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ABSTRACT Chemical abundance anomalies in twin stars have recently been considered tell-tale signs of interactions between stars and planets. While such signals are prevalent, their nature remains a subject of debate. On the one hand, exoplanet formation may induce chemical depletion in host stars by locking up refractory elements. On the other hand, exoplanet engulfment can result in chemical enrichment, and both processes potentially produce similar differential signals. In this study, we aim to observationally disentangle these processes by using the Ca ii infrared triplet to measure the magnetic activity of 125 co-moving star pairs with high signal-to-noise ratio, and high-resolution spectra from the Magellan, Keck, and VLT (Very Large Telescope) telescopes. We find that co-natal star pairs in which the two stars exhibit significant chemical abundance differences also show differences in their magnetic activity, with stars depleted in refractories being magnetically more active. Furthermore, the strength of this correlation between differential chemical abundances and differential magnetic activity increases with condensation temperature. One possible explanation is that the chemical anomaly signature may be linked to planet formation, wherein refractory elements are locked into planets, and the host stars become more active due to more efficient contraction during the pre-main-sequence phase or star–planet tidal and magnetic interactions. 

We demonstrate that contrastive representation learning is a computationally efficient and flexible method to incorporate physical constraints, especially those defined by equalities, in machine-learning-based density functional design. 

Intracellular plant immune receptors, termed NLRs (Nucleotide-binding Leucine-rich repeat Receptors), confer effector-triggered immunity. Sensor NLRs are responsible for pathogen effector recognition. Helper NLRs function downstream of sensor NLRs to transduce signaling and induce cell death and immunity. Activation of sensor NLRs that contain TIR (Toll/interleukin-1receptor) domains generates small molecules that induce an association between a downstream heterodimer signalosome of EDS1 (EnhancedDisease Susceptibility 1)/SAG101 (Senescence-AssociatedGene 101) and the helper NLR of NRG1 (NRequired Gene 1). Autoactive NRG1s oligomerize and form calcium signaling channels largely localized at the plasma membrane (PM). The molecular mechanisms of helper NLR PM association and effector-induced NRG1 oligomerization are not well characterized. We demonstrate that helper NLRs require positively charged residues in their N-terminal domains for phospholipid binding and PM association before and after activation, despite oligomerization and conformational changes that accompany activation. We demonstrate that effector activation of a TIR-containing sensor NLR induces NRG1 oligomerization at the PM and that the cytoplasmic pool of EDS1/SAG101 is critical for cell death function. EDS1/SAG101 cannot be detected in the oligomerized NRG1 resistosome, suggesting that additional unknown triggers might be required to induce the dissociation of EDS1/SAG101 from the previously described NRG1/EDS1/SAG101 heterotrimer before subsequent NRG1 oligomerization. Alternatively, the conformational changes resulting from NRG1 oligomerization abrogate the interface for EDS1/SAG101 association. Our data provide observations regarding dynamic PM association during helper NLR activation and underpin an updated model for effector-induced NRG1 resistosome formation.