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The Energetic X-Ray Imaging Survey Telescope (EXIST)is a mission design concept that uses coded masks seen by Cadmium Zinc Telluride (CZT) detectors to register hard X-rays in the energy region from 10 keV to 600 keV. A partially active or fully active anti-coincidence shield/collimator with a total area of between 15 m2and 35 m2will be used to define the field-of-view of the CZT detectors and to suppress the background of cosmic-ray-induced events. In this paper, we describe the use of a sodium activated cesium iodide shield/collimator to detect gamma-ray bursts (GRBs) and to measure their energy spectra in the energy range from 100 keV up to 10 MeV. We use the code GEANT 4 to simulate the interactions of photons and cosmic rays with the spacecraft and the instrument and the code DETECT2000 to simulate the optical properties of the scintillation detectors. The shield/collimator achieves a $\nu F_\nu$-sensitivity of $3 \times 10^{-9}$erg cm-2s-1and $2 \times 10^{-8}$erg cm-2s-1at 100 keV and 600 keV, respectively. The sensitivity is well matched to that of the coded mask telescope.The broad energy coverage of an EXIST-type mission with active shields will constrain the peak of the spectral energy distribution (SED) for a large number of GRBs. The measurement of the SED peak may be key for determining photometric GRB redshifts and for using GRBs as cosmological probes.

The observed temporal and spectral characteristics and the spatial distribution of gamma-ray bursts (GRBs) are summarized, primarily from data obtained with the BATSE experiment on the Compton Observatory. The availability of these data and the prospects for continued observations are also described.

We present a variational calculation of the envelope wave function of an exciton inside a cube, in the effective mass approximation, with one parameter which plays the part of a Bohr radius. This geometry allows one to reduce the sixfold integrals to threefold integrals which shortens tremendously computer calculations. This wave function is used to obtain the exchange energy and the oscillator strength. The limiting cases (large or small cubes) are recovered. We show that recent experimental results in porous silicon can be explained without further hypothesis.

The cardiac conduction system is a complex network of cells that together orchestrate the rhythmic and coordinated depolarization of the heart. The molecular mechanisms regulating the specification and patterning of cells that form this conductive network are largely unknown. Studies in avian models have suggested that components of the cardiac conduction system arise from progressive recruitment of cardiomyogenic progenitors, potentially influenced by inductive effects from the neighboring coronary vasculature. However, relatively little is known about the process of conduction system development in mammalian species, especially in the mouse, where even the histological identification of the conductive network remains problematic. We have identified a line of transgenic mice where lacZ reporter gene expression delineates the developing and mature murine cardiac conduction system, extending proximally from the sinoatrial node to the distal Purkinje fibers. Optical mapping of cardiac electrical activity using a voltage-sensitive dye confirms that cells identified by the lacZ reporter gene are indeed components of the specialized conduction system. Analysis of lacZ expression during sequential stages of cardiogenesis provides a detailed view of the maturation of the conductive network and demonstrates that patterning occurs surprisingly early in embryogenesis. Moreover, optical mapping studies of embryonic hearts demonstrate that a murine His-Purkinje system is functioning well before septation has completed. Thus, these studies describe a novel marker of the murine cardiac conduction system that identifies this specialized network of cells throughout cardiac development. Analysis of lacZ expression and optical mapping data highlight important differences between murine and avian conduction system development. Finally, this line of transgenic mice provides a novel tool for exploring the molecular circuitry controlling mammalian conduction system development and should be invaluable in studies of developmental mutants with potential structural or functional conduction system defects.

Normal cardiovascular development is exquisitely dependent on the correct dosage of the angiogenic growth factor and vascular morphogen vascular endothelial growth factor (VEGF). However, cardiac expression of VEGF is also robustly augmented during hypoxic insults, potentially mediating the well-established teratogenic effects of hypoxia on heart development. We report that during normal heart morphogenesis VEGF is specifically upregulated in the atrioventricular (AV) field of the heart tube soon after the onset of endocardial cushion formation (i.e. the endocardium-derived structures that build the heart septa and valves). To model hypoxia-dependent induction of VEGF in vivo, we conditionally induced VEGF expression in the myocardium using a tetracycline-regulated transgenic system. Premature induction of myocardial VEGF in E9.5 embryos to levels comparable with those induced by hypoxia prevented formation of endocardial cushions. When added to explanted embryonic AV tissue, VEGF fully inhibited endocardial-to-mesenchymal transformation. Transformation was also abrogated in AV explants subjected to experimental hypoxia but fully restored in the presence of an inhibitory soluble VEGF receptor 1 chimeric protein. Together, these results suggest a novel developmental role for VEGF as a negative regulator of endocardial-to-mesenchymal transformation that underlies the formation of endocardial cushions. Moreover, ischemia-induced VEGF may be the molecular link between hypoxia and congenital defects in heart septation.

