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We present a JWST MIRI medium-resolution spectrometer spectrum (5–27 μ m) of the Type Ia supernova (SN Ia) SN 2021aefx at +415 days past B -band maximum. The spectrum, which was obtained during the iron-dominated nebular phase, has been analyzed in combination with previous JWST observations of SN 2021aefx to provide the first JWST time series analysis of an SN Ia. We find that the temporal evolution of the [Co iii ] 11.888 μ m feature directly traces the decay of ^56 Co. The spectra, line profiles, and their evolution are analyzed with off-center delayed-detonation models. Best fits were obtained with white dwarf (WD) central densities of ρ _c = 0.9−1.1 × 10 ^9 g cm ^−3 , a WD mass of M _WD = 1.33–1.35 M _⊙ , a WD magnetic field of ≈10 ^6 G, and an off-center deflagration-to-detonation transition at ≈0.5 M _⊙ seen opposite to the line of sight of the observer (−30°). The inner electron capture core is dominated by energy deposition from γ -rays, whereas a broader region is dominated by positron deposition, placing SN 2021aefx at +415 days in the transitional phase of the evolution to the positron-dominated regime. The formerly “flat-tilted” profile at 9 μ m now has a significant contribution from [Ni iv ], [Fe ii ], and [Fe iii ] and less from [Ar iii ], which alters the shape of the feature as positrons mostly excite the low-velocity Ar. Overall, the strength of the stable Ni features in the spectrum is dominated by positron transport rather than the Ni mass. Based on multidimensional models, our analysis is consistent with a single-spot, close-to-central ignition with an indication of a preexisting turbulent velocity field and excludes a multiple-spot, off-center ignition.

We present a JWST mid-infrared (MIR) spectrum of the underluminous Type Ia Supernova (SN Ia) 2022xkq, obtained with the medium-resolution spectrometer on the Mid-Infrared Instrument (MIRI) ∼130 days post-explosion. We identify the first MIR lines beyond 14 μ m in SN Ia observations. We find features unique to underluminous SNe Ia, including the following: isolated emission of stable Ni, strong blends of [Ti ii ], and large ratios of singly ionized to doubly ionized species in both [Ar] and [Co]. Comparisons to normal-luminosity SNe Ia spectra at similar phases show a tentative trend between the width of the [Co iii ] 11.888 μ m feature and the SN light-curve shape. Using non-LTE-multi-dimensional radiation hydro simulations and the observed electron capture elements, we constrain the mass of the exploding WD. The best-fitting model shows that SN 2022xkq is consistent with an off-center delayed-detonation explosion of a near-Chandrasekhar mass WD ( ${M}_{{\rm{WD}}}$ ≈1.37 M _⊙ ) of high central density ( ρ _c ≥ 2.0 × 10 ^9 g cm ^−3 ) seen equator-on, which produced M ( ^56 Ni) =0.324 M _⊙ and M ( ^58 Ni) ≥0.06 M _⊙ . The observed line widths are consistent with the overall abundance distribution; and the narrow stable Ni lines indicate little to no mixing in the central regions, favoring central ignition of subsonic carbon burning followed by an off-center deflagration-to-detonation transition beginning at a single point. Additional observations may further constrain the physics revealing the presence of additional species including Cr and Mn. Our work demonstrates the power of using the full coverage of MIRI in combination with detailed modeling to elucidate the physics of SNe Ia at a level not previously possible.

We present a JWST/MIRI low-resolution mid-infrared (MIR) spectroscopic observation of the normal Type Ia supernova (SN Ia) SN 2021aefx at +323 days past rest-frame B -band maximum light. The spectrum ranges from 4 to 14 μ m and shows many unique qualities, including a flat-topped [Ar iii ] 8.991 μ m profile, a strongly tilted [Co iii ] 11.888 μ m feature, and multiple stable Ni lines. These features provide critical information about the physics of the explosion. The observations are compared to synthetic spectra from detailed non–local thermodynamic equilibrium multidimensional models. The results of the best-fitting model are used to identify the components of the spectral blends and provide a quantitative comparison to the explosion physics. Emission line profiles and the presence of electron capture elements are used to constrain the mass of the exploding white dwarf (WD) and the chemical asymmetries in the ejecta. We show that the observations of SN 2021aefx are consistent with an off-center delayed detonation explosion of a near–Chandrasekhar mass ( M _Ch ) WD at a viewing angle of −30° relative to the point of the deflagration to detonation transition. From the strengths of the stable Ni lines, we determine that there is little to no mixing in the central regions of the ejecta. Based on both the presence of stable Ni and the Ar velocity distributions, we obtain a strict lower limit of 1.2 M _⊙ for the initial WD, implying that most sub- M _Ch explosions models are not viable models for SN 2021aefx. The analysis here shows the crucial importance of MIR spectra in distinguishing between explosion scenarios for SNe Ia.

