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S Ferrer

Publications and source records attributed to S Ferrer.

At least 55 records · Page 3Linked to original sources
PubMed1996

Nucleotide sequence of plasmid p4028, a cryptic plasmid from Leuconostoc oenos.

The Leuconostoc oenos plasmid p4028 was cloned in pBlueScript (SK+), and its complete nucleotide sequence was determined. The analysis of the nucleotide sequence revealed five open reading frames, all of them located on the same strand and grouped in two clusters separated by a short noncoding stretch. A similarity search against the other sequences deposited in the EMBL and GenBank databases showed that p4028 has no significant similarity with any of the sequences checked. Nevertheless, a putative ATP-binding motif was found in ORF2. A more detailed analysis of this ORF suggests that it could encode for a DNA-dependent ATPase.

Amino Acid Sequence↗
PubMed1996

Cloning and characterization of two Serratia marcescens genes involved in core lipopolysaccharide biosynthesis.

Bacteriocin 28b from Serratia marcescens binds to Escherichia coli outer membrane proteins OmpA and OmpF and to lipopolysaccharide (LPS) core (J. Enfedaque, S. Ferrer, J. F. Guasch, J. Tomás, and M. Requé, Can. J. Microbiol. 42:19-26, 1996). A cosmid-based genomic library of S. marcescens was introduced into E. coli NM554, and clones were screened for bacteriocin 28b resistance phenotype. One clone conferring resistance to bacteriocin 28b and showing an altered LPS core mobility in polyacrylamide gel electrophoresis was found. Southern blot experiments using DNA fragments containing E. coli rfa genes as probes suggested that the recombinant cosmid contained S. marcescens genes involved in LPS core biosynthesis. Subcloning, isolation of subclones and Tn5tac1 insertion mutants, and sequencing allowed identification of two apparently cotranscribed genes. The deduced amino acid sequence from the upstream gene showed 80% amino acid identity to the KdtA protein from E. coli, suggesting that this gene codes for the 3-deoxy-manno-octulosonic acid transferase of S. marcescens. The downstream gene (kdtX) codes for a protein showing 20% amino acid identity to the Haemophilus influenzae kdtB gene product. The S. marcescens KdtX protein is unrelated to the KdtB protein of E. coli K-12. Expression of the kdtX gene from S. marcescens in E. coli confers resistance to bacteriocin 28b.

Amino Acid Sequence↗
PubMed1996

Genetic evidence for an activator required for induction of colicin-like bacteriocin 28b production in Serratia marcescens by DNA-damaging agents.

Bacteriocin 28b production is induced by mitomycin in wild-type Serratia marcescens 2170 but not in Escherichia coli harboring the bacteriocin 28b structural gene (bss). Studies with a bss-lacZ transcriptional fusion showed that mitomycin increased the level of bss gene transcription in S. marcescens but not in the E. coli background. A S. marcescens Tn5 insertion mutant was obtained (S. marcescens 2170 reg::Tn5) whose bacteriocin 28b production and bss gene transcription were not increased by mitomycin treatment. Cloning and DNA sequencing of the mutated region showed that the Tn5 insertion was flanked by an SOS box sequence and three genes that are probably cotranscribed (regA, regB, and regC). These three genes had homology to phage holins, phage lysozymes, and the Ogr transcriptional activator of P2 and related bacteriophages, respectively. Recombinant plasmid containing this wild-type DNA region complemented the reg::Tn5 regulatory mutant. A transcriptional fusion between a 157-bp DNA fragment, containing the apparent SOS box upstream of the regA gene, and the cat gene showed increased chloramphenicol acetyltransferase activity upon mitomycin treatment. Upstream of the bss gene, a sequence similar to the consensus sequence proposed to bind Ogr protein was found, but no sequence similar to an SOS box was detected. Our results suggest that transcriptional induction of bacteriocin 28b upon mitomycin treatment is mediated by the regC gene whose own transcription would be LexA dependent.

