[Comprehensive re-annotation of protein-coding genes for prokaryotic genomes by Z-curve and similarity-based methods].

The development of sequencing technology has generated huge genomic sequencing information and largely enriched public genetic resources. To analyze such big data, the algorithms and tools for comparison and annotation of genomes are updated continually, enabling genome annotation with higher accuracy via various annotation tools. Many prokaryotic genomes in public database were sequenced and assembled more than a decade ago, and they contained multiple genes with unknown functions. To improve the current annotation for those genomes in NCBI, we re-annotate 1587 bacterial and archaeal genomes using multiple prokaryotic gene recognition algorithms/softwares and gene expression data. The 33 Z-curve variables were applied to recognize sequences that were over-annotated to genes of 1587 bacterial and archaeal genomes deposited in public databases, and a total of 3092 sequences belonging to 177 genomes were recognized as sequences over-annotated as protein-coding genes. Next, 4447 protein-coding genes with unknown functions from 939 genomes were annotated with definite functions by similarity search. Finally, we recognized 2003 missed protein-coding genes that belong to known COG (clusters of orthologous groups of proteins) of nine genomes using three methods (ZCURVE 3.0, Glimmer 3.02 and Prodigal), which are accurate and frequently used for gene finding. Their algorithms are different and complementary. This is a comprehensive study for re-annotation of bacterial and archaeal genomes with new tools combining multi-omics data, which should provide a reference for annotation of newly sequenced strains, and also benefit further fundamental researches with the bacterial gene sequences obtained after re-annotation.

Ischemic Preconditioning-Induced SOCS-1 Protects Rat Intestinal Ischemia Reperfusion Injury via Degradation of TRAF6.

BACKGROUND: The inflammatory immune response plays an important role in mesenteric ischemia and ischemia-reperfusion injury. Toll-like receptor 4 (TLR4) is a critical receptor in transduction of the inflammatory response and plays an important role in intestinal homeostasis. Tumor necrosis factor receptor-associated factor 6 (TRAF6), known as a key adaptor protein downstream of TLR4, is involved in the inflammatory response by activating multiple apoptotic signaling pathways. However, mechanisms of the suppressor of cytokine signaling-1 (SOCS-1) in regulating cell inflammation and apoptosis are still obscure. OBJECTIVES: To investigate the TLR4-TRAF6 signaling pathway in intestinal ischemia and reperfusion injury, as well as SOCS-1 expression after ischemic preconditioning in the rat intestine. METHODS: The small bowel ischemia, ischemia-reperfusion, and preconditioning models were induced using ligation of the superior mesenteric artery in male Sprague-Dawley rats; then, the mRNA and protein levels of TLR4, TRAF6, and SOCS-1 were analyzed using real-time PCR, Western blot, and immunohistochemistry, respectively. RESULTS: The expression of TLR4 and TRAF6 was gradually increased with increasing intestinal ischemia duration, but increased substantially after ischemia-reperfusion injury. After ischemic preconditioning, TLR4 and TRAF6 expressions decreased; however, expression of SOCS-1 and the TLR4-TRAF6 pathway inhibitor was increased. CONCLUSION: These data show that ischemic preconditioning may induce the activation of SOCS-1 to inhibit the TLR4-TRAF6 signaling pathway, thereby playing a protective role in ischemia-reperfusion injury.