Dynkin Diagrams and Integrable Models Based on Lie Superalgebras

An analysis is given of the structure of a general two-dimensional Toda field theory involving bosons and fermions which is defined in terms of a set of simple roots for a Lie superalgebra. It is shown that a simple root system for a superalgebra has two natural bosonic root systems associated with it which can be found very simply using Dynkin diagrams; the construction is closely related to the question of how to recover the signs of the entries of a Cartan matrix for a superalgebra from its Dynkin diagram. The significance for Toda theories is that the bosonic root systems correspond to the purely bosonic sector of the integrable model, knowledge of which can determine the bosonic part of the extended conformal symmetry in the theory, or its classical mass spectrum, as appropriate. These results are applied to some special kinds of models and their implications are investigated for features such as supersymmetry, positive kinetic energy and generalized reality conditions for the Toda fields. As a result, some new families of integrable theories with positive kinetic energy are constructed, some containing a mixture of massless and massive degrees of freedom, others being purely massive and supersymmetric, involving a number of coupled sine/sinh-Gordon theories.Comment: 31 pages; plain TeX, macros included; 5 main Figs., more in tables; v2: minor but confusing inaccuracy corrected in statement of one proposition (already corrected in published version

Super-W(infinity) Asymptotic Symmetry of Higher-Spin AdS(3) Supergravity

We consider (2+1)-dimensional (N, M)-extended higher-spin anti-de Sitter supergravity and study its asymptotic symmetries. The theory is described by the Chern-Simons action based on a real, infinite-dimensional higher-spin superalgebra. We specify consistent boundary conditions on the higher-spin super-gauge connection corresponding to asymptotically anti-de Sitter spacetimes. We then determine the residual gauge transformations that preserve these asymptotic conditions and compute their Poisson bracket algebra. We find that the asymptotic symmetry is enhanced from the higher-spin superalgebra to some (N,M)-extended super-W(infinity) nonlinear superalgebra. The latter has the same classical central charge as pure Einstein gravity. Special attention is paid to the (1,1)-case. Truncation to the bosonic sector yields the previously found W(infinity) algebra, while truncation to the underlying finite-dimensional superalgebra reproduces the N-extended superconformal algebra (in its nonlinear version for N>2). We discuss string theory realization of these higher-spin anti-de Sitter supergravity theories as well as relations to previous treatments of super-W(infinity) in the literature.Comment: References added. (N>2)-Extended supersymmetric models argued to be rigid with respect to lambda-deformation. Comments on G(3)-case adde

Defining the mode, energetics and specificity with which a macrocyclic hexaoxazole binds to human telomeric G-quadruplex DNA

Oxazole-containing macrocycles represent a promising class of anticancer agents that target G-quadruplex DNA. We report the results of spectroscopic studies aimed at defining the mode, energetics and specificity with which a hexaoxazole-containing macrocycle (HXDV) binds to the intramolecular quadruplex formed by the human telomeric DNA model oligonucleotide d(T2AG3)4 in the presence of potassium ions. HXDV binds solely to the quadruplex nucleic acid form, but not to the duplex or triplex form. HXDV binds d(T2AG3)4 with a stoichiometry of two drug molecules per quadruplex, with these binding reactions being coupled to the destacking of adenine residues from the terminal G-tetrads. HXDV binding to d(T2AG3)4 does not alter the length of the quadruplex. These collective observations are indicative of a nonintercalative ‘terminal capping’ mode of interaction in which one HXDV molecule binds to each end of the quadruplex. The binding of HXDV to d(T2AG3)4 is entropy driven, with this entropic driving force reflecting contributions from favorable drug-induced alterations in the configurational entropy of the host quadruplex as well as in net hydration. The ‘terminal capping’ mode of binding revealed by our studies may prove to be a general feature of the interactions between oxazole-containing macrocyclic ligands (including telomestatin) and intramolecular DNA quadruplexes

Effects of histone deacetylase inhibitor FR901228 on expression level of telomerase reverse transcriptase in oral cancer

We speculated whether or not the expression level of telomerase reverse transcriptase (hTERT) would be modulated by agents targeting epigenetics in oral cancer cell lines. Although hTERT is known to be targeted by epigenetic changes, it remains unclear how chemoagents targeting epigenetics work on hTERT transcription. In the present study, the epigenetic effects of histone deacetylase (HDAC) inhibitor FR901228 on hTERT transcription were analysed by RT-PCR in oral cancer cell lines. The mRNA expression of hTERT was upregulated after exposure to FR901228 in hTERT-negative Hep2 cells, even in the hTERT highly expressed SAS and KB cells. Moreover, co-treatment of protein synthesis inhibitor cycloheximide (CHX) resulted in the induction of hTERT transcription by FR901228. This suggests that the induction of hTERT by FR901228 requires de novo protein synthesis to some extent and is more likely a direct than an indirect effect on epigenetic changes such as histone acetylation / deacetylation. We further examined the effect of FR901228 on c-myc protein, which is one of the main hTERT transcription activators. FR901228 repressed c-myc protein only in the absence of CHX, dependent of the enhancement of de novo protein synthesis. Our results indicate that c-myc protein is repressed indirectly by FR901228 but may not contribute FR901228-induced hTERT transcription. The present study showed that the HDAC inhibitor FR901228 induced the hTERT gene by a complex mechanism that involved other transcription factors except for c-myc, in addition to the inhibition of histone deacetylation