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Biomedical subjects

E J Strauss

Publications and source records attributed to E J Strauss.

9 recordsLinked to original sources
PubMed1997

Microbial pathogenesis: genomics and beyond.

The growing number of complete microbial genome sequences provides a powerful tool for studying the biology of microorganisms. In combination with assays for function, genomic-based approaches can facilitate efficient and directed research strategies to elucidate mechanisms of bacterial pathogenicity. As genomic information accrues, the challenge remains to construct a picture of the biology that accurately reflects how individual genes collaborate to create the complex world of microbial specialization.

Animals↗
PubMed1997

An Edwardsiella tarda strain containing a mutation in a gene with homology to shlB and hpmB is defective for entry into epithelial cells in culture.

Edwardsiella tarda is an enteric pathogen that causes diarrhea, wound infections, and death due to septicemia. This species is capable of invading human epithelial cell lines, and we have now been able to follow the entry and replication of E. tarda within tissue culture host cells. E. tarda escapes from the endocytic vacuole within minutes of entry and then replicates within the cytoplasm. Unlike other well-studied bacteria that replicate and reside in the cytoplasm, we never observed this organism moving directly from cell to cell; instead the bacteria spread by lysing the plasma membrane after several rounds of replication. Efforts to study the interactions of E. tarda with tissue culture cells are complicated by the presence of a potent cytotoxin that the bacterium produces. Using transposon mutagenesis, we isolated a noncytotoxic strain of E. tarda. This mutant is also defective for hemolysin production. The dual phenotype of this strain is consistent with the hypothesis that cytotoxicity is due to the previously characterized E. tarda hemolysin activity. The nonhemolytic strain is also unable to enter HEp-2 cells. The disrupted gene has sequence similarity to members of a family of genes required for transport and activation of the hemolysin genes, shlA and hpmA. A cosmid bearing 40 kb of E. tarda DNA, including wild-type copies of the E. tarda homologs of the transporter-activator protein and the hemolysin itself, confers hemolytic, cytotoxic, and invasive abilities upon normally nonhemolytic, noncytotoxic, and noninvasive strains of Escherichia coli. Sequence data indicate that the genes required for hemolytic activity are linked to a transposable element, suggesting that they arose in the E. tarda genome by horizontal transfer.

Adhesins, Bacterial↗
PubMed1995

Bacterial pathogenesis. When a turn off is a turn on.

Pathogenic bacteria express distinct sets of genes at different stages in their life cycles; inappropriate expression of normally repressed genes during host colonization can interfere with bacterial survival.

Bacteria↗
PubMed1994

PRP28, a 'DEAD-box' protein, is required for the first step of mRNA splicing in vitro.

We previously reported the isolation of PRP28, a gene in Saccharomyces cerevisiae whose activity is required for the first step of nuclear mRNA splicing in vivo. Sequence analysis revealed that PRP28 is included in the 'DEAD-box' gene family, members of which are thought to function as ATP-dependent RNA helicases. Genetic interactions led us to suggest that PRP28 is functionally associated with the U4/U5/U6 snRNP. We have now purified the PRP28 protein from S. cerevisiae and demonstrated that it is required for the first step of splicing in vitro. Interestingly, PRP28 is not a stably associated snRNP protein. Strand displacement assays indicate that PRP28 does not exhibit RNA helicase activity, suggesting that an additional factor or factors may be required for its activation.

Adenosine Triphosphatases↗
PubMed1991

A cold-sensitive mRNA splicing mutant is a member of the RNA helicase gene family.

We have isolated a cold-sensitive mutant of Saccharomyces cerevisiae in which the first step of mRNA splicing is inhibited. The growth and splicing defects are recessive and cosegregate, thus defining a single essential gene (PRP28). The wild-type PRP28 gene was cloned, and sequence analysis reveals extensive homology to a family of proteins that are thought to function as ATP-dependent RNA helicases. The cold sensitivity is caused by a glycine-to-glutamic acid change in a conserved sequence motif. Interestingly, double mutants containing conditional alleles of PRP28 and PRP24, which encodes a U6 snRNA-binding protein, are inviable. In addition, a suppressor of prp28-1 is a mutant allele of PRP8, which encodes a U5 protein, thus linking PRP28 with U5. These data are consistent with a scenario in which PRP28 acts to unwind the U4/U6 base-pairing interaction in the U4/U6/U5 snRNP, facilitating the first covalent step of splicing.

Amino Acid Sequence↗
PubMedDate not supplied

Molecular mechanisms of bacterial virulence: type III secretion and pathogenicity islands.

Recently, two novel but widespread themes have emerged in the field of bacterial virulence: type III secretion systems and pathogenicity islands. Type III secretion systems, which are found in various gram-negative organisms, are specialized for the export of virulence factors delivered directly to host cells. These factors subvert normal host cell functions in ways that seem beneficial to invading bacteria. The genes encoding several type III secretion systems reside on pathogenicity islands, which are inserted DNA segments within the chromosome that confer upon the host bacterium a variety of virulence traits, such as the ability to acquire iron and to adhere to or enter host cells. Many of these segments of DNA appear to have been acquired in a single step from a foreign source. The ability to obtain complex virulence traits in one genetic event, rather than by undergoing natural selection for many generations, provides a mechanism for sudden radical changes in bacterial-host interactions. Type III secretion systems and pathogenicity islands must have played critical roles in the evolution of known pathogens and are likely to lead to the emergence of novel infectious diseases in the future.

Bacterial Proteins↗