Therefore, it seems that most (if not all) changes that could affect the functions of the encoded proteins have been removed by the action of purifying selection. Functional analysis of the nested consortium Most endosymbiotic systems analyzed to date at the genomic level have a nutritional basis, and many of them involve the biosynthesis of essential amino acids that are in short supply in the host diet. The metabolic pathways leading to amino acid biosynthesis in the T. princeps-M. GSK461364 manufacturer endobia consortium found in P. citri were recently analyzed in detail by McCutcheon and von Dohlen [16] and, therefore, they will

not be dealt with in this study. These authors also stated that T. princeps is unable to perform DNA replication, recombination or repair by itself, and the same applies to translation. They speculate that a passive mechanism such as cell lysis could provide T. princeps with the needed gene products from M. endobia. Our present work provides a detailed analysis of the M. GSK126 mouse endobia functional capabilities, based on a functional analysis of its genome, regarding informational

functions or other intermediate metabolism pathways beyond amino acids biosynthesis. In the following sections these functional capabilities will be analyzed in a comprehensive manner, considering both endosymbiotic partners, in order to identify CH5424802 molecular weight putative additional levels of complementation between them. DNA repair and recombination Contrary to what is found in bacterial endosymbionts with similarly

reduced genomes, M. endobia has quite a complete set of genes for DNA repair and recombination, while none were annotated in the T. princeps genome [16, 19]. Although it has lost the nucleotide excision repair genes (only uvrD is present), M. endobia retains a base excision repair system (the DNA glycosylases encoded by mutM and ung plus xth, the gene encoding exonuclease III, involved in the repair of sites where damaged bases have been removed). The mismatch repair system is also almost complete, since only mutH, encoding the endonuclease needed in this process to cleave the unmethylated strand, has been lost. Additionally, M. endobia also retains almost the entire molecular machinery for homologous recombination (recABCGJ, ruvABC, priAB), which Fluorometholone Acetate could be responsible for the concerted evolution of the duplications in both genomes. In the absence of recD, the RecBC enzyme can still promote recombination, since it retains helicase and RecA loading activity. The missing exonuclease V activity can be replaced by other exonucleases with ssDNA degradation activity in the 5′ → 3′ sense, such of RecJ [30], which has been preserved. The final step in homologous recombination requires the reloading of origin-independent replication machinery. Two replisome reloading systems have been described in E.