Streptococcus agalactiae was isolated from cultured gilthead seabream, Sparus auratus L., and diseased wild Klunzinger's mullet, Liza klunzingeri (Day), in Kuwait Bay, Arabian Gulf. Isolates were catalase negative, β‐haemolytic, Gram‐positive cocci and serogroup B. Experimental infectivity trials with mullet and seabream brain isolates in Nile tilapia, Oreochromis niloticus L., caused 100 and 90% mortality, respectively, within 7 days post‐inoculation indicating virulent S. agalactiae as the bacterial pathogen responsible for the epizootic in Kuwait Bay.

Phylogenetic relationships among Streptococcus agalactiae isolated from piscine, dolphin, bovine and human sources: a dolphin and piscine lineage associated with a fish epidemic in Kuwait is also associated with human neonatal infections in Japan Streptococcus agalactiae, commonly known as group B streptococcus (GBS), is a cause of infectious disease in numerous animal species. This study examined the genetic relatedness of piscine, dolphin and human GBS isolates and bovine GBS reference strains from different geographical regions using serological and molecular serotyping and multilocus sequence typing (MLST) techniques. Piscine isolates originating from Kuwait, Brazil, Israel and the USA were capsular serotype Ia, a serotype previously unreported in GBS isolated from fish. Sequence typing of piscine isolates produced six sequence types (ST-7, ST-257, ST-258, ST-259, ST-260 and ST-261), the latter five representing allelic designations and allelic combinations not previously reported in the S. agalactiae MLST database. Genomic diversity existed between dolphin and piscine GBS isolates from Kuwait and other geographical areas. Piscine GBS isolates from Brazil, Israel, Honduras and the USA appeared to represent a distinct genetic population of strains that were largely unrelated to human and bovine GBS. The Kuwait dolphin and piscine lineage (ST-7, Ia) was also associated with human neonatal infections in Japan. Comparative genomics of piscine, human and bovine GBS could help clarify those genes important for host tropism, the emergence of unique pathogenic clones and whether these hosts act as reservoirs of one another's pathogenic lineages.

Homo-oligomerization of Bax (or Bak) has been hypothesized to be responsible for cell death through the mitochondria-dependent apoptosis pathway. However, partly due to a lack of structural information on the Bax homo-oligomerization and apoptosis inducing domain(s), this hypothesis has remained difficult to test. In this study, we identified a three-helix unit, comprised of the BH3 (helix 2) and BH1 domains (helix 4 and helix 5), as the homo-oligomerization domain of Bax. When targeted to mitochondria, this minimum oligomerization unit induced apoptosis in Bax [Keywords: Bax; homo-oligomerization; apoptotic activity; BH3; Bcl-2 family] Supplemental material is available at http://www.genesdev.org.

BACKGROUNDUnderstanding and managing the evolutionary responses of pests and pathogens to control efforts is essential to human health and survival. Herbicide‐resistant (HR) weeds undermine agricultural sustainability, productivity and profitability, yet the epidemiology of resistance evolution – particularly at landscape scales – is poorly understood. We studied glyphosate resistance in a major agricultural weed, Amaranthus tuberculatus (common waterhemp), using landscape, weed and management data from 105 central Illinois grain farms, including over 500 site‐years of herbicide application records.RESULTSGlyphosate‐resistant (GR) A. tuberculatus occurrence was greatest in fields with frequent glyphosate applications, high annual rates of herbicide mechanism of action (MOA) turnover and few MOAs field−1 year−1. Combining herbicide MOAs at the time of application by herbicide mixing reduced the likelihood of GR A. tuberculatus.CONCLUSIONSThese findings illustrate the importance of examining large‐scale evolutionary processes at relevant spatial scales. Although measures such as herbicide mixing may delay GR or other HR weed traits, they are unlikely to prevent them. Long‐term weed management will require truly diversified management practices that minimize selection for herbicide resistance traits. © 2015 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.

Results of this study do not support the contention that S iniae is a serious public health threat associated with commercially raised fish; rather, it represents a limited risk for older or immunocompromised people who incur puncture wounds while handling and preparing fish.

The balance of selection acting through different fitness components (e.g. fecundity, mating success, survival) determines the potential tempo and trajectory of adaptive evolution. Yet the extent to which the temporal dynamics of phenotypic selection may vary among fitness components is poorly understood. Here, we compiled a database of 3978 linear selection coefficients from temporally replicated studies of selection in wild populations to address this question. Across studies, we find that multi-year selection through mating success and fecundity is stronger than selection through survival, but varies less in direction. We also report that selection through mating success varies more in long-term average strength than selection through either survival or fecundity. The consistency in direction and stronger long-term average strength of selection through mating success and fecundity suggests that selection through these fitness components should cause more persistent directional evolution relative to selection through survival. Similar patterns were apparent for the subset of studies that evaluated the temporal dynamics of selection on traits simultaneously using several different fitness components, but few such studies exist. Taken together, these results reveal key differences in the temporal dynamics of selection acting through different fitness components, but they also reveal important limitations in our understanding of how selection drives adaptive evolution.

