Evolutionary roles of polyploidization-derived structural variations in the phenotypic diversification of Panax species.

Genomic structural variations (SVs) are widespread in plant and animal genomes and play important roles in phenotypic novelty and species adaptation. Frequent whole genome duplications followed by (re)diploidizations have resulted in high diversity of genome architecture among extant species. In this study, we identified abundant genomic SVs in the Panax genus that are hypothesized to have occurred through during the repeated polyploidizations/(re)diploidizations. Our genome-wide comparisons demonstrated that although these polyploidization-derived SVs have evolved at distinct evolutionary stages, a large number of SV-intersecting genes showed enrichment in functionally important pathways related to secondary metabolites, photosynthesis and basic cellular activities. In line with these observations, our metabolic analyses of these Panax species revealed high diversity of primary and secondary metabolites both at the tissue and interspecific levels. In particular, genomic SVs identified at ginsenoside biosynthesis genes, including copy number variation and large fragment deletion, appear to have played important roles in the evolution and diversification of ginsenosides. A further herbivore deterrence experiment demonstrated that, as major triterpenoidal saponins found exclusively in Panax, ginsenosides provide protection against insect herbivores. Our study provides new insights on how polyploidization-derived SVs have contributed to phenotypic novelty and plant adaptation.

Scutellarin ameliorates ischemia/reperfusion injury­induced cardiomyocyte apoptosis and cardiac dysfunction via inhibition of the cGAS­STING pathway.

Ischemic heart disease is a common cardiovascular disease. Scutellarin (SCU) exhibits protective effects in ischemic cardiomyocytes; however, to the best of our knowledge, the protective mechanism of SCU remains unclear. The present study was performed to investigate the protective effect of SCU on cardiomyocytes after ischemia/reperfusion (I/R) injury and the underlying mechanism. Mice were intraperitoneally injected with SCU (20 mg/kg) for 7 days before establishing the heart I/R injury model. Cardiac function was detected using small animal echocardiography, apoptotic cells were visualized using TUNEL staining, the myocardial infarct area was assessed by 2,3,5-triphenyltetrazolium chloride staining, and the protein levels of cyclic GMP-AMP synthase (cGAS), stimulator of interferon genes (STING), Bcl-2, Bax and cleaved Caspase-3 were detected by western blotting. In in vitro experiments, H9c2 cells were pretreated with SCU, RU.521 (cGAS inhibitor) and H-151 (STING inhibitor), before cell hypoxia/reoxygenation (H/R) injury. The viability of H9c2 cells was detected using a Cell Counting Kit-8 assay, the rate of apoptosis was determined by flow cytometry, and the protein expression levels of cGAS, STING, Bcl-2, Bax and cleaved Caspase-3 were detected by western blotting. It was revealed that SCU ameliorated cardiac dysfunction and apoptosis, and inhibited the activation of the cGAS-STING and Bcl-2/Bax/Caspase-3 signaling pathways in I/R-injured mice. It was also observed that SCU significantly increased cell viability and decreased apoptosis in H/R-induced H9c2 cells. Furthermore, H/R increased the expression levels of cGAS, STING and cleaved Caspase-3, and decreased the ratio of Bcl-2/Bax, which could be reversed by treatment with SCU, RU.521 and H-151. The present study demonstrated that the cGAS-STING signaling pathway may be involved in the regulation of the activation of the Bcl-2/Bax/Caspase-3 signaling pathway to mediate I/R-induced cardiomyocyte apoptosis and cardiac dysfunction, which could be ameliorated by SCU treatment.

Phenotypic and transcriptomic responses of the shade-grown species Panax ginseng to variable light conditions.