We analyze 426 observations of the bursting pulsar GRO J1744-28 by Ulyssesand BATSE. Triangulating each burst and statistically combining the triangulation annuli, we obtain a 3 ? error ellipse whose area is 532 arcsec2. The accuracy of this statistical method has been independently verified with observations of the soft gamma repeater SGR 1900+14. The ellipse is fully contained within the 1' radius ASCAerror circle of the soft X-ray counterpart and partially overlaps the 10'' radius ROSATerror circle of a source which may also be the soft X-ray counterpart. A variable source which has been proposed as a possible IR counterpart lies at the edge of the 3 ? error ellipse, making it unlikely from a purely statistical point of view to be associated with the bursting pulsar.

HERG(1) K(+) channel mutations are responsible for one form of dominantly inherited long QT syndrome (LQT). Some LQT mutations exert a dominant negative effect on wild-type current expression. To investigate mechanisms of dominant-negative behavior, we co-expressed wild-type HERG with the A561V mutant in mammalian cells. Transfection with various cDNA ratios produced HERG K(+) current densities that approached a predicted binomial distribution where mutant and wild-type subunits co-assemble in a tetramer with nearly complete dominance. Using C terminus myc-tagged wild-type HERG we specifically followed the mutant's effect on full-length wild-type HERG protein expression. Co-expression with A561V reduced the abundance of full-length wild-type HERG protein comparable to the current reduction. Reduction of wild-type protein was due to decreased synthesis and increased turnover. Conditions facilitating protein folding (growth at 30 degrees C, or in 10% glycerol) resulted in partial rescue from the dominant effect, as did the 26 S proteosome inhibitor ALLN. Thus, for A561V, dominant negative effects result from assembly of wild-type subunits with mutant very early in production leading to rapid recognition of mutant channels and targeting for proteolysis. These results establish protein misfolding, cellular proofreading, and bystander involvement as contributing mechanisms for dominant effects in LQT2.

We demonstrate that the growth mode of GaN, AlN and InN in molecular beam epitaxy is two or three dimensional, depending on the competing kinetics of the metal species (Ga, Al or In) and of N. In this view, we show that the presence of foreign species acting as surfactants profoundly modifies the kinetics of the adatoms, eventually leading to an improvement in both structural and optical properties of the material. Next, we discuss the interplay between the growth mode and the strain relaxation in nitride heterostructures. In particular, we show that GaN and InGaN can experience a Stranski–Krastanov growth mode leading to the formation of quantum dots. A mechanism of quantum dot nucleation is proposed in the case of GaN on AlN.

The influence of foreign species on the growth mode has been studied, with special emphasis on the role of In. It is demonstrated that the growth mode, i.e. 2D or 3D, first depends on the competing kinetics of Ga and N. In this view, we show that the surfactants modify both the Ga droplet formation process and the N desorption rate. Next, we discuss the role of strain relaxation in nitride heterostructures. In particular, we show that GaN and InGaN can experience a Stranski-Krastanow growth mode leading to the formation of quantum dots. A mechanism of quantum dot nucleation is proposed in the case of GaN on AlN.

We observe in strained GaN self-assembled quantum dots grown on an AlN layer, a dramatic modification of the optical emission spectra as the dot size varies. In “large” quantum dots with an average height of 4.1nm, the photoluminescence (PL) peak is centered at 2.95eV, nearly 0.5eV below the bulk GaN bandgap. We attribute this enormous redshift to a giant 5.5MV cm−1piezoelectric field present in our dots. Temperature-dependent PL studies reveal the strongly zero-dimensional character of this QD system and are consistent with an intrinsic PL mechanism.

This paper describes a method of sampling from the Poisson distribution on a computer that appears to be less costly than a recently suggested method in [1]. The proposed method relies on a conventional search using the inverse transform approach for nonintegral μ<7, on a modification of the inverse transform approach that begins the search at the mode for integral μ, and on a combination of these two approaches for nonintegral μ>7. For large μ the sampling cost is proportional to μ1/2. The paper also shows that for μ≥15 an incidental error occurs by using max (0, [μ+Yμ1/2+0.5]) whereY is fromN(0,1). Since the sampling cost ofY is a constant, this approach places an upper bound on the cost of generating a Poisson variate.

