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Bublitz, D. C.

Publications and source records attributed to Bublitz, D. C..

3 recordsLinked to original sources

Bacterial threat assessment of bacteriophage infection is mediated by intracellular polyamine accumulation and Gac/Rsm signaling

When eukaryotic cells are killed by pathogenic microorganisms, damage-associated and pathogen-associated signals are generated that alert other cells of nearby danger. Bacteria can detect the death of their kin; however, how bacteria make threat assessments of cellular injury is largely unexplored. Here we show that polyamines released by lysed bacteria serve as damage-associated molecules in Pseudomonas aeruginosa. In response to exogenous polyamines, Gac/Rsm and cyclic-di-GMP signaling is activated and intracellular polyamine levels increase. In the absence of a threat, polyamines are catabolized, and intracellular polyamines return to basal levels, but cells infected by bacteriophage increase and maintain intracellular polyamine levels, which inhibits phage replication. Phage species not inhibited by polyamines did not trigger polyamine accumulation by P. aeruginosa, suggesting polyamine accumulation and metabolism are targets in the phage-host arms-race. Our results suggest that like eukaryotic cells, bacteria can differentiate damage-associated and pathogen-associated signals to make threat assessments of cellular injury. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=112 SRC="FIGDIR/small/486733v1_ufig1.gif" ALT="Figure 1"> View larger version (34K): org.highwire.dtl.DTLVardef@1f69334org.highwire.dtl.DTLVardef@13a4422org.highwire.dtl.DTLVardef@4f3edeorg.highwire.dtl.DTLVardef@a86c43_HPS_FORMAT_FIGEXP M_FIG C_FIG

microbiology↗

The depletion mechanism can actuate bacterial aggregation by self-produced exopolysaccharides and determine species distribution and composition in bacterial aggregates

Bacteria causing chronic infections are often found in cell aggregates suspended in polymer secretions, and aggregation may be a factor in infection persistence. One aggregation mechanism, called depletion aggregation, is driven by physical forces between bacteria and polymers. Here we investigated whether the depletion mechanism can actuate the aggregating effects of P. aeruginosa exopolysaccharides for suspended (i.e. not surface attached) bacteria, and how depletion affects bacterial inter-species interactions. We found cells overexpressing the exopolysaccharides Pel and Psl, but not alginate remained aggregated after depletion-mediating conditions were reversed. In co-culture, depletion aggregation had contrasting effects on P. aeruginosas interactions with coccus- and rod-shaped bacteria. Depletion caused S. aureus (cocci) and P. aeruginosa (rods) to segregate from each other, S. aureus to resist secreted P. aeruginosa antimicrobial factors, and the species to co-exist. In contrast, depletion aggregation caused P. aeruginosa and Burkholderia sp. to intermix, enhancing type VI secretion inhibition of Burkholderia by P. aeruginosa, leading to P. aeruginosa dominance. These results show that in addition to being a primary cause of aggregation in polymer-rich suspensions, physical forces inherent to the depletion mechanism can actuate the aggregating effects of self-produced exopolysaccharides and determine species distribution and composition of bacterial communities.

microbiology↗

Evolutionary relationships among Massospora spp. (Entomophthorales), obligate pathogens of cicadas

The fungal genus Massospora (Zoopagomycota: Entomophthorales) includes more than a dozen obligate, sexually transmissible pathogenic species that infect cicadas (Hemiptera) worldwide. At least two species are known to produce psychoactive compounds during infection, which has garnered considerable interest for this enigmatic genus. As with many Entomophthorales, the evolutionary relationships and host associations of Massospora spp. are not well understood. The acquisition of M. diceroproctae from Arizona, M. tettigatis from Chile, and M. platypediae from California and Colorado provided an opportunity to conduct molecular phylogenetic analyses and morphological studies to investigate if these fungi represent a monophyletic group and delimit species boundaries. In a three-locus phylogenetic analysis including the D1-D2 domains of the nuclear 28S rRNA gene (28S), elongation factor 1 alpha-like (EFL), and beta-tubulin (BTUB), Massospora was resolved in a strongly supported monophyletic group containing four well-supported genealogically exclusive lineages, based on two of three methods of phylogenetic inference. There was incongruence among the single-gene trees: two methods of phylogenetic inference recovered trees with either the same topology as the 3-gene concatenated tree (EFL), or a basal polytomy (28S, BTUB). Massospora levispora and M. platypediae isolates formed a single lineage in all analyses and are synonymized here as M. levispora. Massospora diceroproctae was sister to M. cicadina in all three single-gene trees and on an extremely long branch relative to the other Massospora, and even the outgroup taxa, which may reflect an accelerated rate of molecular evolution and/or incomplete taxa sampling. The results of the morphological study presented here indicate that spore measurements may not be phylogenetically or diagnostically informative. Despite recent advances in understanding the ecology of Massospora, much about its host range and diversity remains unexplored. The emerging phylogenetic framework can provide a foundation for exploring co-evolutionary relationships with cicada hosts and the evolution of behavior-altering compounds.

microbiology↗