Population genomics of the southern Caspian Sea Vobla Rutilus lacustris

Hydrobiologia - The genus Rutilus is widespread in the western and central Palearctic region. In the Caspian Sea, the taxonomic status of different populations of Rutilus lacustris has...     

Fine-scale population genetic structure of Endangered Caspian Sea trout,Salmo caspius: implications for conservation

Hydrobiologia - Many populations of Caspian Sea trout (Salmo caspius)—a nationally endangered species in Iran—have been extirpated or depleted due to anthropogenic impacts. The Lar...     

Molecular determinants of phospholipid synergy in blood clotting

Many regulatory processes in biology involve reversible association of proteins with membranes. Clotting proteins bind to phosphatidylserine (PS) on cell surfaces, but a clear picture of this interaction has yet to emerge. We present a novel explanation for membrane binding by GLA domains of clotting proteins, supported by biochemical studies, solid-state NMR analyses, and molecular dynamics simulations. The model invokes a single "phospho-L-serine-specific" interaction and multiple "phosphate-specific" interactions. In the latter, the phosphates in phospholipids interact with tightly bound Ca(2+) in GLA domains. We show that phospholipids with any headgroup other than choline strongly synergize with PS to enhance factor X activation. We propose that phosphatidylcholine and sphingomyelin (the major external phospholipids of healthy cells) are anticoagulant primarily because their bulky choline headgroups sterically hinder access to their phosphates. Following cell damage or activation, exposed PS and phosphatidylethanolamine collaborate to bind GLA domains by providing phospho-L-serine-specific and phosphate-specific interactions, respectively.     

Air pollution-induced placental epigenetic alterations in early life: a candidate miRNA approach

Particulate matter (PM) exposure during in utero life may entail adverse health outcomes in later-life. Air pollution's adverse effects are known to alter gene expression profiles, which can be regulated by microRNAs (miRNAs). We investigate the potential influence of air pollution exposure in prenatal life on placental miRNA expression. Within the framework of the ENVIRONAGE birth cohort, we measured the expression of six candidate miRNAs in placental tissue from 210 mother-newborn pairs by qRT-PCR. Trimester-specific PM_2.5 exposure levels were estimated for each mother's home address using a spatiotemporal model. Multiple regression models were used to study miRNA expression and in utero exposure to PM_2.5 over various time windows during pregnancy. The placental expression of miR-21 (?33.7%, 95% CI: ?53.2 to ?6.2, P = 0.022), miR-146a (?30.9%, 95% CI: ?48.0 to ?8.1, P = 0.012) and miR-222 (?25.4%, 95% CI: ?43.0 to ?2.4, P = 0.034) was inversely associated with PM_2.5 exposure during the 2nd trimester of pregnancy, while placental expression of miR-20a and miR-21 was positively associated with 1st trimester exposure. Tumor suppressor phosphatase and tensin homolog (PTEN) was identified as a common target of the miRNAs significantly associated with PM exposure. Placental PTEN expression was strongly and positively associated (+59.6% per 5 µg/m³ increment, 95% CI: 26.9 to 100.7, P < 0.0001) with 3rd trimester PM_2.5 exposure. Further research is required to establish the role these early miRNA and mRNA expression changes might play in PM-induced health effects. We provide molecular evidence showing that in utero PM_2.5 exposure affects miRNAs expression as well as its downstream target PTEN.