Cleft Extensions and Quotients of Twisted Quantum Doubles

Given a pair of finite groups $F, G$ and a normalized 3-cocycle $\omega$ of $G$, where $F$ acts on $G$ as automorphisms, we consider quasi-Hopf algebras defined as a cleft extension $\Bbbk^G_\omega\#_c\,\Bbbk F$ where $c$ denotes some suitable cohomological data. When $F\rightarrow \overline{F}:=F/A$ is a quotient of $F$ by a central subgroup $A$ acting trivially on $G$, we give necessary and sufficient conditions for the existence of a surjection of quasi-Hopf algebras and cleft extensions of the type $\Bbbk^G_\omega\#_c\, \Bbbk F\rightarrow \Bbbk^G_\omega\#_{\overline{c}} \, \Bbbk \overline{F}$. Our construction is particularly natural when $F=G$ acts on $G$ by conjugation, and $\Bbbk^G_\omega\#_c \Bbbk G$ is a twisted quantum double $D^{\omega}(G)$. In this case, we give necessary and sufficient conditions that Rep($\Bbbk^G_\omega\#_{\overline{c}} \, \Bbbk \overline{G}$) is a modular tensor category.Comment: LaTex; 14 page

On the trace of the antipode and higher indicators

We introduce two kinds of gauge invariants for any finite-dimensional Hopf algebra H. When H is semisimple over C, these invariants are respectively, the trace of the map induced by the antipode on the endomorphism ring of a self-dual simple module, and the higher Frobenius-Schur indicators of the regular representation. We further study the values of these higher indicators in the context of complex semisimple quasi-Hopf algebras H. We prove that these indicators are non-negative provided the module category over H is modular, and that for a prime p, the p-th indicator is equal to 1 if, and only if, p is a factor of dim H. As an application, we show the existence of a non-trivial self-dual simple H-module with bounded dimension which is determined by the value of the second indicator.Comment: additional references, fixed some typos, minor additions including a questions and some remark

Dynamics of REL, RELA and IRF1 transcription factor expression in U937 macrophages after dioxin exposure

The aryl hydrocarbon receptor (AhR), a ligand- activated transcription factor, participates in a wide range of critical cellular events in response to endogenous signals or xenobiotic chemicals. 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD) is one of the AhR ligands with a very high binding affinity for the AhR. TCDD is the most toxic among the dioxin xenobiotics and induces a broad spectrum of biological responses, including immunotoxicity and cancer. The complex ligand:AhR:ARNT functions as a transcription factor, binding to the dioxin responsive element (DRE) sequences in the regulatory regions of target genes. Macrophages are key regulators of the innate immune response, as well as one of the first types of cells which respond to chemical stress, so the study of the action of TCDD on these cells is important. Putative DREs were predicted using the SITECON software tool in the regulatory regions of the genes encoding transcription factors REL, RELA and IRF1 expressed in macrophages. Nuclear extract and total RNA were isolated from U937 macrophages treated with 10 nM TCDD (or 0.1 % DMSO as a control) for 1, 3 and 6 hours. The binding of the TCDD:AhR:ARNT transcription complex from the nuclear extract with double-stranded oligonucleotides containing the putative DREs was studied by the EMSA. Isolated RNA was used for the study of the TCDD-mediated alteration of gene expression levels using Real-time PCR with SYBR Green I. Obtained data demonstrate the functional activity of DREs in the IRF1, REL, RELA gene promoters via AhR signaling pathway

Hopf algebras and Markov chains: Two examples and a theory

The operation of squaring (coproduct followed by product) in a combinatorial Hopf algebra is shown to induce a Markov chain in natural bases. Chains constructed in this way include widely studied methods of card shuffling, a natural "rock-breaking" process, and Markov chains on simplicial complexes. Many of these chains can be explictly diagonalized using the primitive elements of the algebra and the combinatorics of the free Lie algebra. For card shuffling, this gives an explicit description of the eigenvectors. For rock-breaking, an explicit description of the quasi-stationary distribution and sharp rates to absorption follow.Comment: 51 pages, 17 figures. (Typographical errors corrected. Further fixes will only appear on the version on Amy Pang's website, the arXiv version will not be updated.

Conditional Tek Promoter-Driven Deletion of Arginyltransferase in the Germ Line Causes Defects in Gametogenesis and Early Embryonic Lethality in Mice

Posttranslational protein arginylation mediated by Ate1 is essential for cardiovascular development, actin cytoskeleton functioning, and cell migration. Ate1 plays a role in the regulation of cytoskeleton and is essential for cardiovascular development and angiogenesis—capillary remodeling driven by in-tissue migration of endothelial cells. To address the role of Ate1 in cytoskeleton-dependent processes and endothelial cell function during development, we produced a conditional mouse knockout with Ate1 deletion driven by Tek endothelial receptor tyrosine kinase promoter expressed in the endothelium and in the germ line. Contrary to expectations, Tek-Ate1 mice were viable and had no visible angiogenesis-related phenotypes; however, these mice showed reproductive defects, with high rates of embryonic lethality in the second generation, at stages much earlier than the complete Ate1 knockout strain. While some of the early lethality originated from the subpopulation of embryos with homozygous Tek-Cre transgene—a problem that has not previously been reported for this commercial mouse strain—a distinct subpopulation of embryos had lethality at early post-implantation stages that could be explained only by a previously unknown defect in gametogenesis originating from Tek-driven Ate1 deletion in premeiotic germs cells. These results demonstrate a novel role of Ate1 in germ cell development

