The first comprehensive comparative analysis of lactobacilli was done by comparing the genomes of Lactobacillus plantarum (3?3 Mb) and Lactobacillus johnsonii (2?0 Mb). L. johnsonii is predominantly found in the gastrointestinal tract, while L. plantarum is also found on plants and plant-derived material, and is used in a variety of industrial fermentations. The L. plantarum and L. johnsonii chromosomes have only 28 regions with conservation of gene order, totalling about 0?75 Mb; these regions are not co-linear, indicating major chromosomal rearrangements. Metabolic reconstruction indicates many differences between L. johnsonii and L. plantarum: numerous enzymes involved in sugar metabolism and in biosynthesis of amino acids, nucleotides, fatty acids and cofactors are lacking in L. johnsonii. Major differences were seen in the number and types of putative extracellular proteins, which are of interest because of their possible role in host-microbe interactions. The differences between L. plantarum and L. johnsonii, both in genome organization and gene content, are exceptionally large for two bacteria of the same genus, emphasizing the difficulty in taxonomic classification of lactobacilli.

A 302-bp noncoding DNA fragment from the DNA replication module of phage phiSfi21 was shown to protect the Streptococcus thermophilus strain Sfi1 from infection by 17 of 25 phages. The phage-inhibitory DNA possesses two determinants, each of which individually mediated phage resistance. The phage-inhibitory activity was copy number dependent and operates by blocking the accumulation of phage DNA. Furthermore, when cloned on a plasmid, the phiSfi21 DNA acts as an origin of replication driven by phage infection. Protein or proteins in the phiSfi21-infected cells were shown to interact with this phage-inhibitory DNA fragment, forming a retarded protein-DNA complex in gel retardation assays. A model in which phage proteins interact with the inhibitory DNA such that they are no longer available for phage propagation can be used to explain the observed bacteriophage resistance. Genome analysis of phiSfi19, a phage that is insensitive to the inhibitory activity of the phiSfi21-derived DNA, led to the characterisation of a variant putative phage replication origin that differed in 14 of 302 nucleotides from that of phiSfi21. The variant origin was cloned and exhibited an inhibitory activity toward phages that were insensitive to the phiSfi21-derived DNA.

Postexercise protein feeding regulates the skeletal muscle adaptive response to endurance exercise, but the transcriptome guiding these adaptations in well-trained human skeletal muscle is uncharacterized. In a crossover design, eight cyclists ingested beverages containing protein, carbohydrate and fat (PTN: 0.4, 1.2, 0.2 g/kg, respectively) or isocaloric carbohydrate and fat (CON: 1.6, 0.2 g/kg) at 0 and 1 h following 100 min of cycling. Biopsies of the vastus lateralis were collected at 3 and 48 h following to determine the early and late transcriptome and regulatory signaling responses via microarray and immunoblot. The top gene ontology enriched by PTN were: muscle contraction, extracellular matrix--signaling and structure, and nucleoside, nucleotide, and nucleic acid metabolism (3 and 48 h); developmental processes, immunity, and defense (3 h); glycolysis, lipid and fatty acid metabolism (48 h). The transcriptome was also enriched within axonal guidance, actin cytoskeletal, Ca2+, cAMP, MAPK, and PPAR canonical pathways linking protein nutrition to exercise-stimulated signaling regulating extracellular matrix, slow-myofibril, and metabolic gene expression. At 3 h, PTN attenuated AMPKα1Thr172 phosphorylation but increased mTORC1Ser2448, rps6Ser240/244, and 4E-BP1-γ phosphorylation, suggesting increased translation initiation, while at 48 h AMPKα1Thr172 phosphorylation and PPARG and PPARGC1A expression increased, supporting the late metabolic transcriptome, relative to CON. To conclude, protein feeding following endurance exercise affects signaling associated with cell energy status and translation initiation and the transcriptome involved in skeletal muscle development, slow-myofibril remodeling, immunity and defense, and energy metabolism. Further research should determine the time course and posttranscriptional regulation of this transcriptome and the phenotype responding to chronic postexercise protein feeding.

Dysregulation of intestinal epithelial cell performance is associated with an array of pathologies whose onset mechanisms are incompletely understood. While whole-genomics approaches have been valuable for studying the molecular basis of several intestinal diseases, a thorough analysis of gene expression along the healthy gastrointestinal tract is still lacking. The aim of this study was to map gene expression in gastrointestinal regions of healthy human adults and to implement a procedure for microarray data analysis that would allow its use as a reference when screening for pathological deviations. We analyzed the gene expression signature of antrum, duodenum, jejunum, ileum, and transverse colon biopsies using a biostatistical method based on a multivariate and univariate approach to identify region-selective genes. One hundred sixty-six genes were found responsible for distinguishing the five regions considered. Nineteen had never been described in the GI tract, including a semaphorin probably implicated in pathogen invasion and six novel genes. Moreover, by crossing these genes with those retrieved from an existing data set of gene expression in the intestine of ulcerative colitis and Crohn's disease patients, we identified genes that might be biomarkers of Crohn's and/or ulcerative colitis in ileum and/or colon. These include CLCA4 and SLC26A2, both implicated in ion transport. This study furnishes the first map of gene expression along the healthy human gastrointestinal tract. Furthermore, the approach implemented here, and validated by retrieving known gene profiles, allowed the identification of promising new leads in both healthy and disease states.