We describe the channel-to-energy calibration of the Spectroscopy Detectors of the Burst and Transient Source Experiment (BATSE) on the Compton Gamma Ray Observatory (GRO). These detectors consist of NaI(Tl) crystals viewed by photomultiplier tubes whose output in turn is measured by a pulse height analyzer. The calibration of these detectors has been complicated by frequent gain changes and by nonlinearities specific to the BATSE detectors. Nonlinearities in the light output from the NaI crystal and in the pulse height analyzer are shifted relative to each other by changes in the gain of the photomultiplier tube. We present the analytical model which is the basis of our calibration methodology, and outline how the empirical coefficients in this approach were determined. We also describe the complications peculiar to the Spectroscopy Detectors, and how our understanding of the detectors' operation led us to a solution to these problems.

The ultrastructural features of the retina in two cases of X-linked recessive and one of autosomal dominant retinitis pigmentosa are described. Histopathologic changes were most apparent in the retinal pigment epithelium (RPE), photoreceptor cells, and retinal vessels. the RPE was foeally absent, focally proliferated, and mostly depigmented. Thickening of the basal membrane of the RPE was present. Photoreceptors were severely reduced in number. Two forms of photoreceptor cell degeneration were observed. In the first form the photoreceptor cells exhibited mitochondrial swelling, wateriness of cytoplasm, and loss of organelles. In the second form the cells showed densified, shrunken cytoplasm with vacuolated mitochondria. In many retinal vessels, endothelial cell and pericytic degeneration were apparent. Pigment-laden macrophages were present in all layers of the retina. A preretinal membrane was observed in the posterior pole of all six eyes and consisted of cellular elements bearing the ultrastructural characteristics of smooth muscle cells. the preretinal membrane may account for the retinal vascular leakage observed in some cases of retinitis pigmentosa.

Nanometer-scale CdTe quantum wires have been fabricated using a two step epitaxial growth process. Modulation of the in-plane lattice constant of a [110]CdTeCdZnTequantum well grown over a [001]CdTeCdZnTestrained superlattice laterally confines the carriers to one dimension. The photoluminescence of these quantum wires presents a large energy shift relative to the unmodulated [110] quantum well (QW) which is strongly dependent on the excitation density. The results compare very well with a theoretical model assuming no relaxation in the structure. With this calculation, the dependence on excitation density of the wire exciton transition energy can be explained by taking into account the lateral piezoelectric field present in these strained modulated [110] structures.

The Cambridge Low Frequency Synthesis Telescope (CLFST) is being used to search for prompt radio emission from GRBs at 151 MHz. For this search a special observing mode has recently been developed; the antennas of the CLFST are split into seven groups which are spaced about 30° apart. When triggered by the real-time signals from the BACODINE system the antennas are slewed to the GRB position, with data being sampled at 1.5 or 3-s intervals. The antennas slew at about 10° per minute, so that an appreciable fraction of the sky can be accessed on timescales of a few minutes - any prompt radio emission from a GRB might be delayed by this timescale due to propagation effects.

The celestial coordinates of gamma-ray burst sources observed with BATSE on GRO are automatically determined and distributed in real time to members of the global scientific community. These data are now being used by more than 20 operations to enable searches for associated transients in a variety of other wavelength or energy regimes to identify the burst source objects. The minimum total delay time from the onset of a burst to the receipt of its coordinates by distant experimenters can be under 4 sec, less than the duration of a typical GRB, and the maximum total delay is 7 sec, or longer, depending on the distribution method. Some improvements to the BACODINE system and a summary of the follow-up observations made by some of the sites are given.

A “repeater statistic” (derived from the two-point angular correlation function and accounting for location errors) is used to identify constraints on the rate of burst repetition from the BATSE 1B catalog. Because of the anisotropic sky exposure, repeating sources should create additional effects in the large-scale distribution of close burst pairs.

Very Large Array (VLA) radio observations of precisely-located GRB error boxes have been performed to search for fading and quiescent emission associated with ?-ray bursts. These observations were made as quickly as 23 hours and as late as 13 years after the time of the burst. Our measurements presented here have found GRB error boxes to be empty of sources to the 80 µJy level (? = 3.6 cm) at 9 months, to 1 mJy (20 cm) at 9 days, and probably to 5 mJy (20 cm) at 23 hours after the bursts.