BACKGROUND AND AIMS: Elucidating how plant species respond to variable light conditions is important to understand the ecological adaptation to heterogeneous natural habitats. Plant performance and its underlying gene regulatory network have been well documented in sun-grown plants. However, the phenotypic and molecular responses of shade-grown plants under variable light conditions have remained largely unclear. METHODS: We assessed the differences in phenotypic performance between Panax ginseng (shade-grown) and Arabidopsis thaliana (sun-grown) under sunlight, shade and deep-shade conditions. To further address the molecular bases underpinning the phenotypic responses, we compared time-course transcriptomic expression profiling and candidate gene structures between the two species. KEY RESULTS: Our results show that, compared with arabidopsis, ginseng plants not only possess a lower degree of phenotypic plasticity among the three light conditions, but also exhibit higher photosynthetic efficiency under shade and deep-shade conditions. Further comparisons of the gene expression and structure reveal that differential transcriptional regulation together with increased copy number of photosynthesis-related genes (e.g. electron transfer and carbon fixation) may improve the photosynthetic efficiency of ginseng plants under the two shade conditions. In contrast, the inactivation of phytochrome-interacting factors (i.e. absent and no upregulation of the PIF genes) are potentially associated with the observed low degree of phenotypic plasticity of ginseng plants under variable light conditions. CONCLUSIONS: Our study provides new insights into how shade-grown plants respond to variable light conditions. Candidate genes related to shade adaptation in ginseng provide valuable genetic resources for future molecular breeding of high-density planting crops.

Bioinformatics Analysis of the MicroRNA-Metabolic Gene Regulatory Network in Neuropathic Pain and Prediction of Corresponding Potential Therapeutics.

Neuropathic pain (NP) involves metabolic processes that are regulated by metabolic genes and their non-coding regulator genes such as microRNAs (miRNAs). Here, we aimed at exploring the key miRNA signatures regulating metabolic genes involved in NP pathogenesis. We downloaded NP-related data from public databases and identified differentially expressed microRNAs (miRNAs) and mRNAs through differential gene expression analysis. The miRNA target prediction was performed, and integration with the differentially expressed metabolic genes (DEMGs) was used for constructing the miRNA-DEMG network. Subsequently, functional enrichment analysis and protein-protein interaction (PPI) analysis were performed to explore the role of DEMGs in the regulatory network. The drug prediction was performed based on the DEMGs in the miRNA-DEMG network. A total of 8251 differentially expressed mRNAs (4193 upregulated and 4058 downregulated), and 959 differentially expressed miRNAs (455 upregulated and 504 downregulated) were identified. Moreover, after target gene prediction, a miRNA-DEMG network composed of 22 miRNAs and 113 mRNAs was constructed. The network was constituted of 135 nodes and 236 edges. We found that DEMGs in the network were mainly enriched in metabolic pathways and metabolic processes. A total of 1200 drugs were predicted as potential therapeutics for NP based on the differentially expressed genes, while 170 drugs were predicted for the DEMGs in the miRNA-DEMG network. Conclusively, our study predicted drugs that may be effective against the metabolic changes induced by miRNA dysregulation in NP. This information will help further reveal the pathological mechanism of NP and provide more treatment options for NP patients.

Left ventricular geometry transition in hypertensive patients with heart failure with preserved ejection fraction.

AIMS: Heart failure with preserved ejection fraction (HFpEF) develops in response to hypertensive left ventricular (LV) hypertrophy and is associated with increased cardiovascular events. Although the progression to systolic heart failure is a known consequence of LV hypertrophy and HFpEF, few data are available on the LV geometry change and frequency of deterioration to systolic dysfunction in this population. METHODS AND RESULTS: We evaluated the baseline and follow-up characteristics in 680 patients with LV hypertrophy and HFpEF in this prospective cohort study. The primary endpoint was 5 year all-cause mortality. The changes of LV geometry and heart failure transition were analysed. Systolic dysfunction [left ventricular ejection fraction (LVEF) < 50%] occurred in 182 patients (26.8%) during a 5 year follow-up. Patients with LVEF deterioration were associated with a lower survival rate. Beta-blocker prescription was a protective factor for preserved LVEF. And concentric LV geometry shifted to eccentric hypertrophy was uncommon (10.6%) during a 5 year follow-up. CONCLUSIONS: A quarter of patients with hypertensive LV hypertrophy and HFpEF progresses to systolic dysfunction during a 5 year follow-up, which was accompanied by poor clinical outcomes. And beta-blocker therapy might play a protective role for preserved LVEF in this population.

Concerted and birth-and-death evolution of 26S ribosomal DNA in Camellia L.

