The 2,272,351-base pair genome of Neisseria meningitidis strain MC58 (serogroup B), a causative agent of meningitis and septicemia, contains 2158 predicted coding regions, 1158 (53.7%) of which were assigned a biological role. Three major islands of horizontal DNA transfer were identified; two of these contain genes encoding proteins involved in pathogenicity, and the third island contains coding sequences only for hypothetical proteins. Insights into the commensal and virulence behavior of N. meningitidis can be gleaned from the genome, in which sequences for structural proteins of the pilus are clustered and several coding regions unique to serogroup B capsular polysaccharide synthesis can be identified. Finally, N. meningitidis contains more genes that undergo phase variation than any pathogen studied to date, a mechanism that controls their expression and contributes to the evasion of the host immune system.

Neisseria meningitidis is a major cause of bacterial septicemia and meningitis. Sequence variation of surface-exposed proteins and cross-reactivity of the serogroup B capsular polysaccharide with human tissues have hampered efforts to develop a successful vaccine. To overcome these obstacles, the entire genome sequence of a virulent serogroup B strain (MC58) was used to identify vaccine candidates. A total of 350 candidate antigens were expressed in Escherichia coli, purified, and used to immunize mice. The sera allowed the identification of proteins that are surface exposed, that are conserved in sequence across a range of strains, and that induce a bactericidal antibody response, a property known to correlate with vaccine efficacy in humans.

Chloroplasts of photosynthetic organisms harness light energy and convert it into chemical energy. In several land plants, GOLDEN2-LIKE (GLK) transcription factors are required for chloroplast development, as glk1 glk2 double mutants are pale green and deficient in the formation of the photosynthetic apparatus. We show here that glk1 glk2 double mutants of Arabidopsis thaliana accumulate abnormal levels of chlorophyll precursors and that constitutive GLK gene expression leads to increased accumulation of transcripts for antenna proteins and chlorophyll biosynthetic enzymes. To establish the primary targets of GLK gene action, an inducible expression system was used in combination with transcriptome analysis. Following induction, transcript pools were substantially enriched in genes involved in chlorophyll biosynthesis, light harvesting, and electron transport. Chromatin immunoprecipitation experiments confirmed the direct association of GLK1 protein with target gene promoters, revealing a putative regulatory cis-element. We show that GLK proteins influence photosynthetic gene expression independently of the phyB signaling pathway and that the two GLK genes are differentially responsive to plastid retrograde signals. These results suggest that GLK genes help to coregulate and synchronize the expression of a suite of nuclear photosynthetic genes and thus act to optimize photosynthetic capacity in varying environmental and developmental conditions.

CD4+CD25+ regulatory T (TR) cells can inhibit a variety of autoimmune and inflammatory diseases, but the precise mechanisms by which they suppress immune responses in vivo remain unresolved. Here, we have used Helicobacter hepaticus infection of T cell–reconstituted recombination-activating gene (RAG)−/− mice as a model to study the ability of CD4+CD25+ TR cells to inhibit bacterially triggered intestinal inflammation. H. hepaticus infection elicited both T cell-mediated and T cell–independent intestinal inflammation, both of which were inhibited by adoptively transferred CD4+CD25+ TR cells. T cell–independent pathology was accompanied by activation of the innate immune system that was also inhibited by CD4+CD25+ TR cells. Suppression of innate immune pathology was dependent on T cell–derived interleukin 10 and also on the production of transforming growth factor β. Thus, CD4+CD25+ TR cells do not only suppress adaptive T cell responses, but are also able to control pathology mediated by innate immune mechanisms.