A nuclear factor 1 binding site mediates the transcriptional activation of a type I collagen promoter by transforming growth factor-beta

Transforming growth factor-beta (TGF-beta) increases the steady-state RNA levels of several fibroblast extracellular matrix proteins. Using DNA transfection, we show that TGF-beta stimulates the activity of the mouse alpha 2(l) collagen promoter 5- to 10-fold in mouse NIH 3T3 and rat osteosarcoma cells. Deletion analysis indicates that a segment of this promoter between -350 and -300, overlapping a nuclear factor 1 (NF1) binding site, is needed for TGF-beta stimulation. A 3 bp substitution mutation abolishing NF1 binding to this site inhibits TGF-beta activation. Insertion of this NF1 binding site 5' to the SV40 early promoter makes the promoter TGF-beta inducible, but the 3 bp substitution does not. Similarly, when the NF1 binding site at the replication origin of adenovirus 2 and 5 is inserted 5' to the SV40 promoter, the promoter responds to TGF-beta. Therefore an NF1 binding site mediates the transcriptional activation of the mouse alpha 2(l) collagen promoter by TGF-beta

Pauli equation and the method of supersymmetric factorization

We consider different variants of factorization of a 2x2 matrix Schroedinger/Pauli operator in two spatial dimensions. They allow to relate its spectrum to the sum of spectra of two scalar Schroedinger operators, in a manner similar to one-dimensional Darboux transformations. We consider both the case when such factorization is reduced to the ordinary 2-dimensional SUSY QM quasifactorization and a more general case which involves covariant derivatives. The admissible classes of electromagnetic fields are described and some illustrative examples are given.Comment: 18 pages, Late

The dimerization domain of SOX9 is required for transcription activation of a chondrocyte-specific chromatin DNA template

Mutations in SOX9, a gene essential for chondrocyte differentiation cause the human disease campomelic dysplasia (CD). To understand how SOX9 activates transcription, we characterized the DNA binding and cell-free transcription ability of wild-type SOX9 and a dimerization domain SOX9 mutant. Whereas formation of monomeric mutant SOX9–DNA complex increased linearly with increasing SOX9 concentrations, formation of a wild-type SOX9–DNA dimeric complex increased more slowly suggesting a more sigmoidal-type progression. Stability of SOX9–DNA complexes, however, was unaffected by the dimerization mutation. Both wild-type and mutant SOX9 activated transcription of a naked Col2a1 DNA template. However, after nucleosomal assembly, only wild-type and not the mutant was able to remodel chromatin and activate transcription of this template. Using a cell line, in which the Col2a1 vector was stably integrated, no differences were seen in the interactions of wild-type and mutant SOX9 with the chromatin of the Col2a1 vector using ChIP. However, the mutant was unable to activate transcription in agreement with in vitro results. We hypothesize that the SOX9 dimerization domain is necessary to remodel the Col2a1 chromatin in order to allow transcription to take place. These results further clarify the mechanism that accounts for CD in patients harboring SOX9 dimerization domain mutations

Invariant vector fields and the prolongation method for supersymmetric quantum systems

The kinematical and dynamical symmetries of equations describing the time evolution of quantum systems like the supersymmetric harmonic oscillator in one space dimension and the interaction of a non-relativistic spin one-half particle in a constant magnetic field are reviewed from the point of view of the vector field prolongation method. Generators of supersymmetries are then introduced so that we get Lie superalgebras of symmetries and supersymmetries. This approach does not require the introduction of Grassmann valued differential equations but a specific matrix realization and the concept of dynamical symmetry. The Jaynes-Cummings model and supersymmetric generalizations are then studied. We show how it is closely related to the preceding models. Lie algebras of symmetries and supersymmetries are also obtained.Comment: 37 pages, 7 table

Pentaquark baryons in SU(3) quark model

We study the SU(3) group structure of pentaquark baryons which are made of four quarks and one antiquark. The pentaquark baryons form {1}, {8}, {10}, {10}-bar, {27}, and {35} multiplets in SU(3) quark model. First, the flavor wave functions of all the pentaquark baryons are constructed in SU(3) quark model and then the flavor SU(3) symmetry relations for the interactions of the pentaquarks with three-quark baryons and pentaquark baryons are obtained.Comment: REVTeX, 36 pages, 8 figures, references added, section for mass sum rules is added, to appear in Phys. Rev.

Chondrocytes Directly Transform into Bone Cells in Mandibular Condyle Growth

For decades, it has been widely accepted that hypertrophic chondrocytes undergo apoptosis prior to endochondral bone formation. However, very recent studies in long bone suggest that chondrocytes can directly transform into bone cells. Our initial in vivo characterization of condylar hypertrophic chondrocytes revealed modest numbers of apoptotic cells but high levels of antiapoptotic Bcl-2 expression, some dividing cells, and clear alkaline phosphatase activity (early bone marker). Ex vivo culture of newborn condylar cartilage on a chick chorioallantoic membrane showed that after 5 d the cells on the periphery of the explants had begun to express Col1 (bone marker). The cartilage-specific cell lineage–tracing approach in triple mice containing Rosa 26tdTomato (tracing marker), 2.3 Col1GFP (bone cell marker), and aggrecan CreERT2 (onetime tamoxifen induced) or Col10-Cre (activated from E14.5 throughout adult stage) demonstrated the direct transformation of chondrocytes into bone cells in vivo. This transformation was initiated at the inferior portion of the condylar cartilage, in contrast to the initial ossification site in long bone, which is in the center. Quantitative data from the Col10-Cre compound mice showed that hypertrophic chondrocytes contributed to ~80% of bone cells in subchondral bone, ~70% in a somewhat more inferior region, and ~40% in the most inferior part of the condylar neck (n = 4, P < 0.01 for differences among regions). This multipronged approach clearly demonstrates that a majority of chondrocytes in the fibrocartilaginous condylar cartilage, similar to hyaline cartilage in long bones, directly transform into bone cells during endochondral bone formation. Moreover, ossification is initiated from the inferior portion of mandibular condylar cartilage with expansion in one direction

Supersymmetrization of Quaternion Dirac Equation for Generalized Fields of Dyons

The quaternion Dirac equation in presence of generalized electromagnetic field has been discussed in terms of two gauge potentials of dyons. Accordingly, the supersymmetry has been established consistently and thereafter the one, two and component Dirac Spinors of generalized quaternion Dirac equation of dyons for various energy and spin values are obtained for different cases in order to understand the duality invariance between the electric and magnetic constituents of dyons.Comment: Key words: Supersymmetry, quaternion, Dirac equation, dyons PACS No.: 11.30.Pb, 14.80.Ly, 03.65.G

Supersymmetric Homogeneous Quantum Cosmologies Coupled to a Scalar Field

Recent work on $N=2$ supersymmetric Bianchi type IX cosmologies coupled to a scalar field is extended to a general treatment of homogeneous quantum cosmologies with explicitely solvable momentum constraints, i.e. Bianchi types I, II, VII, VIII besides the Bianchi type IX, and special cases, namely the Friedmann universes, the Kantowski-Sachs space, and Taub-NUT space. Besides the earlier explicit solution of the Wheeler DeWitt equation for Bianchi type IX, describing a virtual wormhole fluctuation, an additional explicit solution is given and identified with the `no-boundary state'.Comment: 23 PAGE