Listeria genomics

Abstract

The publication of the complete genome sequences of four clinical Listeria monocytogenes isolates and one of its apathogenic relative, Listeria innocua, in 2001 and 2003 has paved the way for major breakthroughs in understanding the biology of L. monocytogenes. The availability of these sequences allowed applying postgenomics analysis to understand virulence and ecology of L. monocytogenes and evolution of the genus Listeria. Comparative genomics now help to unravel the molecular basis of the pathogenesis, the host range, the evolution, and the phenotypic differences among L. monocytogenes isolates and within the genus Listeria. Based on sequence analysis, many new virulence factors have been identified, foremost among them, surface proteins like internalins, in agreement with the expansion of this protein family revealed by genome sequencing. The discovery of a broad transport capacity, in particular, of carbon sources and of unexpected metabolic pathways like the biosynthesis of vitamin B12 and glutathione (GSH) explains the ubiquitous nature of Listeria. Some of the many regulators identified in the genome are now analyzed, demonstrating, e.g., the importance of an orphan two-component regulator DegU in virulence of L. monocytogenes or leading to the identification of a new class of regulators like MogR, the master regulator of flagella expression. Combined with genome analysis, transcriptome studies using microarrays allow for the first time the global and parallel analysis of L. monocytogenes gene expression inside and outside eukaryotic cells. Multiple ongoing sequencing projects allowing multigenome comparisons combined with different postgenomics and functional analyses open the way to a global understanding of the ability of Listeria to adapt to a broad range of environments and hosts and of the multiple aspects of the disease it causes, listeriosis.