BACKGROUND AND AIMS: The ribosomal DNA (rDNA) gene family, encoding ribosomal RNA (rRNA), has long been regarded as an archetypal example illustrating the model of concerted evolution. However, controversy is arising, as rDNA in many eukaryotic species has been proved to be polymorphic. Here, a metagenomic strategy was applied to detect the intragenomic polymorphism as well as the evolutionary patterns of 26S rDNA across the genus Camellia. METHODS: Degenerate primer pairs were designed to amplify the 26S rDNA fragments from different Camellia species. The amplicons were then paired-end sequenced on the Illumina MiSeq platform. KEY RESULTS: An extremely high level of rDNA polymorphism existed universally in Camellia. However, functional rDNA was still the major component of the family, and was relatively conserved among different Camellia species. Sequence variations mainly came from rRNA pseudogenes and favoured regions that are rich in GC. Specifically, some rRNA pseudogenes have existed in the genome for a long time, and have even experienced several expansion events, which has greatly enriched the abundance of rDNA polymorphism. CONCLUSIONS: Camellia represents a group in which rDNA is subjected to a mixture of concerted and birth-and-death evolution. Some rRNA pseudogenes may still have potential functions. Conversely, when released from selection constraint, they can evolve in the direction of decreasing GC content and structural stability through a methylation-induced process, and finally be eliminated from the genome.

High Genetic Diversity With Weak Phylogeographic Structure of the Invasive Spartina alterniflora (Poaceae) in China.

Biological invasion represents a global issue of concern due to its large negative impacts on native ecosystems and society. Elucidating the evolutionary history and genetic basis underpinning invasiveness is critical to understanding how alien species invade and adapt to novel environments. Smooth cordgrass (Spartina alterniflora, 2n = 6x = 62) is a notorious invasive species that causes heavily negative effects on native ecosystems worldwide. Here we addressed the evolutionary mechanisms underlying the invasion and dispersal history of this species along the China coast in the past decades. We employed nine microsatellites and three chloroplast fragments to investigate phylogeographic structure and genetic diversity of 11 native US and 11 invasive Chinese S. alterniflora populations. Demographic history simulation was also performed for both the native and invasive populations, respectively. Comparative genetic analyses of these natural populations revealed that although all the Chinese populations were introduced only once, high level of genetic diversity with weak geographic structure was observed. In particular, both the genetic features and mathematical simulation illustrated very recent population expansion in the Chinese populations. We found that genetic variants identified in native US populations were mixed in the Chinese populations, suggesting the recombination of these original variants during the invasion process. These genetic attributes indicate that Chinese populations might not have experienced a genetic bottleneck during the invasion process. High genetic diversity and genetic admixture might have contributed to the success of invasion of S. alterniflora in China. Our study provides a framework of how the smooth cordgrass spreads along the China coast as well as its potential genetic mechanisms underlying the invasion.

Effects of parental genetic divergence on gene expression patterns in interspecific hybrids of Camellia.

BACKGROUND: The merging of two divergent genomes during hybridization can result in the remodeling of parental gene expression in hybrids. A molecular basis underling expression change in hybrid is regulatory divergence, which may change with the parental genetic divergence. However, there still no unanimous conclusion for this hypothesis. RESULTS: Three species of Camellia with a range of genetic divergence and their F1 hybrids were used to study the effect of parental genetic divergence on gene expression and regulatory patterns in hybrids by RNA-sequencing and allelic expression analysis. We found that though the proportion of differentially expressed genes (DEGs) between the hybrids and their parents did not increase, a greater proportion of DEGs would be non-additively (especially transgressively) expressed in the hybrids as genomes between the parents become more divergent. In addition, the proportion of genes with significant evidence of cis-regulatory divergence increased, whereas with trans-regulatory divergence decreased with parental genetic divergence. CONCLUSIONS: The discordance within hybrid would intensify as the parents become more divergent, manifesting as more DEGs would be non-additively expressed. Trans-regulatory divergence contributed more to the additively inherited genes than cis, however, its contribution to expression difference would be weakened as cis mutations accumulated over time; and this might be an important reason for that the more divergent the parents are, the greater proportion of DEGs would be non-additively expressed in hybrid.

Acidic Preconditioning Protects Against Ischemia-Reperfusion Lung Injury Via Inhibiting the Expression of Matrix Metalloproteinase 9.

