Dominance of Lysobacter sp. in the rhizosphere of two coastal sand dune plant species, Calystegia soldanella and Elymus mollis

Bacterial diversity in the rhizosphere of beach morning glory (Calystegia soldanella) and wild rye (Elymus mollis), two of the major plant species inhabiting the coastal sane dune in Tae-An, Korea, was studied by the analysis of community 16S rRNA gene clones. The amplified rDNA restriction analysis (ARDRA) of the clones using HaeIII exhibited significant differences in the community composition between the two plant species as well as regional differences, but also identified a specific ARDRA pattern that was most common among the clones regardless of plant species. Subsequent sequence analysis indicated that the pattern was that of Lysobacter spp., which is a member of the family Xanthomonadaceae, class Gamma proteobacteria. The Lysobacter clones comprised 50.6% of the clones derived from C. soldanella and 62.5% of those from E. mollis. Other minor patterns included those of Pseudomonas spp., species of Rhizobium, Chryseobacterium spp. and Pantoea spp. among C. soldanella clones, and Pseudomonas sp. and Aeromonas hydrophila among E. mollis clones. It is not yet clear what kind of roles Lysobacter plays in association with sand dune plants, but its universal presence in the rhizosphere, together with the potential of this taxon for antagonistic activity against plant pathogens, suggests that Lysobacter might form a symbiotic relationship with its host plants.     

Evaluation of formulations of Bacillus licheniformis for the biological control of tomato gray mold caused by Botrytis cinerea

Bacillus licheniformis N1, which has previously exhibited potential as a biological control agent, was investigated to develop a biofungicide to control the gray mold of tomato caused by Botrytis cinerea. Various formulations of B. licheniformis N1 were developed using fermentation cultures of the bacteria in Biji medium, and their ability to control gray mold on tomato plants was evaluated. The results of pot experiments led to the selection of the wettable powder formulation N1E, based on corn starch and olive oil, for evaluation of the disease control activity of this bacterium after both artificial infection of the pathogen and natural disease occurrence under production conditions. In plastic-house artificial infection experiments, a 100-fold diluted N1E treatment was found to be the optimum biofungicide spray formulation. This treatment resulted in the significant reduction of symptom development when N1E was applied before Bo. cinerea infection, but not after the infection. Both artificial infection experiments in a plastic house and natural infection experiments under production conditions revealed that the N1E significantly reduced disease severity on tomato plants and flowers. The disease control value of N1E on tomato plants was 90.5% under production conditions, as compared to the 77% conferred by a chemical fungicide, the mixture of carbendazim and diethofencarb (1:1). The prevention of flower infection by N1E resulted in increased numbers of tomato fruits on each plant. N1E treatment also had growth promotion activity, which showed the increased number of tomato fruits compared to fungicide treatment and non-treated control and the increased fruit size compared the non-treated control under production conditions. This study suggests that the corn starch-based formulation of B. licheniformis developed using liquid fermentation will be an effective tool in the biological control of tomato gray mold.     

Determination of functional strength imbalance of the lower extremities

The purposes of this study were (a) to determine whether a significant strength imbalance existed between the left and right or dominant (D) and nondominant (ND) legs and (b) to investigate possible correlations among various unilateral and bilateral closed kinetic chain tests, including a field test, and traditional isokinetic dynamometry used to determine strength imbalance. Fourteen Division I collegiate women softball players (20.2 +/- 1.4 years) volunteered to undergo measures of average peak torque for isokinetic flexion and extension at 60 degrees .s(-1) and 240 degrees .s(-1); in addition, measures of peak and average force of each leg during parallel back squat, 2-legged vertical jump, and single-leg vertical jump and performance in a 5-hop test were examined. Significant differences of between 4.2% and 16.0% were evident for all measures except for average force during single-leg vertical jump between the D and ND limbs, thus revealing a significant strength imbalance. The 5-hop test revealed a significant difference between D and ND limbs and showed a moderate correlation with more sophisticated laboratory tests, suggesting a potential use as a field test for the identification of strength imbalance. The results of this study indicate that a significant strength imbalance can exist even in collegiate level athletes, and future research should be conducted to determine how detrimental these imbalances could be in terms of peak performance for athletes, as well as the implications for injury risk.     

PPARgamma activation induces CD36 expression and stimulates foam cell like changes in rVSMCs

The purpose of the present study was to determine the role of peroxisome proliferator-activated receptor gamma (PPARgamma) activation in smooth muscle cell (SMC) derived form cell formation. Wild and mutant type PPARgamma were delivered by adenovirus then activated with troglitazone. The result of Oil Red O staining and FACS analysis showed that PPARgamma activation induced lipid accumulation in rVSMCs. Furthermore, PPARgamma activation reduced SMC marker genes such as alpha-actin while induced adipocyte differentiation marker genes and lipid metabolism-related genes as evidenced by RT-PCR and fluorescent immunocytochemistry. All these data demonstrate that PPARgamma activation can drive foam cell like change in rVSMCs. Our results strongly suggest that PPARgamma expression induces CD36 expression and adipocyte differentiation gene activation in the process of atherosclerosis and might be one of the crucial events in SMC derived foam cell formation.     

