Conditioned spin and charge dynamics of a single electron quantum dot

In this article we describe the incoherent and coherent spin and charge dynamics of a single electron quantum dot. We use a stochastic master equation to model the state of the system, as inferred by an observer with access to only the measurement signal. Measurements obtained during an interval of time contribute, by a past quantum state analysis, to our knowledge about the system at any time $t$ within that interval. Such analysis permits precise estimation of physical parameters, and we propose and test a modification of the classical Baum-Welch parameter re-estimation method to systems driven by both coherent and incoherent processes.Comment: 9 pages, 9 figure

Simplified example of the closest derived sarcin–ricin sequences in an alignment

<p><b>Copyright information:</b></p><p>Taken from "Modeling RNA tertiary structure motifs by graph-grammars"</p><p></p><p>Nucleic Acids Research 2007;35(5):1726-1736.</p><p>Published online 21 Feb 2007</p><p>PMCID:PMC1865062.</p><p>© 2007 The Author(s)</p> () Two derived sarcin–ricin motif sequences. () All possible matches (bold underlined) of the two sequences in the alignment. () One structural site in the reference () sequence. The first strand matches in the reference sequence at position 20, and the second strand matches at position 40. For each sequence of the alignment, we choose the positions (bold underlined), among all possible matches, that minimizes the Manhattan distance. () Resulting alignment. The closest matches, in each sequence, are shown in bold-underlined characters

Cross-evolutionary screen for brain-specific ASEs found in human.

<p>Of the 93 mouse candidate ASEs for conserved brain-specificity, 89 had orthologous regions in human. Of these, 62 ASEs gave good data by PCR on 6 human tissue cDNAs: brain, heart, muscle, kidney, liver and lung. The psi values are shown in the heat map; the genes are clustered on both axes according to their psi values. X-axis clustering shows the brain, heart/muscle and liver/kidney/lung have 3 distinct splicing profiles. Y axis clustering groups the genes based on their psi values’ patterns across tissues; the brain-specific ASEs cluster at the bottom of the heat map but the clustering also distinguishes some ASEs in the centre that splice similarly in brain/heart/muscle as distinct from liver/kidney/lung.</p

Switch-like tissue-specific ASEs are conserved in all vertebrates.

<p>RT-PCR was performed on 15 genes across human, mouse and zebrafish. The 9 genes shown have conserved switch-like splicing in all three vertebrate species. Brain-specific splice forms are indicated with a red arrow. The alternative kidney/liver-specific forms are indicated with a double-headed blue arrow. The different, expected and found, PCR sizes for the long and short form of each gene in each species are given in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0125998#pone.0125998.s005" target="_blank">S1 Table</a>.</p

Nine vertebrate brain specific alternative splice events.

<p><b>a. Primary structures of proteins encoded by the 9 human genes with vertebrate conserved brain-specific splicing.</b> Shown are the annotated human proteins with the regions of the nine splice events indicated by red boxes. TM: transmembrane region; β-APP C-ter: C-terminus of the β Amyloid Precursor Protein (pf10515); CAP-Gly: Cytoskeletal-Associated protein (pf00225); HELP: Hydrophibic EMAP-Like Protein (pf03451); WD40: β-transducin repeat (pf00400); SiP: Signal peptide; Ig: Immunoglobulin-like domain (pf00047); FN3: Fibronectin type III domain (pf00041); AT-hook: DNA-binding for A/T-rich regions (pf02178); PHD finger: Plant HomeoDomain (Cys)4-His-(Cys)3 (pf00628). Gene names are labelled with a ¹ if exclusion of the alternatively splice regions directly affects structural domains. Note all ASEs are multiples of 3 nucleotides, thus all the alternative splicing events confer in frame peptide omission or insertion. <b>b. Brain-specific alternative splicing is conserved in vertebrates, and possibly beyond, in microtubule-associated genes.</b> Metazoan genomes in Ensembl were searched for paralogs and orthologs of each target gene and for the presence (yellow) or absence (gray) of potential ASEs (Accession numbers are shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0125998#pone.0125998.s005" target="_blank">S1 Table</a>). Yellow indicates that alternatively spliced mRNAs were detected in EST databases. Orange indicates that there were too few ESTs to conclude. Green indicates the absence of both genomic and EST data. Duplications are indicated by thick lines along with the names of the duplicated genes. An indication of the function of each gene is given on the right.</p

Genomewide screen for brain-specific ASEs in mouse.

<p>PCR primers were designed across all the simple ASEs in the mouse RefSeq collection [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0125998#pone.0125998.ref010" target="_blank">10</a>] and RT-PCR was performed on three mouse tissue cDNA;. 809 PCRs gave good data; the psi values are shown for mouse brain, kidney and liver. The ASEs have been clustered according to the shift between brain and the two other tissues, indicated by the difference in psi values. 93 ASE psi values shifted more than 50% between brain and both of the other tissues (see the top and bottom of the heat map). Numerical data are given in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0125998#pone.0125998.s005" target="_blank">S1 Table</a>.</p

Neural splicing dynamics.

<p><b>a. The 9 conserved brain-specific ASEs shifts during zebrafish embryogenesis.</b> Time-course of splicing of the nine vertebrate brain-specific ASEs during the first two days of zebrafish embryogenesis, spanning 2 to 48 hours post fertilisation (hpf). The red arrows indicate the commencement of expression of the brain-specific AS transcript. <b>b. Splicing of 13 genes pivots from predominantly one AS transcript isoform to the other upon neural differentiation of stem cells between days 6–10.</b> 93 ASEs were assayed by PCR and their psi values were evaluated during neural stem cell differentiation. 56 ASEs gave good data for all time points (see <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0125998#pone.0125998.s005" target="_blank">S1 Table</a>). Chart showing the psi values of 13 ASEs whose psi values shift more than 50% during the time-course.</p

Role of MBNL1 and RBFOX1 in splicing regulation.

<p>(<b>A–C</b>) <b>A.</b> Venn diagram representing the overlap of hits obtained by knocking down MBNL1 and RBFOX1 in the HFN embryonic muscle cell line. In panels <b>B</b> and <b>C</b>, Venn diagrams are presented to illustrate events coregulated by MBNL1 and RBFOX1 that are mis-spliced in embryonic DM1 lines or and DM1 adult samples. The number and identity of the ASEs in each category are indicated. Gene names in bold indicate that the splicing shift for those ASEs occur in the reverse direction to the DM1 mis-splice.</p

Splicing defects in a mouse strain expressing CUG repeats.

<p>Total RNA from muscle tissues of transgenic C57BL6 mice expressing 600 and 1200 CUG-repeats were screened for alternative splicing defects. We interrogated 172 ASEs in genes reported to be susceptible to changes in HSA^LR and MBNL knockout mice <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0107324#pone.0107324-Du1" target="_blank">[14]</a>. Using a false discovery rate threshold (<i>q-</i>value) of 0.05 and |ΔΨ| greater than 5 percentage points, we identified 24 ASEs in CUG1200 (black bars) that are significantly different from WT (white bars). Changes that were also significant in CUG600 (grey bars) are indicated with an asterisk. Results are presented in histograms by order of significance based on <i>q</i>-values.</p

Alternative splicing events co-regulated by MBNL1 and RBFOX1.

<p>Genes in bold are mis-spliced in DM1 tissues.</p><p>Alternative splicing events co-regulated by MBNL1 and RBFOX1.</p