BACKGROUND: Acidic preconditioning (APC) has been demonstrated to protect against ischemia-reperfusion (IR)-induced lung injury, which could occur during lung transplantation or cardiopulmonary bypass. However, the pathophysiological mechanisms underlying IR lung injury and APC protection are not completely understood. The key factors responsible for the protective effects of APC are not clear. In this study, bioinformatics was used to predict the potential key factor in IR lung injury and explore the important mediator of the APC protective effect in IR lung injury. METHODS: First, we screened GSE6730, which is related to both lung injury and IR in Gene Expression Omnibus, and STRING was used later to select the genes in GSE6730 needed in the future. Animal models were established and classified to validate the effect of matrix metalloproteinase 9 (MMP-9) on lung injury after IR by adding a selective inhibitor (4-phenoxyphenylsulfonyl) methylthiirane, MMP-9 inhibitor. Next, for better understanding of APC inhibition of the expression of MMP-9 in lung injury, assessment of lung tissues, Western blot analysis, and RNA extraction and reverse transcription quantitative polymerase chain reaction were conducted. RESULTS: MMP-9 was identified to be overexpressed after IR according to the analysis on GSE67370. MMP-9 was an unknown gene in relation to acute lung injury and found to be associated with interleukin (IL)-1B, IL-6, and IL-8. The expressions of these inflammatory factors, including MMP-9, were all elevated in IR. Furthermore, lung injury was ameliorated, and the level of MMP-9 was lower when an MMP-9 inhibitor, (4-phenoxyphenylsulfonyl) methylthiirane, was added. Compared with group IR, APC reversed the ischemia-induced lung injury, and the level of MMP-9 was lower, and the concentrations of IL-1ß, IL-6, and IL-8 were decreased. CONCLUSIONS: Our findings reveal a novel mechanism indicating that IR induces higher expression of MMP-9 in lung injury by increasing the expression of inflammation-related factors. APC might protect against IR lung injury by inhibiting the expression of MMP-9.

PPARγ agonist use and recurrence of atrial fibrillation after successful electrical cardioversion.

Inflammation is associated with atrial fibrillation (AF), and peroxisome proliferator-activated receptor-gamma (PPARγ) agonists have anti-inflammatory properties. We tested whether pioglitazone reduced AF recurrence after electrical cardioversion (EC) by modifying systemic inflammation. In this randomized and prospective trial, patients with persistent AF and type 2 diabetes mellitus were randomized into a pioglitazone group (n=48) or a control group (n=49) before EC. Treatment was continued for 3 months or until AF recurred. Serum inflammatory markers [high sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6) and tumour necrosis factor-α (TNF-α)] were measured at baseline and follow-up. During the 3-month follow-up, AF recurred in 22 (45.8%) patients of the pioglitazone-treated and 24 (49.0%) patients of the control group (P=0.756). However, the 3 inflammatory markers were significantly lowered with pioglitazone treatment during follow-up. Cox proportional hazards regression models showed that the predictors of recurrence included AF history (relative risk RR 1.002, 95% CI 1.003-1.061, P =0.037) and the left atrial diameter (RR 1.131, 95% CI 1.029-1.242, P = 0.010). In conclusion, while reducing some inflammatory markers, the PPARγ agonist pioglitazone did not affect the recurrence of AF after EC.

Rapamycin Inhibits Cardiac Hypertrophy by Promoting Autophagy via the MEK/ERK/Beclin-1 Pathway.

Rapamycin, also known as sirolimus, is an antifungal agent and immunosuppressant drug used to prevent organ rejection in transplantation. However, little is known about the role of rapamycin in cardiac hypertrophy and the signaling pathways involved. Here, the effect of rapamycin was examined using phenylephrine (PE) induced cardiomyocyte hypertrophy in vitro and in a rat model of aortic banding (AB) - induced hypertrophy in vivo. Inhibition of MEK/ERK signaling reversed the effect of rapamycin on the up-regulation of LC3-II, Beclin-1 and Noxa, and the down-regulation of Mcl-1 and p62. Silencing of Noxa or Beclin-1 suppressed rapamycin-induced autophagy, and co-immunoprecipitation experiments showed that Noxa abolishes the inhibitory effect of Mcl-1 on Beclin-1, promoting autophagy. In vivo experiments showed that rapamycin decreased AB-induced cardiac hypertrophy in a MEK/ERK dependent manner. Taken together, our results indicate that rapamycin attenuates cardiac hypertrophy by promoting autophagy through a mechanism involving the modulation of Noxa and Beclin-1 expression by the MEK/ERK signaling pathway.

