THE MASS-RADIUS RELATION OF YOUNG STARS. I. USCO 5, AN M4.5 ECLIPSING BINARY IN UPPER SCORPIUS OBSERVED BY K2

We present the discovery that UScoCTIO 5, a known spectroscopic binary in the Upper Scorpius star-forming region (P = 34 days, Mtot sin(i) = 0.64 M⊙), is an eclipsing system with both primary and secondary eclipses apparent in K2 light curves obtained during Campaign 2. We have simultaneously fit the eclipse profiles from the K2 light curves and the existing RV data to demonstrate that UScoCTIO 5 consists of a pair of nearly identical M4.5 stars with MA = 0.329 ± 0.002 M⊙, RA = 0.834 ± 0.006 R⊙, MB = 0.317 ± 0.002 M⊙, and RB = 0.810 ± 0.006 R⊙. The radii are broadly consistent with pre-main-sequence ages predicted by stellar evolutionary models, but none agree to within the uncertainties. All models predict systematically incorrect masses at the 25%-50% level for the HR diagram position of these mid-M dwarfs, suggesting significant modifications to mass-dependent outcomes of star and planet formation. The form of the discrepancy for most model sets is not that they predict luminosities that are too low, but rather that they predict temperatures that are too high, suggesting that the models do not fully encompass the physics of energy transport (via convection and/or missing opacities) and/or a miscalibration of the SpT-Teff scale. The simplest modification to the models (changing Teff to match observations) would yield an older age for this system, in line with the recently proposed older age of Upper Scorpius (τ ∼ 11 Myr)

The Obliquity of HIP 67522 b: A 17 Myr Old Transiting Hot, Jupiter-sized Planet

HIP 67522 b is a 17 Myr old, close-in (P orb = 6.96 days), Jupiter-sized (R = 10 R ⊕) transiting planet orbiting a Sun-like star in the Sco-Cen OB association. We present our measurement of the system's projected orbital obliquity via two spectroscopic transit observations using the CHIRON spectroscopic facility. We present a global model that accounts for large surface brightness features typical of such young stars during spectroscopic transit observations. With a value of | λ | = 5.8-5.7+2.8 it is unlikely that this well-aligned system is the result of a high-eccentricity-driven migration history. By being the youngest planet with a known obliquity, HIP 67522 b holds a special place in contributing to our understanding of giant planet formation and evolution. Our analysis shows the feasibility of such measurements for young and very active stars

TESS hunt for young and maturing exoplanets (THYME). IV. Three small planets orbiting a 120 Myr old star in the pisces-eridanus stream

Young exoplanets can offer insight into the evolution of planetary atmospheres, compositions, and architectures. We present the discovery of the young planetary system TOI 451 (TIC 257605131, Gaia DR2 4844691297067063424). TOI 451 is a member of the 120 Myr old Pisces-Eridanus stream (Psc-Eri). We confirm membership in the stream with its kinematics, its lithium abundance, and the rotation and UV excesses of both TOI 451 and its wide-binary companion, TOI 451 B (itself likely anM-dwarf binary).We identified three candidate planets transiting in the Transiting Exoplanet Survey Satellite data and followed up the signals with photometry from Spitzer and ground-based telescopes. The system comprises three validated planets at periods of 1.9, 9.2, and 16 days, with radii of 1.9, 3.1, and 4.1 R⊗, respectively. The host star is near-solar mass with V=11.0 and H = 9.3 and displays an infrared excess indicative of a debris disk. The planets offer excellent prospects for transmission spectroscopy with the Hubble Space Telescope and the James Webb Space Telescope, providing the opportunity to study planetary atmospheres that may still be in the process of evolving

Mitochondrial Ca2+ uptake requires sustained Ca2+ release from the endoplasmic reticulum.

We analyzed the role of inositol 1,4,5-trisphosphate-induced Ca(2+) release from the endoplasmic reticulum (ER) (i) in powering mitochondrial Ca(2+) uptake and (ii) in maintaining a sustained elevation of cytosolic Ca(2+) concentration ([Ca(2+)](c)). For this purpose, we expressed in HeLa cells aequorin-based Ca(2+)-sensitive probes targeted to different intracellular compartments and studied the effect of two agonists: histamine, acting on endogenous H(1) receptors, and glutamate, acting on co-transfected metabotropic glutamate receptor (mGluR1a), which rapidly inactivates through protein kinase C-dependent phosphorylation and thus causes transient inositol 1,4,5-trisphosphate production. Glutamate induced a transient [Ca(2+)](c) rise and drop in ER luminal [Ca(2+)] ([Ca(2+)](er)), and then the ER refilled with [Ca(2+)](c) at resting values. With histamine, [Ca(2+)](c) after the initial peak stabilized at a sustained plateau, and [Ca(2+)](er) decreased to a low steady-state value. In mitochondria, histamine evoked a much larger mitochondrial Ca(2+) response than glutamate ( approximately 15 versus approximately 65 microm). Protein kinase C inhibition, partly relieving mGluR1a desensitization, reestablished both the [Ca(2+)](c) plateau and the sustained ER Ca(2+) release and markedly increased the mitochondrial Ca(2+) response. Conversely, mitochondrial Ca(2+) uptake evoked by histamine was drastically reduced by very transient ( approximately 2-s) agonist applications. These data indicate that efficient mitochondrial Ca(2+) uptake depends on the preservation of high Ca(2+) microdomains at the mouth of ER Ca(2+) release sites close to mitochondria. This in turn depends on continuous Ca(2+) release balanced by Ca(2+) reuptake into the ER and maintained by Ca(2+) influx from the extracellular space