Prime movers : mechanochemistry of mitotic kinesins

Mitotic spindles are self-organizing protein machines that harness teams of multiple force generators to drive chromosome segregation. Kinesins are key members of these force-generating teams. Different kinesins walk directionally along dynamic microtubules, anchor, crosslink, align and sort microtubules into polarized bundles, and influence microtubule dynamics by interacting with microtubule tips. The mechanochemical mechanisms of these kinesins are specialized to enable each type to make a specific contribution to spindle self-organization and chromosome segregation

The morphofunctional and biochemical characteristics of opisthorchiasis-associated cholangiocarcinoma in a Syrian hamster model

The validity of experimental models of pathologies is one of the key challenges in translational medicine. Cholangiocarcinoma, or bile duct cancer, ranks second among oncological diseases of the liver. There is a strong association between bile duct cancer and parasitic infestation of the liver caused by trematodes in the family Opisthorchiidae. We have recently demonstrated that cholangiocarcinoma can develop in Syrian hamsters (Mesocricetus auratus) infected by Opisthorchis felineus and administered with dimethylnitrosamine. However, there is still no description of how this experimental model can possibly be used in translational research. The aim of this work was to study the morphological, functional and biochemical characteristics during cholangiocarcinoma development in Syrian hamsters infected by O. felineus and administered with dimethylnitrosamine. The experi­ment lasted 30 weeks with combined exposure to dimethylnitrosamine in drinking water at a dose of 12.5 ppm and a single injection of 50 metacercariae O. felineus. It was shown that the development of cholangiocarcinoma (18 weeks) increased the total number of basophils, eosinophils and monocytes, the relative number of granulocytes, the amount of total and direct bilirubin, and cholesterol and ALT levels, but reduced the relative number of lymphocytes. Based on pathological, morphometric and biochemical analyses, our model has characteristics similar to those in patients with opisthorchiasisassociated cholangiocarcinoma. Thus, this model can be used to test anticancer drugs, to study the mechanisms of cholangiocarcinogenesis and to search for molecular markers for early diagnosis of bile duct cancer

Phosphorylation controls autoinhibition of cytoplasmic linker protein-170

Author Posting. © American Society for Cell Biology, 2010. This article is posted here by permission of American Society for Cell Biology for personal use, not for redistribution. The definitive version was published in Molecular Biology of the Cell 21 (2010): 2661-2673, doi:10.1091/mbc.E09-12-1036.Cytoplasmic linker protein (CLIP)-170 is a microtubule (MT) plus-end-tracking protein that regulates MT dynamics and links MT plus ends to different intracellular structures. We have shown previously that intramolecular association between the N and C termini results in autoinhibition of CLIP-170, thus altering its binding to MTs and the dynactin subunit p150Glued (J. Cell Biol. 2004: 166, 1003–1014). In this study, we demonstrate that conformational changes in CLIP-170 are regulated by phosphorylation that enhances the affinity between the N- and C-terminal domains. By using site-directed mutagenesis and phosphoproteomic analysis, we mapped the phosphorylation sites in the third serine-rich region of CLIP-170. A phosphorylation-deficient mutant of CLIP-170 displays an "open" conformation and a higher binding affinity for growing MT ends and p150Glued as compared with nonmutated protein, whereas a phosphomimetic mutant confined to the "folded back" conformation shows decreased MT association and does not interact with p150Glued. We conclude that phosphorylation regulates CLIP-170 conformational changes resulting in its autoinhibition.This work was supported by National Institutes of Health grant GM-25062 (to G.G.B.); Netherlands Organization for Scientific Research grants (to A. A. and N. G.); a Cancer Genomics Centre grant (to J.v.H.); and Presidential Program of Russian Academy of Sciences and RFBP grant 05-04-4915 (to E.S.N.)

The elegans of spindle assembly

The Caenorhabditis elegans one-cell embryo is a powerful system in which to study microtubule organization because this large cell assembles both meiotic and mitotic spindles within the same cytoplasm over the course of 1 h in a stereotypical manner. The fertilized oocyte assembles two consecutive acentrosomal meiotic spindles that function to reduce the replicated maternal diploid set of chromosomes to a single-copy haploid set. The resulting maternal DNA then unites with the paternal DNA to form a zygotic diploid complement, around which a centrosome-based mitotic spindle forms. The early C. elegans embryo is amenable to live-cell imaging and electron tomography, permitting a detailed structural comparison of the meiotic and mitotic modes of spindle assembly