SAP97 has been shown to interact with the C-terminus of NMDA and a-amino-3-hydroxy-5-methyl-4isoxazolepropionic acid receptors. Recently, SAP97 has also been implicated in trafficking of NMDARs at the cell surface by sorting them through an unconventional secretory pathway. In this study, we report a novel role for Lomitapide Mesylate DlgS97 and SAP97 in the development of Cinoxacin tolerance to ethanol. By testing multiple independently isolated dlg1 alleles, we determined that DlgS97 is required for the development of rapid ethanol tolerance in Drosophila. We further demonstrate that hypomorphic mutants of Nmdar1, encoding the Drosophila NMDA receptor 1 subunit, or Camguk/Caki, encoding the homolog of CASK that interacts with the L27 domain of DlgS97, exhibit reduced ethanol tolerance. Co-immunoprecipitation of dNR1 and DlgS97 confirmed a physical interaction of DlgS97 and NMDARs. We propose that this interaction is of functional relevance to ethanol tolerance development. Lastly, we show that adult mice with reduced expression of SAP97 display deficits in the development of rapid tolerance to the sedative/hypnotic effects of ethanol, measured using regain of the loss of righting response. Unless otherwise stated, adult male flies were used for all experiments. Flies were collected under CO2 anesthesia 2�C3 days before experiments. Ethanol sensitivity and tolerance were quantified using the inebriometer, an apparatus that measures the loss of postural control with increasing time of exposure to ethanol vapor of a sample population of flies. To quantify ethanol tolerance, a sample of,120 flies was exposed to ethanol vapor at a relative flow rate of 60/40 ethanol vapor/humidified air for 30 min, transferred to large vials containing fly food, and allowed to recover from sedation for an additional 3.5 hr. In parallel, a second, control sample otherwise identically treated was exposed to humidified air without ethanol at an equivalent total flow rate and allowed to recover. Following recovery, each pair of ethanol pre-exposed and control samples were assayed using side-by-side inebriometers. Placenta is a highly specialized temporary organ responsible for the normal progression of pregnancy in mammals. Defects in implantation, placental development and maturation lead to complications in pregnancy and newborns. Aberrant placental expression of apoptosis and inflammation-related genes in early pregnancy was found in recurrent miscarriage and hydatidiform mole samples. Altered placental transcription of metabolic regulatory genes has been associated to affected fetal growth and maternal pregnancy complications such as preeclampsia and gestational diabetes mellitus. Differential expression of some genes is common to several pregnancy complications, serving as biomarkers for malfunctioning placenta. Despite the great importance of placenta in mediating the rapid physiological changes in pregnancy, data on the temporal dynamics of human placental gene expression are limited. Large-scale differences in DNA 
methylation levels between first, second and third trimesters support the gestational-age dependent function of placental genes. So far, only three published studies focus on gene expression in term placenta compared to either early or mid-gestation pregnancy, or both. All studies agree that global gene expression undergoes a profound transformation at the end of pregnancy, affecting up to 25% of placental transcriptome and involving coordinated up- or downregulation of functionally linked loci to achieve rapid changes in placental function.