Resveratrol-induced autophagy promotes survival and attenuates doxorubicin-induced cardiotoxicity.

Resveratrol (RSV) has many biological effects, including antitumor and antiviral activities, and vascular protection. Recent studies have suggested that RSV exerts its antitumor effects through induction of autophagy by an unknown mechanism. Doxorubicin (DOX) is a wide spectrum antitumor drug, but its clinical application is limited by its cardiotoxicity. This study evaluated whether the manipulation of autophagy could attenuate the cardiotoxic effects of DOX in vitro as well as in a rat model of DOX-induced cardiotoxicity. We found that DOX induced H9C2 cell apoptosis by inhibiting AMPK activation and promoting pro-apoptotic protein expression through p38MAPK/p53 signaling. RSV-treated H9C2 cells showed increased autophagy through the AMPK/mTOR/Ulk1 pathway. When DOX and RSV were combined, apoptosis was decreased, despite a slight increase in the autophagy ratio. The same result was observed in the rat model of DOX-induced cardiotoxicity. Injection with DOX or RSV alone, or in combination, for a week, resulted in a reduced apoptotic ratio in the combination group compared with the DOX alone group. Our results strongly indicate that this co-treatment strategy with RSV can attenuate the cardiotoxic effects of DOX. Our findings may have important clinical implications.

Connective tissue growth factor: a predictor of recurrence after catheter ablation in patients with nonparoxysmal atrial fibrillation.

BACKGROUND: Although catheter ablation can effectively eliminate atrial fibrillation (AF), the progression of atrial remodeling increases the risk of recurrence. We, therefore, examined the possibility of determining the postablation prognosis of patients with AF using biomarkers of atrial structural remodeling and serum connective tissue growth factor (CTGF) level, and measured its changes after catheter ablation. METHODS: Subjects were 400 consecutive patients (308 with paroxysmal AF and 92 with nonparoxysmal AF [persistent and long-standing persistent AF]) who underwent catheter ablation for drug-resistant AF. Serum CTGF levels were measured before and 2 months after ablation. RESULTS: During the follow-up period of 20.5 ± 6.9 (8-30) months, 61 patients (66%) with nonparoxysmal AF and 95 patients (31%) with paroxysmal AF had recurrence after catheter ablation. Recurrence was associated with higher "baseline CTGF level" in patients with nonparoxysmal AF (936.5 ± 93.1 ng/mL vs 746.3 ± 56.9 ng/mL, P = 0.007) instead of patients with paroxysmal AF (851.6 ± 97.6 ng/mL vs 807.6 ± 99.1 ng/mL, P = 0.921). In nonparoxysmal AF, the recurrence subgroup also had larger left atrial diameter (LAD; 47.1 ± 5.2 mm vs 39.5 ± 4.3 mm, P = 0.035) compared with the nonrecurrence subgroup, and "baseline serum CTGF" and LAD were shown to be independent predictors for postablation recurrence by a Cox proportional hazards model. However, the 2-month postablation elevations of CTGF in patients with recurrence were not significantly different from that in patients without recurrence in nonparoxysmal AF. CONCLUSION: Our finding indicates that "baseline serum CTGF level" is an independent predictor for recurrence in patients with nonparoxysmal AF following catheter ablation. Two-month postablation elevation in CTGF has no association with recurrence.

New aspects of HERG K⁺ channel function depending upon cardiac spatial heterogeneity.