SUMO-specific protease SUSP4 positively regulates p53 by promoting Mdm2 self-ubiquitination

The p53 tumour suppressor has a key role in the control of cell growth and differentiation, and in the maintenance of genome integrity. p53 is kept labile under normal conditions, but in response to stresses, such as DNA damage, it accumulates in the nucleus for induction of cell-cycle arrest, DNA repair or apoptosis. Mdm2 is an ubiquitin ligase that promotes p53 ubiquitination and degradation. Mdm2 is also self-ubiquitinated and degraded. Here, we identified a novel cascade for the increase in p53 level in response to DNA damage. A new SUMO-specific protease, SUSP4, removed SUMO-1 from Mdm2 and this desumoylation led to promotion of Mdm2 self-ubiquitination, resulting in p53 stabilization. Moreover, SUSP4 competed with p53 for binding to Mdm2, also resulting in p53 stabilization. Overexpression of SUSP4 inhibited cell growth, whereas knockdown of susp4 by RNA interference (RNAi) promoted of cell growth. UV damage induced SUSP4 expression, leading to an increase in p53 levels in parallel with a decrease in Mdm2 levels. These findings establish a new mechanism for the elevation of cellular p53 levels in response to UV damage.     

Senescence-associated beta-galactosidase is lysosomal beta-galactosidase

Replicative senescence limits the proliferation of somatic cells passaged in culture and may reflect cellular aging in vivo. The most widely used biomarker for senescent and aging cells is senescence-associated beta-galactosidase (SA-beta-gal), which is defined as beta-galactosidase activity detectable at pH 6.0 in senescent cells, but the origin of SA-beta-gal and its cellular roles in senescence are not known. We demonstrate here that SA-beta-gal activity is expressed from GLB1, the gene encoding lysosomal beta-D-galactosidase, the activity of which is typically measured at acidic pH 4.5. Fibroblasts from patients with autosomal recessive G(M1)-gangliosidosis, which have defective lysosomal beta-galactosidase, did not express SA-beta-gal at late passages even though they underwent replicative senescence. In addition, late passage normal fibroblasts expressing small-hairpin interfering RNA that depleted GLB1 mRNA underwent senescence but failed to express SA-beta-gal. GLB1 mRNA depletion also prevented expression of SA-beta-gal activity in HeLa cervical carcinoma cells induced to enter a senescent state by repression of their endogenous human papillomavirus E7 oncogene. SA-beta-gal induction during senescence was due at least in part to increased expression of the lysosomal beta-galactosidase protein. These results also indicate that SA-beta-gal is not required for senescence.     

Single molecule analysis indicates stimulation of MUTYH by UV-DDB through enzyme turnover

The oxidative base damage, 8-oxo-7,8-dihydroguanine (8-oxoG) is a highly mutagenic lesion because replicative DNA polymerases insert adenine (A) opposite 8-oxoG. In mammalian cells, the removal of A incorporated across from 8-oxoG is mediated by the glycosylase MUTYH during base excision repair (BER). After A excision, MUTYH binds avidly to the abasic site and is thus product inhibited. We have previously reported that UV-DDB plays a non-canonical role in BER during the removal of 8-oxoG by 8-oxoG glycosylase, OGG1 and presented preliminary data that UV-DDB can also increase MUTYH activity. In this present study we examine the mechanism of how UV-DDB stimulates MUTYH. Bulk kinetic assays show that UV-DDB can stimulate the turnover rate of MUTYH excision of A across from 8-oxoG by 4–5-fold. Electrophoretic mobility shift assays and atomic force microscopy suggest transient complex formation between MUTYH and UV-DDB, which displaces MUTYH from abasic sites. Using single molecule fluorescence analysis of MUTYH bound to abasic sites, we show that UV-DDB interacts directly with MUTYH and increases the mobility and dissociation rate of MUTYH. UV-DDB decreases MUTYH half-life on abasic sites in DNA from 8800 to 590 seconds. Together these data suggest that UV-DDB facilitates productive turnover of MUTYH at abasic sites during 8-oxoG:A repair.     

Natal origin and dispersal of problem saltwater crocodiles in the Darwin Harbor,Australia

Management programs that successfully recovered wild saltwater crocodile (Crocodylus porosus) populations in the Northern Territory of Australia did so with an expanding commitment to maintaining public safety. One aspect of the program is the ongoing removal of resident and immigrant crocodiles within Darwin Harbor (since 1979), the main urban center. We determined the likely sources of crocodiles caught as problem animals between 2015–2017 by comparing recently developed methods for population assignment. Depending on the assignment model used, we estimated that between 30% and 50% of crocodiles in Darwin Harbor originated from the Adelaide and Mary rivers, and the Kakadu region east of Darwin, and between 20% and 30% of crocodiles originated from the Finniss, Reynolds, and Daly rivers southwest of Darwin. Saltwater crocodiles occur at particularly high densities in these catchments. The remainder came from a mixture of different sources across the Northern Territory. The most common animals captured were immature (150–180 cm) males that have traveled 100–200 km. We did not identify any relationships between the distance from the inferred origin to Darwin Harbor and the size and sex of the crocodiles, or the year of capture. The targeted removal of crocodiles from specific sites such as Darwin Harbor, near where most people live, improves public safety in the highest risk areas, without compromising abundant source populations in most areas.