Amino Acid Sequence↗
PubMed1996

Bacteriocin 28b from Serratia marcescens N28b: identification of Escherichia coli surface components involved in bacteriocin binding and translocation.

Serratia marcescens N28b produces bacteriocin 28b, active against Escherichia coli. Bacteriocin sensitivity tests performed on a collection of E. coli envelope mutants, and isolation and characterization of E. coli bacteriocin-28b-insensitive mutants, showed that the core lipopolysaccharide, outer membrane proteins OmpA and OmpF, and TolQ, TolA, and TolB proteins are involved in bacteriocin 28b lethal activity. These mutants are assayed for bacteriocin 28b sensitivity under normal and bypass conditions, and their bacteriocin-binding ability was determined. The results obtained suggest that the core lipopolysaccaride and outer membrane proteins OmpA and OmpF are involved in bacteriocin 28b binding. Furthermore, bacteriocin 28b translocation requires proteins TolA, TolB, and TolQ.

Bacterial Outer Membrane Proteins↗
PubMed1996

[Cerebral toxoplasmosis in patients with human immunodeficiency virus (HIV) infection. Clinico-radiological and therapeutic aspects in 63 patients].

We have retrospectively reviewed 63 cases of encephalic toxoplasmosis (ET) in HIV-infected patients in order to determine clinical and radiological characteristics, the diagnostic value of serologic determinations, and the response to antioxoplasmic therapy. ET was the AIDS-defining condition in 44% of the patients. Eighty of the patients had a CD4 cell count < 100/microliters when ET was diagnosed. Only 4.8% of the patients had been taking anti-Pneumocytis carinii prophylaxis with cotrimoxazol. The most frequent clinical presentation was focal neurologic signs in 80.9% of the patients, with headache and fever in 53.3% and 42.4%, respectively. The most frequent cerebral CT finding was hipodense lesions (92%) with ring enhancement (68.9%). They were most frequently had a hemisferic location. Seroconversion was detected in two patients (6%), whereas 55 patients had serologic evidence of latent infection by Toxoplasma gondii (87.3%). Ninety eight percent of the patients were treated with sulphadiazine plus pyrimethamine. However, such therapy should be discontinued in 22% of them and switched to clindamycin plus pyrimethamine. The overall mortality rate during the acute phase of the disease was 7.9%, but 41.4% of the survivors exhibited neurologic sequelae. Relapsing ET was detected in 33.3% of the patients, and it was usually due to discontinuation of treatment. The mean survival time after the diagnosis of ET was 11.5 months. ET is the most common opportunistic infection of the central nervous system among our AIDS patients. Primary prophylaxis for toxoplasmic infection seems advisable in our epidemiologic environment, when CD4 cell count is less than 200/microliters and there is serologic evidence of latent infection. Acute ET usually has a good response to therapy, and the acute mortality rate is low. However, most of the survivors will remain with neurologic sequelae. The high frequency of adverse effects to sulphamide therapy with clindamycin make the need of alternative treatment strategies urgent.

Acquired Immunodeficiency Syndrome↗
PubMed1995

A 17 kDa outer-membrane protein (Omp4) from Serratia marcescens confers partial resistance to bacteriocin 28b when expressed in Escherichia coli.

A cosmid-based genomic library of Serratia marcescens N28b was introduced into Escherichia coli and clones were screened for a bacteriocin 28b insensitive phenotype. One clone was found that showed partial resistance to bacteriocin 28b. By using Tn5tac1 insertions it was shown that this phenotype was due to the expression in E. coli of an outer-membrane protein of 17 kDa (Omp4). The DNA region defined by insertion mutagenesis was sequenced and found to contain an ORF of 515 bp. The deduced amino acid sequence has 172 residues with a theoretical molecular mass of 18.4 kDa. The protein contains an N-terminal signal sequence of 24 amino acid residues and, when compared to other enterobacterial outer-membrane proteins, most closely resembles a family of small outer-membrane proteins of Enterobacteriaceae whose known functions appear to be related with virulence. Immunoblotting experiments showed that Omp4 is present in 15 biotypes of S. marcescens. The bacteriocin 28b resistance phenotype conferred on E. coli by Omp4 appears to be pleiotropic since overexpression of the Omp4-encoding gene leads to a decrease in the amount of OmpA, OmpF and/or OmpC; OmpA and OmpF are the receptors for bacteriocin 28b in E. coli.