The BATSE/COMPTEL/NMSU Rapid Response Network (RRN) was formed to provide rapid follow-up of?-ray bursts imaged by the COMPTEL instrument on the Compton Gamma-Ray Observatory. The RRN consists of ˜ 22 professional observatories located around the world spanning both northern and southern hemispheres. Also included in the RRN is the Airforce GEODSS network. The goal of the RRN is to perform optical and radio observations of COMPTEL error boxes as soon after the burst as possible. We present results from the first two years of operation of this network.

Optical studies were made of two well-located gamma-ray burst regions in the Southern Hemisphere using the 1.5 m telescope at the Cerro Tololo Inter-American Observatory in Chile. Multi-filter image tube plates and UBV photometry surveys were made of both regions. The field of the 19 November, 1978 gamma-ray burst shows no early star or star with unusual colors out to several diameters of the nominal error box. The region of the 5 March, 1979 gamma-ray burst, which includes N49, contains several blue giants in the LMC, two of which deserve further study.

The research program in gamma-ray burst astronomy at the NASA/Marshall Space Flight Center is described. Large-area scintillation detector arrays have been flown on high-altitude balloons, and an array is being developed for the Gamma-Ray Observatory. The design of these detectors is described along with results obtained from previous balloon flights.

A deep optical search of the “Network Synthesis” localization for the SGR B1900+14 and the nearby ROSAT source error box has yielded an unusual source positionally coincident with an IRAS source. We present optical and IR data describing this source.

We present preliminary results from deep optical searches of small (=~5 arcmin2) GRB error boxes determined using the Third Interplanetary Network (IPN3). Two of these fields also have been found to have historical OT events located within the IPN3 error boxes. We compare the preliminary results of these searches to those reported for the larger IPN1 error boxes. The small size of the IPN3 error boxes should allow a test of the hypothesis suggested by the IPN1 study that there are excess QSOs associated with the GRB fields.

The BATSE and OSSE instrument teams have modified flight software to promptly (within 2 min of trigger) slew the OSSE detectors to burst locations determined on-board by BATSE. This enables OSSE to make sensitive searches for prompt and delayed post-burst line and continuum emission above 50 keV. In the best cases our sensitivity will be more than an order of magnitude better than any other search in this energy range. We expect to slew to 1–2 bursts per month, based on the OSSE FOV and BATSE event rate. Detections or limits from continued operation of this system may provide significant constraints on burst models. As an example of the observations made using this system, we present preliminary limits for post-burst emission from GRB 950223 on several time scales.

Intracellular Ca2+ release in muscle is governed by functional communication between the voltage-dependent L-type Ca2+ channel and the intracellular Ca2+ release channel by processes that are incompletely understood. We previously showed that sorcin binds to cardiac Ca2+ release channel/ryanodine receptors and decreases channel open probability in planar lipid bilayers. In addition, we showed that sorcin antibody immunoprecipitates ryanodine receptors from metabolically labeled cardiac myocytes along with a second protein having a molecular weight similar to that of the alpha1 subunit of cardiac L-type Ca2+ channels. We now demonstrate that sorcin biochemically associates with cardiac and skeletal muscle L-type Ca2+ channels specifically within the cytoplasmically oriented C-terminal region of the alpha1 subunits, providing evidence that the second protein recovered by sorcin antibody from cardiac myocytes was the 240-kDa L-type Ca2+ channel alpha1 subunit. Anti-sorcin antibody immunoprecipitated full-length alpha1 subunits from cardiac myocytes, C2C12 myotubes, and transfected non-muscle cells expressing alpha1 subunits. In contrast, the anti-sorcin antibody did not immunoprecipitate C-terminal truncated forms of alpha1 subunits that were detected in myotubes. Recombinant sorcin bound to cardiac and skeletal HIS6-tagged alpha1 C termini immobilized on Ni2+ resin. Additionally, anti-sorcin antibody immunoprecipitated C-terminal fragments of the cardiac alpha1 subunit exogenously expressed in mammalian cells. The results identified a putative sorcin binding domain within the C terminus of the alpha1 subunit. These observations, along with the demonstration that sorcin accumulated substantially during physiological maturation of the excitation-contraction coupling apparatus in developing postnatal rat heart and differentiating C2C12 muscle cells, suggest that sorcin may mediate interchannel communication during excitation-contraction coupling in heart and skeletal muscle.

