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24. The Intriguing Evolutionary Journey of Enteroinvasive E-coli (EIEC) toward Pathogenicity

Author

Pasqua, Martina, Michelacci, Valeria, Di Martino, Maria Letizia, Tozzoli, Rosangela, Grossi, Milena, Colonna, Bianca, Morabito, Stefano, Prosseda, Gianni, Pasqua, Martina, Michelacci, Valeria, Di Martino, Maria Letizia, Tozzoli, Rosangela, Grossi, Milena, Colonna, Bianca, Morabito, Stefano, and Prosseda, Gianni

Abstract

Among the intestinal pathogenic Escherichia coli, enteroinvasive E. coli (EIEC) are a group of intracellular pathogens able to enter epithelial cells of colon, multiplicate within them, and move between adjacent cells with a mechanism similar to Shigella, the ethiological agent of bacillary dysentery. Despite EIEC belong to the same pathotype of Shigella, they neither have the full set of traits that define Shigella nor have undergone the extensive gene decay observed in Shigella. Molecular analysis confirms that EIEC are widely distributed among E. coli phylogenetic groups and correspond to bioserotypes found in many E. coli serogroups. Like Shigella, also in EIEC the critical event toward a pathogenic life-style consisted in the acquisition by horizontal gene transfer of a large F-type plasmid (pINV) containing the genes required for invasion, intracellular survival, and spreading through the intestinal mucosa. In Shigella, the ample gain in virulence determinants has been counteracted by a substantial loss of functions that, although important for the survival in the environment, are redundant or deleterious for the life inside the host. The pathoadaptation process that has led Shigella to modify its metabolic profile and increase its pathogenic potential is still in infancy in EIEC, although maintenance of some features typical of E. coli might favor their emerging relevance as intestinal pathogens worldwide, as documented by recent outbreaks in industrialized countries. In this review, we will discuss the evolution of EIEC toward Shigella-like invasive forms going through the epidemiology, including the emergence of new virulent strains, their genome organization, and the complex interactions they establish with the host.

Published
2017
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34. Multifactor Regulation of the MdtJI Polyamine Transporter in Shigella

Author

Leuzzi, Adriano, primary, Di Martino, Maria Letizia, additional, Campilongo, Rosaria, additional, Falconi, Maurizio, additional, Barbagallo, Marialuisa, additional, Marcocci, Lucia, additional, Pietrangeli, Paola, additional, Casalino, Mariassunta, additional, Grossi, Milena, additional, Micheli, Gioacchino, additional, Colonna, Bianca, additional, and Prosseda, Gianni, additional

Published
2015
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43. Molecular and Functional Profiling of the Polyamine Content in Enteroinvasive E. coli : Looking into the Gap between Commensal E. coli and Harmful Shigella

Author

Campilongo, Rosaria, primary, Di Martino, Maria Letizia, additional, Marcocci, Lucia, additional, Pietrangeli, Paola, additional, Leuzzi, Adriano, additional, Grossi, Milena, additional, Casalino, Mariassunta, additional, Nicoletti, Mauro, additional, Micheli, Gioacchino, additional, Colonna, Bianca, additional, and Prosseda, Gianni, additional

Published
2014
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47. Nfix Regulates Fetal-Specific Transcription in Developing Skeletal Muscle

Author

Messina, Graziella, primary, Biressi, Stefano, additional, Monteverde, Stefania, additional, Magli, Alessandro, additional, Cassano, Marco, additional, Perani, Laura, additional, Roncaglia, Elena, additional, Tagliafico, Enrico, additional, Starnes, Linda, additional, Campbell, Christine E., additional, Grossi, Milena, additional, Goldhamer, David J., additional, Gronostajski, Richard M., additional, and Cossu, Giulio, additional

Published
2010
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48. v-jun oncogene prevents terminal differentiation and suppresses muscle-specific gene expression in ASV-17-infected muscle cells

Author

Grossi, Milena, Calconi, Attilio, and Tato', Franco

Subjects
v-jun, Genes, jun, Myofibrils, retroviral oncogenes, Muscles, Animals, cell transformation, Cell Differentiation, myogenic differentiation, Cell Transformation, Viral, Quail, Cell Division
Abstract

Infection of replicating quail myoblasts with avian sarcoma virus 17 (ASV-17) results in the inhibition of terminal differentiation into multinucleated myotubes and in the acquisition of anchorage-independent proliferation. Expression of v-jun, the ASV-17 oncogene, concomitantly leads to the accumulation of the gag-jun polyprotein P65 in the nucleus and to the lack of expression of typical differentiation-specific genes such as myosin heavy chain (MHC) and alpha-actinin. Surprisingly, expression of desmin, the muscle-specific subunit of intermediate filaments, is conserved in ASV-17-transformed myoblasts. Analysis of clonal strains of transformed myoblasts suggests that (i) suppression of morphological and biochemical differentiation depends on the absence of muscle-specific gene transcripts; (ii) inhibition of muscle differentiation by v-jun does not depend on the transcriptional silencing of MyoD, a muscle-specific regulatory gene; (iii) expression of desmin is compatible with proliferation of ASV-17-transformed cells and is independent of v-jun and MyoD levels of expression. The present data suggest that nuclear localization of v-jun prevents terminal differentiation in myoblasts and selectively down-regulates muscle-specific genes in terminally differentiated myotubes. In this respect, the behaviour of v-jun is quite different from that of v-myc, thus suggesting that these two oncogenes, although both encoding nuclear proteins, may have different mechanisms of action.

Published
1991

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