HERG K(+) channel, the genetic counterpart of rapid delayed rectifier K(+) current in cardiac cells, is responsible for many cases of inherited and drug-induced long QT syndromes. HERG has unusual biophysical properties distinct from those of other K(+) channels. While the conventional pulse protocols in patch-clamp studies have helped us elucidate these properties, their limitations in assessing HERG function have also been progressively noticed. We employed AP-clamp techniques using physiological action potential waveforms recorded from various regions of canine heart to study HERG function in HEK293 cells and identified several novel aspects of HERG function. We showed that under AP-clamp IHERG increased gradually with membrane repolarization, peaked at potentials around 20-30 mV more negative than revealed by pulse protocols and at action potential duration (APD) to 60%-70% full repolarization, and fell rapidly at the terminal phase of repolarization. We found that the rising phase of IHERG was conferred by removal of inactivation and the decaying phase resulted from a fall in driving force, which were all determined by the rate of membrane repolarization. We identified regional heterogeneity and transmural gradient of IHERG when quantified with the area covered by IHERG trace. In addition, we observed regional and transmural differences of IHERG in response to dofetilide blockade. Finally, we characterized the influence of HERG function by selective inhibition of other ion currents. Based on our results, we conclude that the distinct biophysical properties of HERG reported by AP-clamp confer its unique function in cardiac repolarization thereby in antiarrhythmia and arrhythmogenesis.

Beneficial effects of pioglitazone on atrial structural and electrical remodeling in vitro cellular models.

It has been demonstrated that atrial remodeling contributes toward atrial fibrillation (AF) maintenance and angiotensin II (AngII) is involved in the pathogenesis of atrial remodeling. Peroxisome proliferator-activated receptor-γ (PPAR-γ) agonists have been shown to inhibit atrial remodeling. However, the underlying mechanisms are poorly understood. In the present study we investigated the regulating effects of PPAR-γ agonist on AngII-induced atrial structural and electrical remodeling in vitro cellular models. The effects of pioglitazone on AngII-induced connective tissue growth factor (CTGF) expression and cell proliferation were assessed in primary-cultured mouse atrial fibroblasts. The influences of pioglitazone on AngII-induced L-type calcium channel (ICa-L) α1c expression and current density were evaluated in atrial myocytes (HL-1). Pioglitazone attenuated AngII-induced CTGF expression and proliferation in atrial fibroblasts, and pioglitazone also inhibited the expression or phosphorylation of AngII-induced transforming growth factor-ß1 (TGF-ß1), tumor necrosis factor receptor associated factor 6 (TRAF6), TGF-ß-associated kinase 1 (TAK1) and Smad2/3. In HL-1 cells, pioglitazone suppressed AngII-induced ICa-L α1c expression and current density as well as CAMP responsive element binding protein (CREB) phosphorylation. Besides, pioglitazone inhibited AngII-induced production of AngII type I receptor (AT1R) and downregulation of PPAR-γ in both atrial fibroblasts and HL-1 cells. In conclusion, Pioglitazone suppresses AngII-induced CTGF expression and proliferation in atrial fibroblasts, which might be at least in part related with its inhibitory effects on TGF-ß1/Smad2/3 and TGF-ß1/TRAF6/TAK1 signaling pathways. Moreover, pioglitazone also attenuates AngII-induced ICa-L remodeling in HL-1 cells, which might be at least in part associated with its inhibitory effect on CREB phosphorylation. It is suggested that PPAR-γ agonist may have potential applications in preventing atrial remodeling.

Resveratrol attenuates doxorubicin-induced cardiomyocyte apoptosis in lymphoma nude mice by heme oxygenase-1 induction.

Doxorubicin (DOX) has been used in a variety of human malignancies for decades, in particular of lymphoma. But increased cardiomyocyte apoptosis has been implicated in its cardiotoxicity. Resveratrol (RES) generates cardiovascular protective effects by heme oxygenase-1(HO-1)-mediated mechanism. The present study was designed to determine whether RES protected cardiomyocyte against apoptosis through induction of HO-1 in lymphoma nude mouse in vivo. After being developed into lymphoma model, 40 male Balb/c nude mice were randomized to one of the following four treatments (10 mice per group): control, DOX, DOX + RES and DOX + RES + HO-1 inhibitor (zinc protoporphyrin IX, ZnPP). The results showed that DOX injection markedly decreased the body weight, the heart weight and the ratio of heart weight to body weight, but inversely increased cardiomyocyte apoptosis and the level of serum lactate dehydrogenase and creatine kinase. Moreover, DOX injection attenuated HO-1 expression and enzymatic activity as well as increased P53 expression, modulated Bcl-2/Bax expression and enhanced caspase 3 activity. These cardiotoxic effects of DOX were ameliorated by its combination with RES. However, the protective effects of RES were reversed by the addition of ZnPP. Taken together, it is concluded that HO-1 plays a core role for protective action of RES in DOX-induced cardiomyocyte apoptosis in lymphoma nude mice.