This study was conducted to evaluate the effect of dietary levels of distiller’s dried grains with solubles (DDGS) on growth, body composition, hematology, and resistance of Nile tilapia, Oreochromis niloticus, to Streptococcus iniae challenge. Five isocaloric diets containing DDGS at levels of 0, 10, 20, and 40%, and 40% DDGS + lysine (Diets 1–5) as partial replacements of a combination of soybean meal (SBM) and corn meal (CM) on an equal protein basis were fed to juvenile Nile tilapia (9.41 ± 0.14 g) for 10 wk. Fish fed Diet 4 had the lowest weight gain (WG), feed efficiency ratio, protein efficiency ratio (PER), and whole‐body protein. Supplementation of lysine to the 40% DDGS diet (Diet 5) improved WG and PER. Hematological and immunological parameters were not affected by dietary treatment. There were no significant differences among the average number of days to first mortality after S. iniae challenge and cumulative mortality 14 d postchallenge among fish in various treatments. DDGS can be incorporated in tilapia diet at a level of 20% as a substitute for a combination of SBM and CM without affecting their growth performance, body composition, hematological parameters, immune response, and resistance to S. iniae infection.

Chelatable zinc is important in brain function, and its homeostasis is maintained to prevent cytotoxic overload. However, certain pathologic events result in intracellular zinc accumulation in lysosomes and mitochondria. Abnormal lysosomes and mitochondria are common features of the human lysosomal storage disorder known as mucolipidosis IV (MLIV). MLIV is caused by the loss of TRPML1 ion channel function. MLIV cells develop large hyperacidic lysosomes, membranous vacuoles, mitochondrial fragmentation, and autophagic dysfunction. Here, we observed that RNA interference of mucolipin-1 gene (TRPML1) in HEK-293 cells mimics the MLIV cell phenotype consisting of large lysosomes and membranous vacuoles that accumulate chelatable zinc. To show that abnormal chelatable zinc levels are indeed correlated with MLIV pathology, we quantified its concentration in cultured MLIV patient fibroblast and control cells with a spectrofluorometer using N-(6-methoxy-8-quinolyl)-p-toluene sulfonamide fluorochrome. We found a significant increase of chelatable zinc levels in MLIV cells but not in control cells. Furthermore, we quantified various metal isotopes in whole brain tissue of TRPML1 ؊/؊ null mice and wild-type littermates using inductively coupled plasma mass spectrometry and observed that the zinc-66 isotope is markedly elevated in the brain of TRPML1 ؊/؊ mice when compared with controls. In conclusion, we show for the first time that the loss of TRPML1 function results in intracellular chelatable zinc dyshomeostasis. We propose that chelatable zinc accumulation in large lysosomes and membranous vacuoles may contribute to the pathogenesis of the disease and progressive cell degeneration in MLIV patients.Zinc (Zn 2ϩ ) is a redox-inert yet crucial trace element for virtually all organisms. Zn 2ϩ is second to iron in biological trace metal abundance and is known to play an important role in human brain function (1, 2). Some enzymes require Zn 2ϩ as co-factors, but many proteins use it for structural stability and thus are tightly bound (non-chelatable form) (3). A chelatable pool of Zn 2ϩ is present in cells, most notably in glutamatergic vesicles, and gets released at the neuronal synapse during normal and pathological states (4, 5). Because high levels of chelatable Zn 2ϩ or any trace metals produce cellular and mitochondrial toxicity (1, 6, 7), it is imperative that Zn 2ϩ homeostasis is actively maintained inside and outside of the cells. Certain pathological events such as epilepsy, cerebral stroke, and traumatic brain injury result in uncontrolled release and accumulation of chelatable Zn 2ϩ in neurons (1, 8) via voltage-gated or calcium-permeable ion channels (9). Furthermore, endosomes, autophagosomes, and lysosomes, which are critical organelles involved in the recycling and degradation of many proteins, are known compartments where chelatable Zn 2ϩ accumulates upon cellular perturbation (10 -12). Interestingly, chelatable Zn 2ϩ appears to mediate vacuolar formation in primary retinal cells exposed to ethambutol (an anti...