Quantitative trait loci mapping reveals candidate pathways regulating cell cycle duration in \u3cem\u3ePlasmodium falciparum\u3c/em\u3e

Background: Elevated parasite biomass in the human red blood cells can lead to increased malaria morbidity. The genes and mechanisms regulating growth and development of Plasmodium falciparum through its erythrocytic cycle are not well understood. We previously showed that strains HB3 and Dd2 diverge in their proliferation rates, and here use quantitative trait loci mapping in 34 progeny from a cross between these parent clones along with integrative bioinformatics to identify genetic loci and candidate genes that control divergences in cell cycle duration. Results: Genetic mapping of cell cycle duration revealed a four-locus genetic model, including a major genetic effect on chromosome 12, which accounts for 75% of the inherited phenotype variation. These QTL span 165 genes, the majority of which have no predicted function based on homology. We present a method to systematically prioritize candidate genes using the extensive sequence and transcriptional information available for the parent lines. Putative functions were assigned to the prioritized genes based on protein interaction networks and expression eQTL from our earlier study. DNA metabolism or antigenic variation functional categories were enriched among our prioritized candidate genes. Genes were then analyzed to determine if they interact with cyclins or other proteins known to be involved in the regulation of cell cycle. Conclusions: We show that the divergent proliferation rate between a drug resistant and drug sensitive parent clone is under genetic regulation and is segregating as a complex trait in 34 progeny. We map a major locus along with additional secondary effects, and use the wealth of genome data to identify key candidate genes. Of particular interest are a nucleosome assembly protein (PFL0185c), a Zinc finger transcription factor (PFL0465c) both on chromosome 12 and a ribosomal protein L7Ae-related on chromosome 4 (PFD0960c)

Quantifying the impact of phonon scattering on electrical and thermal transport in quantum dots

We report the inclusion of phonon scattering to our recently established numerical package QmeQ for transport in quantum dot systems. This enables straightforward calculations for a large variety of devices. As examples we show (i) transport in a double-dot structure, where energy relaxation is crucial to match the energy difference between the levels, and (ii) the generation of electrical power by contacting cold electric contacts with quantum dot states, which are subjected to heated phonons.Comment: Accepted manuscript for the special volume of the EPJ-ST,dedicated to FQMT1

Theory of Transmission through disordered superlattices

We derive a theory for transmission through disordered finite superlattices in which the interface roughness scattering is treated by disorder averaging. This procedure permits efficient calculation of the transmission thr ough samples with large cross-sections. These calculations can be performed utilizing either the Keldysh or the Landauer-B\"uttiker transmission formalisms, both of which yield identical equations. For energies close to the lowest miniband, we demonstrate the accuracy of the computationally efficient Wannier-function approximation. Our calculations indicate that the transmission is strongly affected by interface roughness and that information about scale and size of the imperfections can be obtained from transmission data.Comment: 12 pages, 6 Figures included into the text. Final version with minor changes. Accepted by Physical Review