Convergence Theorem for Non-commutative Feynman Graphs and Renormalization

We present a rigorous proof of the convergence theorem for the Feynman graphs in arbitrary massive Euclidean quantum field theories on non-commutative R^d (NQFT). We give a detailed classification of divergent graphs in some massive NQFT and demonstrate the renormalizability of some of these theories.Comment: Latex, 71 pages, many postscript figures; v2: Comments on massless case added/corrected in sec.8, refs. adde

Prediction of quantitative phenotypes based on genetic networks: a case study in yeast sporulation

<p>Abstract</p> <p>Background</p> <p>An exciting application of genetic network is to predict phenotypic consequences for environmental cues or genetic perturbations. However, <it>de novo </it>prediction for quantitative phenotypes based on network topology is always a challenging task.</p> <p>Results</p> <p>Using yeast sporulation as a model system, we have assembled a genetic network from literature and exploited Boolean network to predict sporulation efficiency change upon deleting individual genes. We observe that predictions based on the curated network correlate well with the experimentally measured values. In addition, computational analysis reveals the robustness and hysteresis of the yeast sporulation network and uncovers several patterns of sporulation efficiency change caused by double gene deletion. These discoveries may guide future investigation of underlying mechanisms. We have also shown that a hybridized genetic network reconstructed from both temporal microarray data and literature is able to achieve a satisfactory prediction accuracy of the same quantitative phenotypes.</p> <p>Conclusions</p> <p>This case study illustrates the value of predicting quantitative phenotypes based on genetic network and provides a generic approach.</p

Non-Abelian Wilson Surfaces

A definition of non-abelian genus zero open Wilson surfaces is proposed. The ambiguity in surface-ordering is compensated by the gauge transformations.Comment: JHEP Latex, 10 pages, 6 figures; v2, refs and comments added in sec.

A note on correlation functions in AdS_5/SYM_4 correspondence on the Coulomb branch

We compute certain two-point functions in D=4, ${\cal N}=4$, SU(N) SYM theory on the Coulomb branch using SUGRA/SYM duality and find an infinite set of first order poles at masses of order $({\rm Higgs~scale})/(g_{YM} \sqrt{N})$.Comment: 8 pages, 2 figures, latex. v2: typos in Eqs.3,20,23,24 corrected. References adde

Prediction of regulatory elements in mammalian genomes using chromatin signatures

<p>Abstract</p> <p>Background</p> <p>Recent genomic scale survey of epigenetic states in the mammalian genomes has shown that promoters and enhancers are correlated with distinct chromatin signatures, providing a pragmatic way for systematic mapping of these regulatory elements in the genome. With rapid accumulation of chromatin modification profiles in the genome of various organisms and cell types, this chromatin based approach promises to uncover many new regulatory elements, but computational methods to effectively extract information from these datasets are still limited.</p> <p>Results</p> <p>We present here a supervised learning method to predict promoters and enhancers based on their unique chromatin modification signatures. We trained Hidden Markov models (HMMs) on the histone modification data for known promoters and enhancers, and then used the trained HMMs to identify promoter or enhancer like sequences in the human genome. Using a simulated annealing (SA) procedure, we searched for the most informative combination and the optimal window size of histone marks.</p> <p>Conclusion</p> <p>Compared with the previous methods, the HMM method can capture the complex patterns of histone modifications particularly from the weak signals. Cross validation and scanning the ENCODE regions showed that our method outperforms the previous profile-based method in mapping promoters and enhancers. We also showed that including more histone marks can further boost the performance of our method. This observation suggests that the HMM is robust and is capable of integrating information from multiple histone marks. To further demonstrate the usefulness of our method, we applied it to analyzing genome wide ChIP-Seq data in three mouse cell lines and correctly predicted active and inactive promoters with positive predictive values of more than 80%. The software is available at <url>http://http:/nash.ucsd.edu/chromatin.tar.gz</url>.</p

Are M-atrix theory and Maldacena's conjecture related?

We give arguments in the support of a relation between M-atrix theory and Maldacena's conjecture. M-atrix theory conjecture implies the equivalence of 11-D light-cone supergravity and strongly-coupled (0+1)-D SYM. Maldacena's SUGRA/SYM duality conjecture implies, in the one dimensional SYM case, the equivalence between strongly-coupled (0+1)-D SYM and 11-D supergravity compactified on a spatial circle in the formal Seiberg-Sen limit. Using the classical equivalence between 11-D supergravity on a light-like circle and on a spatial circle in the formal Seiberg-Sen limit, we argue that in the (0+1)-D SYM case, the large-N M-atrix theory in the supergravity regime is equivalent to SUGRA/SYM duality.Comment: 10 pages, LATEX; v2: references added; v3: An expanded discussion of the flat space interpretation and some other clarifying remarks added. References and acknowledgments added; v4: Final version, to appear in PL

Detection of single nucleotide variations in expressed exons of the human genome using RNA-Seq

Whole-genome resequencing is still a costly method to detect genetic mutations that lead to altered forms of proteins and may be associated with disease development. Since the majority of disease-related single nucleotide variations (SNVs) are found in protein-coding regions, we propose to identify SNVs in expressed exons of the human genome using the recently developed RNA-Seq technique. We identify 12 176 and 10 621 SNVs, respectively, in Jurkat T cells and CD4+ T cells from a healthy donor. Interestingly, our data show that one copy of the TAL-1 proto-oncogene has a point mutation in 3′ UTR and only the mutant allele is expressed in Jurkat cells. We provide a comprehensive dataset for further understanding the cancer biology of Jurkat cells. Our results indicate that this is a cost-effective and efficient strategy to systematically identify SNVs in the expressed regions of the human genome

Cyclin D1 integrates G9a-mediated histone methylation.

Lysine methylation of histones and non-histone substrates by the SET domain containing protein lysine methyltransferase (KMT) G9a/EHMT2 governs transcription contributing to apoptosis, aberrant cell growth, and pluripotency. The positioning of chromosomes within the nuclear three-dimensional space involves interactions between nuclear lamina (NL) and the lamina-associated domains (LAD). Contact of individual LADs with the NL are dependent upon H3K9me2 introduced by G9a. The mechanisms governing the recruitment of G9a to distinct subcellular sites, into chromatin or to LAD, is not known. The cyclin D1 gene product encodes the regulatory subunit of the holoenzyme that phosphorylates pRB and NRF1 thereby governing cell-cycle progression and mitochondrial metabolism. Herein, we show that cyclin D1 enhanced H3K9 dimethylation though direct association with G9a. Endogenous cyclin D1 was required for the recruitment of G9a to target genes in chromatin, for G9a-induced H3K9me2 of histones, and for NL-LAD interaction. The finding that cyclin D1 is required for recruitment of G9a to target genes in chromatin and for H3K9 dimethylation, identifies a novel mechanism coordinating protein methylation