Mycobacteriophages are viruses that infect mycobacterial hosts such as Mycobacterium smegmatis and Mycobacterium tuberculosis. All mycobacteriophages characterized to date are dsDNA tailed phages, and have either siphoviral or myoviral morphotypes. However, their genetic diversity is considerable, and although sixty-two genomes have been sequenced and comparatively analyzed, these likely represent only a small portion of the diversity of the mycobacteriophage population at large. Here we report the isolation, sequencing and comparative genomic analysis of 18 new mycobacteriophages isolated from geographically distinct locations within the United States. Although no clear correlation between location and genome type can be discerned, these genomes expand our knowledge of mycobacteriophage diversity and enhance our understanding of the roles of mobile elements in viral evolution. Expansion of the number of mycobacteriophages grouped within Cluster A provides insights into the basis of immune specificity in these temperate phages, and we also describe a novel example of apparent immunity theft. The isolation and genomic analysis of bacteriophages by freshman college students provides an example of an authentic research experience for novice scientists.

Bacillus thuringiensis Kurstaki, a bacterium that is a source of biopesticides and a safe simulant for pathogenic Bacillus species, was used to isolate seven unique bacteriophages. The phage genomes were sequenced and ranged in size from 158,100 to 163,019 bp encoding 290-299 genes, and the GC content of ~38% was similar to that of the host bacterium. All phages had terminal repeats 2-3 kb long. Three of the phages encoded tRNAs and three contained a self-splicing intron in the DNA polymerase gene. They were categorized as a single cluster (>60% nucleotide conservation) containing three subclusters (>80% nucleotide conservation), supported by genomic synteny and phylogenetic analysis. Considering the published genomes of phages that infect the genus Bacillus and noting the ability of many of the Bacillus cereus group phages to infect multiple species, a clustering system based on gene content is proposed.

The pectoral spine of catfishes is an antipredator adaptation that can be bound, locked, and rubbed against the cleithrum to produce stridulation sounds. We describe muscle morphology of the pectoral spines and rays in six species in four genera of North American ictalurid catfishes. Since homologies of catfish pectoral muscles have not been universally accepted, we designate them functionally as the spine abductor and adductor and the arrector dorsalis and ventralis. The four muscles of the remaining pectoral rays are the superficial and deep (profundal) abductors and adductors. The large spine abductor and spine adductor are responsible for large amplitude movements, and the smaller arrector dorsalis and arrector ventralis have more specialized functions, that is, spine elevation and depression, respectively, although they also contribute to spine abduction. Three of the four spine muscles were pennate (the abductor and two arrectors), the spine adductor can be pennate or parallel, and ray muscles have parallel fibers. Insertions of pectoral muscles are similar across species, but there is a shift of origins in some muscles, particularly of the superficial abductor of the pectoral rays, which assumes a midline position in Ictalurus and increasingly more lateral placement in Ameiurus (one quarter way out from the midline), and Pylodictis and Noturus (half way out). Coincident with this lateral shift, the attachments of the hypaxial muscle to the ventral girdle become more robust. Comparison with its sister group supports the midline position as basal and lateral migration as derived. The muscles of the pectoral spine are heavier than muscles of the remaining rays in all species but the flathead, supporting the importance of specialized spine functions above typical movement. Further, spine muscles were larger than ray muscles in all species but the flathead catfish, which lives in water with the fastest currents.

Hypercholesterolemia (HC) is an established risk factor for atherosclerosis and vascular endothelial dysfunction. Paradoxically, we and other investigators have found that animals with HCL are more resistant to myocardial ischemia-reperfusion (Isch-Rep) injury. However, the molecular mechanisms underlying this clinically relevant ischemia-resistant phenotype remain poorly understood. To this context, the present study was designed to identify novel molecular mediators for the HC-induced cardioprotection against Isch-Rep injury. Adult male C57BL/6J wild-type (C57BL-WT) mice and homozygous apolipoprotein E knockout (APOE-KO) mice were fed with regular rodent chow. The hearts were isolated and subjected to 20 min of zero-flow global Isch and 30 min of Rep in Langendorff mode. Infarct size and ventricular contractile function were assessed. Blood samples were collected from each mouse after the heart isolation procedure to measure serum total cholesterol (TCL). As summarized in Table 1 , the APOE-KO mice had developed HC, which was accompanied with significantly better post-Isch cardiac contractile function (DF and ±df/dt max ) and smaller infarct size as compared with C57BL-WT control mice. In a parallel series of experiments, heart tissues were collected from C57BL-WT and APOE-KO mice and total tissue lysates were prepared for Western blot analysis. We found significant enhancement in cardiac expression of caveolin 1 (Cav-1) and metallothionein (MT) in APOE-KO mice, whereas caveolin 3 (Cav-3) and T-complex protein 1beta (TCP-1beta) were significantly downregulated under HC. Electron microscopy revealed a selective increase in caveolae density on the endothelial cell membranes of APOE-KO mice. This study has provided the first evidence demonstrating that the remarkable ischemia-resistant phenotype of HC is associated with enhanced expression of two cytoprotective proteins - Cav-1 and MT in the heart. This research has received full or partial funding support from the American Heart Association, AHA National Center. Table 1