We present a calculation of the Zeeman splitting of the light- and heavy-hole excitons that takes into account the uniaxial strain due to lattice mismatch as well as the interface-enhanced paramagnetism. In the CdTe quantum well, the strain raises the light-hole band edge with respect to the heavy-hole one. The shallower well allows a larger penetration of the Cd 1− x Mn x Te barrier region by the light hole. This adds to the effect of the lighter effective mass, leading to an "anomalous" enhancement of the Zeeman splitting of the light-hole exciton. We find that the ratio of the light- to heavy-hole exciton splitting (between the σ and σ components) increases with the quantum well width eventually exceeding unity, in agreement with experimental data.

The large Area Detectors (LADs) of the BATSE experiment aboard the Compton Gamma-ray Observatory have been used recently as the first hard X-ray all-sky imager at energies between 20 keV and 300 keV. The Earth occultation process is formulated in terms of a curved Radon transform convoluted by a step transform in a selected field of view (FOV) ranging from 5°×5° to 40°×40°. The Maximum Entropy Method is then used to reconstruct an image in the hard X-ray sky. Multiple images of different regions of the sky can be produced simultaneously. A source location accuracy of 0.1° for strong sources and a sensitivity limit of 100 mCrab have been achieved in an one-day integration period.

Sorcin is a widely expressed, 22-kDa Ca2+-binding protein initially identified in multidrug-resistant cells. In the heart, sorcin localizes to the dyadic junctions of transverse tubules and sarcoplasmic reticulum and coimmunoprecipitates with the Ca2+ release channel/ryanodine receptor (RyR) (Meyers, M. B., Pickel, V. M., Sheu, S.-S., Sharma, V. K., Scotto, K. W., and Fishman, G. I. (1995) J. Biol. Chem. 270, 26411-26418). We have investigated a possible functional interaction between sorcin and cardiac RyR using purified recombinant sorcin in [3H]ryanodine binding experiments and single channel recordings of RyR. The open probability of single RyR was decreased significantly by the addition of sorcin to the cytoplasmic side of the channel (IC50 approximately 480 nM). In addition, sorcin completely inhibited [3H]ryanodine binding with an IC50 approximately 700 nM. Inhibition occurred over a wide range of [Ca2+], and sorcin-modulated RyR remained Ca2+-dependent. Furthermore, caffeine-activated RyRs were also inhibited by sorcin at low [Ca2+] (pCa 7), suggesting that Ca2+ is not an obligatory factor for sorcin inhibition of RyR. Comparisons of these inhibitory effects with those of calmodulin and calpain, proteins structurally related to sorcin, suggested that the interaction of sorcin with cardiac RyR was distinct from and independent of either of these modulatory proteins. Phosphorylation of sorcin with the catalytic subunit of protein kinase A significantly decreased the ability of sorcin to modulate RyR. These results suggest that sorcin may modulate RyR function in a normal cell environment and that the level of modulation is in turn influenced by signaling pathways that increase protein kinase A activity.

The mechanisms regulating cardiac muscle differentiation and development are incompletely understood. To examine the relationships between cardiocyte proliferation and differentiation, we tested the ability of a fragment from the rat beta myosin heavy-chain (MHC beta) gene to correctly target expression of a thermolabile simian virus 40 large tumor antigen allele (tsA58) in the developing mouse. Transgene expression in the heart was observed as early as 10 days postconception and was developmentally regulated in parallel with the endogenous MHC beta gene. Expression was also detected in developing skeletal muscle, although at low levels. Despite the temperature sensitivity of the mutant large tumor antigen protein, a subset of transgenic mice in several lineages developed marked cardiac and skeletal myopathies.

We have cloned a protein from bovine brain, brain-derived voltage-dependent anion channel 1 (BR1-VDAC), that is identical to a recently sequenced plasmalemmal-bound porin from human lymphocytes. mRNA hybridization indicates that BR1-VDAC is widely distributed throughout nervous and nonnervous tissues. In situ localization substantiated that the BR1-VDAC is associated with the plasmalemma of astrocytes. A monoclonal antibody that recognizes the N terminus of the BR1-VDAC protein completely blocks an astrocytic high-conductance anion channel that has electrophysiological similarities with the mitochondrial VDAC. Since the high-conductance anion channel in astrocytes has been shown to respond to hypoosmotic solutions, its molecular identification provides the basis for a better understanding of volume regulation in brain tissue.

