertinib ic50 were applied to the status data on HPV detection, VL and CD4 cell count. The following four states

were defined for the VL model (Fig. 1a) to describe the high-risk HPV detection and clearance rates with time-varying VL: 1 = none of the high-risk HPV types (HPV negative) and HIV VL >400 copies/mL; 2 = at least one of the high-risk HPV types detected (HPV positive) and VL > 400 copies/mL; 3 = HPV negative and VL ≤ 400 copies/mL, and 4 = HPV positive and VL ≤ 400 copies/mL. A multi-state model describes a process where an individual is in one of the specified states at any time. An individual’s status at any time can be categorized as one of the four states above, and changes in the state can be followed. The choice of 400 copies/mL was based on the lower limit of quantification of the Roche assay at the time of A5029. To illustrate the assumed state structure, suppose a woman begins in state 1. She may acquire HPV without improvement of VL (transition to state

2), or she may remain HPV negative with improvement 17-AAG supplier of VL (transition to state 3). State 4 may be reached from state 1 via state 2 (change in HPV status first) or state 3 (change in VL first), but not directly from state 1; that is, we assume that simultaneous changes in HPV status and VL do not occur biologically. (However, Cell Penetrating Peptide state 4 may be observed after state 1 in the previous visit.) From state 2, the woman may clear HPV and return to state 1, or she may retain HPV and transition to state 4 with decreased VL. From state 3, she may acquire HPV while

maintaining VL status (transition to state 4), or her VL may increase while she remains HPV negative (transition to state 1). From state 4, she may clear HPV and transition to state 3, or remain HPV positive while her VL increases (transition to state 2). She may also remain in any of the states for the remainder of the study. The analysis methods of Kalbfleisch and Lawless [12] were applied to account for the lack of exact times of HPV detection and clearance. The methods also account for differences in visit times, numbers of visits and initial states among the study participants. The transition rates, or cause-specific hazard rates, are denoted by λs in Figure 1. For instance, λ12 represents the hazard rate for acquiring HPV when VL remains >400 copies/mL and λ34 represents the rate when VL remains ≤400 copies/mL. For HPV clearance rates, λ21 represents the rate for clearing HPV when VL remains >400 copies/mL, and λ43 represents the rate for clearing HPV when VL remains ≤400 copies/mL. To describe the changes in HIV-related status, λ13 represents the rate from VL > 400 to ≤ 400 copies/mL without HPV, and λ24 that with HPV.

The lysogens were grown in LB medium for 16 h, and then directly

The lysogens were grown in LB medium for 16 h, and then directly subjected to β-galactosidase assay. Among 36 strains tested, the high activity of β-galactosidase was detected only for the envZ/ompR null mutant (Fig. 1a), indicating the involvement of OmpR in cysK regulation. To confirm whether or not EnvZ/OmpR repress other five representative genes, cysP, cysD, nirB, cysE, and cysJ, all encoding enzymes for cysteine synthesis, were examined in the envZ/ompR null mutant. The promoters for three genes, cysK, cysP, and cysJ, were induced in the mutant (Fig. 1b). All three genes are known to be under the control of CysB, suggesting that EnvZ/OmpR represses

not only cysK but at least other three CysB regulon genes. Recently small regulator RNAs, OmrA and OmrB,

were identified to repress cysK gene (Guillier & Gottesman, Barasertib manufacturer 2006). EnvZ/OmpR activates omrAB transcription, suggesting that EnvZ/OmpR may repress Trichostatin A cysK expression via OmrAB small regulatory RNAs. For detailed mapping of the promoter region of cysK, we isolated six different fragments of cysK promoter and constructed six species of cysK-lacZ protein fusion genes, which were introduced into the genome of wild-type (BW25113) and envZ/ompR null mutant (BW26424) (for details see Tables S1 and S2). The β-galactosidase activity was measured in these lysogens, each including a different cysK-lacZ protein fusion. Expression from the fusion genes coding CysK N-terminal fragments down to more than 100 amino acids fused to LacZ increased in ΔenvZ/ompR mutant (Fig. 2a). In contrast, the LacZ activity of the fusion gene coding the CysK N-terminal eight amino acids fused to LacZ did not increase in the ΔenvZ/ompR mutant (Fig. 2a, NN9001 and NN16003). In parallel, we also constructed transcriptional fusions using the cysK promoter containing cysK N-terminal eight amino acids (TU4217, TU42300, and TU42600 in Fig. 2b). Expression of all the cysK-lacZ transcriptional fusions was significantly increased ifenprodil (Figs 1 and 2b). We actually detected CysK-LacZ fusion protein from NN2001 and NN9001 but not that from NN1001 and NN9001 by western blotting (Fig. 2c). The CysK-LacZ

fusion protein expressed from NN2001 and NN9001 was of a similar molecular size of intact β-galactosidae (114 KDa). One possibility is that the hitherto predicted initiation codon may not be functional for CysK translation since a SD-like element is located at immediate upstream of 97th methionine (for sequence see Fig. 2c). CysK annotated in genome database may have a deletion of 10.3 KDa corresponding N-terminal 95 amino acids. The unique β-α-β-α domain, called Cap domain, at N-terminus of CysK has been believed to function as the substrate binding site (Burkhard et al., 1998, 1999, 2000), but our finding suggests that the revised sequence of CysK protein lacks this Cap domain. We then tried to identify possible trans-active elements affecting the expression of the CysB regulon.