CHARACTERIZING THE COOL KOIs. V. KOI-256: A MUTUALLY ECLIPSING POST-COMMON ENVELOPE BINARY

We report that Kepler Object of Interest 256 (KOI-256) is a mutually eclipsing post-common envelope binary (ePCEB), consisting of a cool white dwarf (M = 0.592 +/- 0.089 MSun, R = 0.01345 +/- 0.00091 RSun, Teff = 7100 +/- 700 K) and an active M3 dwarf (M = 0.51 +/- 0.16 MSun, R = 0.540 +/- 0.014 RSun, Teff = 3450 +/- 50 K) with an orbital period of 1.37865 +/- 0.00001 days. KOI-256 is listed as hosting a transiting planet-candidate by Borucki et al. and Batalha et al.; here we report that the planet-candidate transit signal is in fact the occultation of a white dwarf as it passes behind the M dwarf. We combine publicly-available long- and short-cadence Kepler light curves with ground-based measurements to robustly determine the system parameters. The occultation events are readily apparent in the Kepler light curve, as is spin-orbit synchronization of the M dwarf, and we detect the transit of the white dwarf in front of the M dwarf halfway between the occultation events. The size of the white dwarf with respect to the Einstein ring during transit (REin = 0.00473 +/- 0.00055 RSun) causes the transit depth to be shallower than expected from pure geometry due to gravitational lensing. KOI-256 is an old, long-period ePCEB and serves as a benchmark object for studying the evolution of binary star systems as well as white dwarfs themselves, thanks largely to the availability of near-continuous, ultra-precise Kepler photometry.Comment: To be published in the Astrophysical Journa

Impaired Amino Acid Transport At The Blood Brain Barrier Is A Cause Of Autism Spectrum Disorder

Autism spectrum disorders (ASD) are a group of genetic disorders often overlapping with other neurological conditions. We previously described abnormalities in the branched-chain amino acid (BCAA) catabolic pathway as a cause of ASD. Here, we show that the solute carrier transporter 7a5 (SLC7A5), a large neutral amino acid transporter localized at the bloodbrainbarrier (BBB), has an essential role in maintaining normal levels of brain BCAAs. In mice, deletion of Slc7a5 from the endothelial cells of theBBBleads to atypical brain amino acid profile, abnormal mRNA translation, and severe neurological abnormalities. Furthermore, we identified several patients with autistic traits and motor delay carrying deleterious homozygous mutations in the SLC7A5 gene. Finally, we demonstrate that BCAA intracerebroventricular administration ameliorates abnormal behaviors in adult mutant mice. Our data elucidate a neurological syndrome defined by SLC7A5 mutations and support an essential role for the BCAA in human brain function.WoSScopu