Avicennia marina (Forssk.) Vierh is distributed in patches along the Farasan archipelago coast and is the most common mangrove species in the Red Sea. However, to date, no studies have been directed towards understanding its genetic variation in the Farasan archipelago. In this investigation, genetic variations within and among natural populations of Avicennia marina in the Farasan archipelago were studied using 15 microsatellite markers. The study found 142 alleles on 15 loci in nine populations. The observed (Ho) and expected (He) heterozygosity values were 0.351 and 0.391, respectively, which are much lower than those of earlier studies on A. marina in the Arabian Gulf. An inbreeding effect from self-pollination might explain its heterozygote deficiency. Population genetic differentiation (FST = 0.301) was similar to other mangrove species. Our findings suggest that the sea current direction and coastal geomorphology might affect genetic dispersal of A. marina. The more isolated populations with fewer connections by sea currents exhibited lower genetic variation and differentiation between populations. The genetic clustering of populations fell into three main groups—Group 1 (populations of Farasan Alkabir Island), Group 2 (populations of Sajid Island), and Group 3 (mix of one population of Farasan Alkabir Island and a population of Zifaf Island). More genetic variation and less genetic differentiation occurred when the population was not isolated and had a direct connection with sea currents. Both of these factors contributed to limited propagule dispersal and produced significant structures among the population. It is expected that the results of this research will be useful in determining policy and species-conservation strategies and in the rehabilitation of A. marina mangrove stands on the Farasan islands in an effort to save this significant natural resource.
Optimization of pluripotent stem cell expansion and differentiation is facilitated by biological tools that permit non-invasive and dynamic monitoring of pluripotency, and the ability to select for an undifferentiated input cell population. Here we report on the generation and characterisation of clonal human embryonic stem (HES3, H9) and human induced pluripotent stem cell lines (UQEW01i-epifibC11) that have been stably modified with an artificial EOS(C3+) promoter driving expression of EGFP and puromycin resistance-conferring proteins. We show that EGFP expression faithfully reports on the pluripotency status of the cells in these lines and that antibiotic selection allows for an efficient elimination of differentiated cells from the cultures. We demonstrate that the extinction of the expression of the pluripotency reporter during differentiation closely correlates with the decrease in expression of conventional pluripotency markers, such as OCT4 (POU5F1), TRA-1-60 and SSEA4 when screening across conditions with various levels of pluripotency-maintaining or differentiation-inducing signals. We further illustrate the utility of these lines for real-time monitoring of pluripotency in embryoid bodies and microfluidic bioreactors.
This study investigated if the well‐reported anti‐tumor effects of resveratrol (RES) is mediated by modulation levels of galectin‐3 (GAL‐3), an anti‐apoptotic lectin that is highly overexpressed in ovarian cancer cells. SKOV3 and OVCAR‐3 OC cells were untreated or incubated with DMOS or increasing concentrations of RES (25, 50, 100 μM) for 72 hr. RES, in a dose‐dependent manner and in both cell lines, induced cell death and inhibited cell migration and invasion It also downregulated Bcl‐2 levels, increased cleaved caspase‐3, and GAL‐3 protein (but not mRNA) levels, suggesting increased breakdown. These effects were associated with reduced levels of p‐NF‐κB P65, p‐IKKα/β, and p‐Akt, major targets of Gal‐3. Further investigation showed that RES enhanced levels of miR‐424‐3p which is able to degrade GAL‐3. Conclusion: Findings of this study suggest that RES induced apoptosis in cancerous cells is associated with increased levels of miR‐424‐3p and reduced levels of GAL‐3.
Practical applications
This study highlights a possible mechanism by which RES could enhance cell death in OC cells and enhances their sensitivity to cisplatin. RES apoptotic effect and enhancement of OC cells to chemotherapy were associated with decreased abundance of GAL‐3, a common cell survival molecule that promotes tumorigenesis and increased transcription of miR‐424‐3p that has the ability to degrade cellular GAL‐3. These findings add a possible new mechanism by which RES acts and opens a window for further research to understand its mechanism of action.
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