A role for calcium influx in the regulation of mitochondrial calcium in endothelial cells.

By using an endothelial cell line (ECV304), derived from human umbilical vein and transfected with recombinant aequorin targeted to the mitochondrial matrix, we find that stimulation with ATP evokes long lasting increases in mitochondrial Ca2+ ([Ca2+]m) that largely depend on Ca2+ influx. In these cells, the release of stored Ca2+ is inefficient at elevating [Ca2+]m. Consequently it appears that in ECV304 cells, bulk cytosolic Ca2+ ([Ca2+]c) is the main determinant of [Ca2+]m changes. In ECV304 cells < 4% of mitochondria are within 700 nm of the endoplasmic reticulum as opposed to 65% in HeLa cells, whereas 14% are within 700 nm of the inner surface of the plasma membrane, compared with < 6% in HeLa cells. Following Ca2+ depletion, readdition of extracellular Ca2+ evokes an increase in [Ca2+]m but not in [Ca2+]c. Under these conditions, microdomains of high [Ca2+]c may occur beneath the plasma membrane of ECV304 cells resulting in the preferential elevation of Ca2+ in mitochondria located in this region. A model is discussed in which the localization of mitochondria with respect to Ca2+ sources is the main determinant of their in situ Ca2+ uptake kinetics. Thus, in any given cell type mitochondria may be localized to suit the energy and metabolic demands of their physiological actions

Drp-1-dependent division of the mitochondrial network blocks intraorganellar Ca2+ waves and protects against Ca2+-mediated apoptosis.

By transiently or stably overexpressing the mitochondrial fission factor dynamin-related protein-1 (Drp-1), we evaluated the role of mitochondrial division in organelle Ca2+ homeostasis and apoptotic signaling. Quantitative 3D digital microscopy revealed a split mitochondrial network in Drp-1-overexpressing cells without changes in cell viability. High-speed mitochondrial [Ca2+] ([Ca2+]m) imaging revealed propagating intramitochondrial Ca2+ waves in intact cells, which were blocked in the Drp-1-fragmented network, leaving a fraction of individual mitochondria without substantial [Ca2+]m elevation. Consequently, in Drp-1-expressing cells the apoptotic efficacy of ceramide, which causes a Ca2+-dependent perturbation of mitochondrial structure and function, was drastically reduced. Conversely, the sensitivity to staurosporine-induced apoptosis, previously shown to be directly triggered by Drp-1-dependent recruitment of proapoptotic proteins to mitochondria, was enhanced. These results demonstrate that the regulated process of mitochondrial fusion and fission controls the spatiotemporal properties of mitochondrial Ca2+ responses and, thus, physiological and pathological consequences of cellular Ca2+ signals

Targeting of reporter molecules to mitochondria to measure calcium, ATP, and pH.

The study of isolated mitochondria, dating back to the 60ties, has provided a wealth of information on the biochemical routes allowing these organelles, deriving from the adaptation of primordial symbionts, to couple oxidation of substrates to the production of ATP. In this work, concepts were acquired (such as, to name a few, the chemiosmotic mechanism of energy conservation, the import into mitochondria of most organelle proteins, the existence of a resident genome with a different genetic code encoding the remaining 13 polypeptides) that are now established dogmas of modern biology. At the same time, the availability of highly efficient probes and imaging systems has allowed cell biologists to obtain a deep insight into how extracellular signals are conveyed and translated in living cells. An example of this insight has been the demonstration that a variety of extracellular stimuli cause a rise in intracellular Ca2+ concentration of high spatio-temporal complexity, that in turn is specifically decoded by intracellular effectors. Among these effectors are mitochondria themselves, that, endowed with low-affinity transport system for Ca2+, can however be recruited by microdomains generated in their proximity by the opening of Ca2+ channels