[Study of bacteria-lysis abilities and growth conditions of 4 Bdellovibrio].

Bdellovibrio can lyse pathogenic bacteria and clean up waters. 4 strains of Bdellovibrio sp., designated Bh04-4, Bh04-41a, Bh04-A + and Bh04-1f, were isolated from seawaters used Bh04 as host bacterium. After confirmation to be Bdellovibrio sp. by electron microscopy and specific PCR method, their growth conditions and lytic ability on 61 bacteria from various sources were performed. Results showed that all four Bdellovibrio grew in salinity in the range of between 1% and 3%, with 3% salinity being the most suitable one. They grew in the range of temperature from 15 to 30 degrees C, with 20 - 25 degrees C as their best growth temperature. These four Bdellovibrio only grew on live host bacteria rather than the dead ones. When 61 strains of bacteria were used as hosts, Bh04-4 lysed 21 strains, corresponding to 34.4% of lysis ability (21/61), Bh04-41a lysed 24 strains (39.3% lysis ability), Bh04-A + lysed 40 strains (65.6% lysis ability) and Bh04-1f 43 strains (70.5% lysis ability). Taken all four Bdellovibrio together, they lysed 55 out of 61 strains, amounting to 90.2% lysis ability. Results fully demonstrate the potential application of Bdellovibrio in lysing pathogenic bacteria from the marine environments.

Fitness estimation through performance comparison of F1 hybrids with their parental species Oryza rufipogon and O. sativa.

BACKGROUND AND AIMS: Introgression of crop genes into populations of wild relatives has important implications for germplasm conservation as well as for the persistence of novel transgenes in wild populations. Studies of hybrid fitness can be used to evaluate the potential for introgression to occur following episodes of interspecific hybridization. METHODS: This study estimated relative fitness of interspecific hybrids through performance comparison of F(1) hybrids with their parental species, a cultivated rice (Oryza sativa) Minghui-63 and perennial common wild rice (O. rufipogon) under the cultivation conditions. KEY RESULTS: Compared with their parents, the hybrids had the lowest values of seedling survival ability, pollen viability and seed production; intermediate values of seed germination, spikelet production and flag leaf areas; and the highest values of plant height, number of tillers and panicles. The hybrids performed poorly at the stage of sexual reproduction, although they had a slightly higher hybrid vigour at the vegetative growth stage and better tillering ability than their wild parent. There were no significant differences in composite fitness across the whole life-history between the hybrids and their wild parental species. CONCLUSIONS: Rice genes, including transgenes, might persist in wild rice populations through vegetative and sexual reproduction. Further studies are needed to examine whether the extent of gene flow from rice is sufficiently significant to influence genetic diversity in wild populations of O. rufipogon, a species that has become endangered in some regions of south-east Asia.

Gene flow from cultivated rice (Oryza sativa) to its weedy and wild relatives.

BACKGROUND AND AIMS: Transgene escape through gene flow from genetically modified (GM) crops to their wild relative species may potentially cause environmental biosafety problems. The aim of this study was to assess the extent of gene flow between cultivated rice and two of its close relatives under field conditions. METHODS: Experiments were conducted at two sites in Korea and China to determine gene flow from cultivated rice (Oryza sativa L.) to weedy rice (O. sativa f. spontanea) and common wild rice (O. rufipogon Griff.), respectively, under special field conditions mimicking the natural occurrence of the wild relatives in Asia. Herbicide resistance (bar) and SSR molecular finger printing were used as markers to accurately determine gene flow frequencies from cultivated rice varieties to their wild relatives. KEY RESULTS: Gene flow frequency from cultivated rice was detected as between approx. 0.011 and 0.046 % to weedy rice and between approx. 1.21 and 2.19 % to wild rice under the field conditions. CONCLUSIONS: Gene flow occurs with a noticeable frequency from cultivated rice to its weedy and wild relatives, and this might cause potential ecological consequences. It is recommended that isolation zones should be established with sufficient distances between GM rice varieties and wild rice populations to avoid potential outcrosses. Also, GM rice should not be released when it has inserted genes that can significantly enhance the ecological fitness of weedy rice in regions where weedy rice is already abundant and causing great problems.