Six patients with various genetic types of retinitis pigmentosa and ten carriers of the X-linked recessive type were studied by vitreous fluorophotometry. Kinetic vitreous fluorophotometry showed an alteration of the blood-retinal barrier (BRB) in patients with retinitis pigmentosa, even in those who had minimal fundoscopic abnormalities and only minor changes on the electroretinogram. Furthermore, an alteration of the BRB could be detected in the carriers of the X-linked recessive form of retinitis pigmentosa. In general, higher concentration of fluorescein in the vitreous correlated topographically with the extent of photoreceptor and retinal pigment epithelial disease, as well as with the presence of leakage from retinal capillaries.

Color vision testing was performed on a group of ten black tyrosinase-positive albino patients and a group of normal subjects. Testing was accomplished by means of a Farnsworth-Munsell (F-M) 100-hue test and Nagel anomaloscope. As a group, the albino patients showed an increase in number of errors scored on the FM-100 hue test, without any specific axis in the majority of cases. Results on the Nagel anomaloscope showed a ‘widening’ into the red end of the Rayleigh equation. A possible explanation for this apparent widening is discussed, which emphasizes anticipated results of matching ranges obtained on extrafoveal cones.

Multilocus linkage analysis of 62 family pedigrees with X chromosome-linked retinitis pigmentosa (XLRP) was undertaken to determine the presence of possible multiple disease loci and to reliably estimate their map location. Multilocus homogeneity tests furnished convincing evidence for the presence of two XLRP loci, the likelihood ratio being 6.4 x 10(9):1 in favor of two versus a single XLRP locus and gave accurate estimates for their map location. In 60-75% of the families, location of an XLRP gene was estimated at 1 centimorgan distal to OTC, and in 25-40% of the families, an XLRP locus was located halfway between DXS14 (p58-1) and DXZ1 (Xcen), with an estimated recombination fraction of 25% between the two XLRP loci. There is also good evidence for a third XLRP locus, midway between DXS28 (C7) and DXS164 (pERT87), supported by a likelihood ratio of 293:1 for three versus two XLRP loci.

The eight-band k·pmethod and the envelope function approximation is used to describe the infrared inter-subband absorption in Si–Si1−xGex–Si quantum wells. The valence and conduction bands are explicitly taken into account leading to an accurate description of the mixing of the conduction and valence band functions. Both as-grownand interdiffused (annealed) quantum wells are discussed.

DNA samples from 161 unrelated patients with autosomal dominant retinitis pigmentosa were screened for point mutations in the rhodopsin gene by using the polymerase chain reaction and denaturing gradient gel electrophoresis. Thirty-nine patients were found to carry 1 of 13 different point mutations at 12 amino acid positions. The presence or absence of the mutations correlated with the presence or absence of retinitis pigmentosa in 174 out of 179 individuals tested in 17 families. The mutations were absent from 118 control subjects with normal vision.

The connexins form a family of membrane spanning proteins that assemble into gap junction channels. The biophysical properties of these channels are dependent upon the constituent connexin isoform. To begin identifying the molecular basis for gap junction channel behavior in the human heart, a tissue that expresses connexin43, we used site-directed mutagenesis to generate mutant cDNAs of human connexin43 with shortened cytoplasmic tail domains. Premature stop codons were inserted, resulting in proteins corresponding in length to the mammalian isoforms connexin32 and connexin26, which are expressed primarily in liver. All constructs restore intercellular coupling when they are transfected into SKHep1 cells, a human hepatoma line that is communication deficient. Whereas wild-type connexin43 transfectants display two distinct unitary conductance values of about 60 and 100 pS, transfectants expressing the mutant proteins, from which 80 and 138 amino acids have been deleted, exhibit markedly different single-channel properties, with unitary conductance values of about 160 and 50 pS, respectively. Junctional conductance of channels composed of wild-type connexin43 is less voltage-sensitive compared with transfectants expressing wild-type connexin32. However, neither of the connexin43 truncation mutants alters this relative voltage insensitivity. These results suggest that the cytoplasmic tail domain is an important determinant of the unitary conductance event of gap junction channels but not their voltage dependence. Furthermore, since the mutant connexins are missing several consensus phosphorylation sites, modification of these particular sites may not be required for membrane insertion or assembly of human connexin43 into functional channels.