Genetic structure of a regionally endangered orchid, the dark red helleborine (Epipactis atrorubens) at the edge of its distribution

Abstract The genetic structure and diversity of species is determined by both current population dynamics and historical processes. Population genetic structure at the edge of the distribution is often expected to differ substantially from populations at the centre, as these edge populations are often small and fragmented. In addition, populations located in regions that have experienced repeated glaciations throughout the Pleistocene, may still carry imprints from the genetic consequences of frequent distribution shifts. Using chloroplast DNA sequences and nuclear microsatellite markers we studied the genetic structure of Epipactis atrorubens at the northern edge of its distribution. Contrary to populations in the centre of the distribution, populations at the northern range are regionally endangered as they are small and disjunct. Sequence data of 2 chloroplast loci and allelic data from 6 nuclear microsatellite markers were obtained from 297 samples from Finland, Estonia and Russia. We sought for genetic indicators of past population processes, such as post-glacial colonisation history of E. atrorubens. As expected, we observed low genetic variation, in terms of numbers of substitutions, haplotypes and alleles, and significant levels of differentiation, especially pronounced in the chloroplast DNA. These features suggest that the edge populations could be prone to extinction

Large-scale assessment of pros and cons of autopsy-derived or tumor-matched tissues as the norms for gene expression analysis in cancers

Normal tissues are essential for studying disease-specific differential gene expression. However, healthy human controls are typically available only in postmortal/autopsy settings. In cancer research, fragments of pathologically normal tissue adjacent to tumor site are frequently used as the controls. However, it is largely underexplored how cancers can systematically influence gene expression of the neighboring tissues. Here we performed a comprehensive pan-cancer comparison of molecular profiles of solid tumor-adjacent and autopsy-derived “healthy” normal tissues. We found a number of systemic molecular differences related to activation of the immune cells, intracellular transport and autophagy, cellular respiration, telomerase activation, p38 signaling, cytoskeleton remodeling, and reorganization of the extracellular matrix. The tumor-adjacent tissues were deficient in apoptotic signaling and negative regulation of cell growth including G2/M cell cycle transition checkpoint. We also detected an extensive rearrangement of the chemical perception network. Molecular targets of 32 and 37 cancer drugs were over- or underexpressed, respectively, in the tumor-adjacent norms. These processes may be driven by molecular events that are correlated between the paired cancer and adjacent normal tissues, that mostly relate to inflammation and regulation of intracellular molecular pathways such as the p38, MAPK, Notch, and IGF1 signaling. However, using a model of macaque postmortal tissues we showed that for the 30 min – 24-hour time frame at 4ºC, an RNA degradation pattern in lung biosamples resulted in an artifact “differential” expression profile for 1140 genes, although no differences could be detected in liver. Thus, such concerns should be addressed in practice

Mechanism of the sulphurisation of phosphines and phosphites using 3-amino-1,2,4-dithiazole-5-thione (Xanthane Hydride)

Contrary to a previous report, the sulfurisation of phosphorus(III) derivatives by 3-amino-1,2,4-dithiazole-5-thione (xanthane hydride) does not yield carbon disulfide and cyanamide as the additional reaction products. The reaction of xanthane hydride with triphenyl phosphine or trimethyl phosphite yields triphenyl phosphine sulfide or trimethyl thiophosphate, respectively, and thiocarbamoyl isothiocyanate which has been trapped with nucleophiles. The reaction pathway involves initial nucleophilic attack of the phosphorus at sulfur next to the thiocarbonyl group of xanthane hydride followed by decomposition of the phosphonium intermediate formed to products. The Hammett -values for the sulfurisation of substituted triphenyl phosphines and triphenyl phosphites in acetonitrile are –1.0. The entropies of activation are very negative (–114 ± 15 J mol–1 K–1) with little dependence on solvent which is consistent with a bimolecular association step leading to the transition state. The negative values of S and values indicate that the rate limiting step of the sulfurisation reaction is formation of the phosphonium ion intermediate which has an early transition state with little covalent bond formation. The site of nucleophilic attack has been also confirmed using computational calculation