Amino Acid Sequence↗
PubMed1995

Protection against bacteriocin 28b in Serratia marcescens is apparently not related to the expression of an immunity gene.

The gene encoding bacteriocin 28b from Serratia marcescens N28b (bss gene) has been cloned in Escherichia coli and its nucleotide sequence has been determined. The genetic determinants coding for other well-characterized bacteriocins from enterobacteria (colicins) are located in plasmids and they have always been shown to contain a gene responsible for immunity located downstream from the bacteriocin structural gene. In some cases there is another gene located downstream from the immunity gene, which is responsible for bacteriocin release. Analysis of bacteriocin 28b release and the sensitivity to this bacteriocin of E. coli strains harbouring recombinant plasmids containing the bss gene showed that bacteriocin 28b is not released from the cell in these strains and that their phenotypic insensitivity is not associated with any region close to the structural gene. The nucleotide sequence of the region downstream from the bss gene contains two putative open reading frames transcribed in the opposite direction to the bss gene. These open reading frames apparently encode proteins that seem not to be involved in bacteriocin immunity or release. Moreover, a S. marcescens N28b genomic library was screened and no immunity gene was found. Therefore, bacteriocin 28b differs greatly from the bacteriocins from other enterobacteria, and in the following senses it is unique: firstly, the gene encoding bacteriocin 28b seems to be located on the chromosome, and secondly, insensitivity to this bacteriocin in S. marcescens N28b is not associated with the expression of an immunity gene.

Amino Acid Sequence↗
PubMed1995

[Eosinophilic pustular folliculitis in acquired immunodeficiency syndrome. Report of 6 cases].

Eosinophilic pustulous foliculitis (EPF) is a rare dermatosis which has been reported in association with the human immunodeficiency virus infection. Six patients infected with HIV are reported with advanced disease in whom the diagnosis of EPF was made. All patients has a highly pruritic follicular papular rash. In all cases the pathology study revealed a mixed inflammatory infiltrate with predominance of eosinophils at the infundibulum of the pilous folliculi. Two patients had eosinophilia in peripheral blood. Therapy with antihistaminic agents and topical corticosteroids was ineffective in all cases. A favourable therapeutic response was achieved with phototherapy associated with the topic application of disodium cromoglycate 4%.

Adult↗
PubMed1994

Transformation of Aspergillus parasiticus using autonomously replicating plasmids from Aspergillus nidulans.

A genetic transformation system for the aflatoxin-producing fungus Aspergillus parasiticus using two autonomously replicating plasmids from A. nidulans (ARp1 and pDHG25) is reported. Transformation frequencies using the plasmid pDHG25 were from 5 x 10(2) to 2.5 x 10(4) transformants per 10(6) viable protoplasts and microgram DNA. The stability of the plasmids in the transformants was also studied. This transformation system offers a new opportunity to clone genes related to aflatoxin production using appropriate aflatoxin-defective mutants.

Aspergillus↗
PubMed1994

[Polyneuropathies and dysglobulinemias].

We review the concept fo Monoclonal Gammopathy emphasizing that the so called benign forms, with or without polyneuropathy can have an unpredictable evolution. Polyneuropathies associated to monoclonal gammopathy-IgM, IgG, IgA, Waldestrom's disease, Multiple myeloma, Osteosclerotic myeloma (POEMS), Amyloidosis and Cryoglobulinemias are reviewed. They generally are solely sensory, sensorimotor or rarely, solely motor. The importance of neuro-physiological studies and nerve biopsy is emphasized. For progressive forms, treatment with plasmapheresis, immunotherapy, corticoids or intravenous gammaglobulin is suggested.

Aged↗