Taste receptor cells use multiple signaling mechanisms to detect different taste stimuli in the oral cavity. Ionic stimuli (sour, salty) interact directly with ion channels to elicit responses, whereas bitter, sweet, and umami tastants activate G protein-coupled receptors to initiate phospholipase C (PLC)-dependent release of calcium from intracellular stores. However, the precise role for PLC in taste responses remains unclear. One study reported that bitter, sweet, and umami detection is abolished in PLCbeta2 knock-out animals, indicating that the perception of these stimuli depends solely on PLCbeta2. In contrast, another study found that PLCbeta2 knock-out mice have a reduced, but not abolished, capacity to detect these taste qualities, suggesting a PLCbeta2-independent signaling pathway may be involved in the detection of taste stimuli. Since PLCbeta2-expressing taste cells do not have conventional synapses or express voltage-gated calcium channels (VGCCs), we sought to determine if any taste cells responding to bitter express VGCCs. We characterized calcium responses generated by bitter stimuli to activate the PLC pathway and 50 mM KCl to activate VGCCs. Comparisons of evoked calcium responses found that these two stimuli generated significantly different responses. Surprisingly, although most responsive taste cells responded to bitter or 50 mM KCl, some taste cells responded to both. Analysis of dual responsive cells found that bitter responses were inhibited by the PLC inhibitor U73122. Immunocytochemical analysis detected PLCbeta3 and IP(3)R1, indicating the presence of multiple PLC signaling pathways in taste cells.

Sensory systems have evolved to collect information about the environment. Each system has developed to gather specific data that are pertinent to an organism's needs, and consequently the systems vary in their abilities to detect external stimuli such as light, sound, vibration, magnetic fields, or chemicals. Although not all sensory systems are present in all organisms, all organisms, even those at the single-cell level, have the ability to detect chemicals in the environment. Chemical detection likely evolved out of organisms' needs to detect food sources and avoid potentially harmful compounds. Higher-level organisms developed two sensory systems to detect environmental chemicals: olfaction and taste. Olfaction is used in many behaviors, such as kin recognition and mate selection, whereas taste is used primarily to determine whether potential food items will be ingested or rejected. The sense of taste involves the detection of five taste qualities: bitter, sweet, salty, sour, and umami, which is the detection of amino acids, specifically glutamate. Because the chemical structures of taste qualities are diverse, numerous mechanisms are used by taste cells to detect these stimuli. This review focuses on our current understanding of the signaling mechanisms used by taste cells to transduce stimulus signals.

The diverse functions of retinal amacrine cells are reliant on the physiological properties of their synapses. Here we examine the role of mitochondria as Ca(2+) buffering organelles in synaptic transmission between GABAergic amacrine cells. We used the protonophore p-trifluoromethoxy-phenylhydrazone (FCCP) to dissipate the membrane potential across the inner mitochondrial membrane that normally sustains the activity of the mitochondrial Ca(2+) uniporter. Measurements of cytosolic Ca(2+) levels reveal that prolonged depolarization-induced Ca(2+) elevations measured at the cell body are altered by inhibition of mitochondrial Ca(2+) uptake. Furthermore, an analysis of the ratio of Ca(2+) efflux on the plasma membrane Na-Ca exchanger to influx through Ca(2+) channels during voltage steps indicates that mitochondria can also buffer Ca(2+) loads induced by relatively brief stimuli. Importantly, we also demonstrate that mitochondrial Ca(2+) uptake operates at rest to help maintain low cytosolic Ca(2+) levels. This aspect of mitochondrial Ca(2+) buffering suggests that in amacrine cells, the normal function of Ca(2+)-dependent mechanisms would be contingent upon ongoing mitochondrial Ca(2+) uptake. To test the role of mitochondrial Ca(2+) buffering at amacrine cell synapses, we record from amacrine cells receiving GABAergic synaptic input. The Ca(2+) elevations produced by inhibition of mitochondrial Ca(2+) uptake are localized and sufficient in magnitude to stimulate exocytosis, indicating that mitochondria help to maintain low levels of exocytosis at rest. However, we found that inhibition of mitochondrial Ca(2+) uptake during evoked synaptic transmission results in a reduction in the charge transferred at the synapse. Recordings from isolated amacrine cells reveal that this is most likely due to the increase in the inactivation of presynaptic Ca(2+) channels observed in the absence of mitochondrial Ca(2+) buffering. These results demonstrate that mitochondrial Ca(2+) buffering plays a critical role in the function of amacrine cell synapses.

Estrogen stimulation of the production of teh yolk protein precursor vitellogenin was demonstrated in immature Kemp's ridley sea turtles. 17beta-Estradiol injection elicited an increase in serum estrogen, protein, protein phosphorus, and total calcium within 7 days. Associated with these changes was the appearance of a single, dimethylformamide-precipitable, 205-kDa estradiol-induced serum protein, which became the predominant serum protein identified by polyacrylamide gel electrophoresis. The effects of estradiol injection were maintained for 3 months following termination of estradiol administration, despite a decline in serum estrogen levels. Although studies in other species have indicated that changes in circulating vitellogenin levels can influence thyroid hormone transport, no changes were observed throughout the study in total blood levels of thyroxine or triiodothyronine or protein binding of these hormones. We conclude that in the immature Kemp's ridley estrogen induces the synthesis and secretion of a vitellogenin which resembles that of other reptiles, but which does not influence thyroid hormone transport. The prolonged presence of vitellogenin in the blood may be due to a lack of an active ovarian uptake mechanism in these immature animals.