Hidden Order in the Cuprates

We propose that the enigmatic pseudogap phase of cuprate superconductors is characterized by a hidden broken symmetry of d(x^2-y^2)-type. The transition to this state is rounded by disorder, but in the limit that the disorder is made sufficiently small, the pseudogap crossover should reveal itself to be such a transition. The ordered state breaks time-reversal, translational, and rotational symmetries, but it is invariant under the combination of any two. We discuss these ideas in the context of ten specific experimental properties of the cuprates, and make several predictions, including the existence of an as-yet undetected metal-metal transition under the superconducting dome.Comment: 12 pages of RevTeX, 9 eps figure

Plakoglobin is essential for myocardial compliance but dispensable for myofibril insertion into adherens junctions

Plakoglobin (gamma-catenin), a member of the armadillo family of proteins, is a constituent of the cytoplasmic plaque of cardiac junctions and is involved in anchorage of cytoskeletal filaments to specific cadherins. Its genetic inactivation leads to an embryonic lethal phenotype due to heart dysfunction related to an impairment in the architecture of intercalated discs and in the stability of the heart tissue. To elucidate the functional consequences of the loss of plakoglobin for myofibrillar function, we monitored passive stress-strain relationship and contractility parameters of demembranated embryonic fibers. Heart fibers obtained from plakoglobin-deficient embryonic mice were significantly less compliant than were fibers from wild-type embryos. This difference was especially pronounced at lower fiber extension levels: at 120% of slack length, compliance was 2.5-fold lower in plakoglobin-deficient mice than in the corresponding wild-type group. Contractile paramenters (force per cross-section; Ca2+ sensitivity of isometric force and shortening velocity at near-zero load) were comparable in all experimental groups. Therefore, we suggest that plakoglobin is important for cardiac compliance but not necessary for the attachment of the myofibrillar apparatus to adherens junctions. Thus, we conclude that the loss of function of desmosomes and the profound disarrangement of junctional components in plakoglobin null embryos is associated with a decreased passive compliance, which may explain the ventricular rupture and consequent pericardial tamponade in embryos lacking plakoglobin

Differential expression and association of calcium channel alpha1B and beta subunits during rat brain ontogeny

Calcium functions as an essential second messenger during neuronal development and synapse acquisition. Voltage-dependent calcium channels (VDCC), which are critical to these processes, are heteromultimeric complexes composed of alpha1, alpha2/delta, and beta subunits. beta subunits function to direct the VDCC complex to the plasma membrane as well as regulate its channel properties. The importance of beta to neuronal functioning was recently underscored by the identification of a truncated beta4 isoform in the epileptic mouse lethargic (lh) (Burgess, D. L., Jones, J. M., Meisler, M. H., and Noebels, J. L. (1997) Cell 88, 385-392). The goal of our study was to investigate the role of individual beta isoforms (beta1b, beta2, beta3, and beta4) in the assembly of N-type VDCC during rat brain development. By using quantitative Western blot analysis with anti-alpha1B-directed antibodies and [125I-Tyr22]omega-conotoxin GVIA (125I-CTX) radioligand binding assays, we observed that only a small fraction of the total alpha1B protein present in embryonic and early postnatal brain expressed high affinity 125I-CTX-binding sites. These results suggested that subsequent maturation of alpha1B or its assembly with auxiliary subunits was required to exhibit high affinity 125I-CTX binding. The temporal pattern of expression of beta subunits and their assembly with alpha1B indicated a developmental pattern of expression of beta isoforms: beta1b increased 3-fold from P0 to adult, beta4 increased 10-fold, and both beta2 and beta3 expression remained unchanged. As the beta component of N-type VDCC changed during postnatal development, we were able to identify both immature and mature forms of N-type VDCC. At P2, the relative contribution of beta is beta1b > beta3 >> beta2, whereas at P14 and adult the distribution is beta3 > beta1b = beta4. Although we observed no beta4 associated with the alpha1B at P2, beta4 accounted for 14 and 25% of total alpha1B/beta subunit complexes in P14 and adult, respectively. Thus, of the beta isoforms analyzed, only the beta4 was assembled with the rat alpha1B to form N-type VDCC with a time course that paralleled its level of expression during rat brain development. These results suggest a role for the beta4 isoform in the assembly and maturation of the N-type VDCC