GADD34 induces autophagy through the suppression of the mTOR pathway during starvation Habibul Bari Shozib. Choline acetyltransferase mutations cause myasthenic syndrome (CMS-EA) associated with episodic apnea in humans

Keisuke Kuroda Reevaluation of DISC1 using knockout mice and new antibodies Qiang Qiang 17-AAG, an Hsp90 inhibitor, ameliorates polyglutamine-mediated motor neuron degeneration Mohammad Nizam uddin GADD34 induces autophagy through the suppression of the mTOR pathway during starvation Habibul Bari Shozib. Choline acetyltransferase mutations cause myasthenic syndrome (CMS-EA) associated with episodic apnea in humans Hirotaka Nagai Diameter of multi-walled carbon nanotubes and nanofibres is a critical factor in mesothelial injury and subsequent inflammation Molecular pathomechanism of aberrant splicing of exon P3A in CHRNA1 due to a mutation causes congenital myasthenic syndrome Each presentation will last 10 minutes followed by 2 minutes for questions. Title: Reevaluation of DISC1 using knockout mice and new antibodies Background: Translocation of the Disrupted in Schizophrenia 1 (DISC1) gene is associated with schizophrenia. This gene was originally identified in the large Scottish family in which a balanced t(1;11) translocation that co-segregates with schizophrenia and other major mental illnesses. This translocation disrupts the DISC1 locus, and may result in loss of function via haplo-insufficiency or dominant-negative effects of a predicted truncated protein product. Recent studies have reported many functions and many interacting proteins of DISC1. According to these studies, DISC1 has multiple splice variants, expresses in both neuron and glia, and plays multiple roles in neuronal development through its interactions with different partners. Problem: in vivo functions of DISC1 have not been defined, particularly in knockout mice. Hypothesis: DISC1 is essential for normal embryonic development, and loss of DISC1 will produce abnormal, schizophrenic mice. Methods: DISC1 knockout mice, and novel DISC1 antibodies, were generated to evaluate the effects of DISC1 in vivo. Results: Unexpectedly, DISC1 homozygous deletion mice are viable and fertile, and no gross phenotype is observed. Using our novel antibodies, we also found that DISC1 does not have splicing variants, does not express in some mice strains, and is detected in many tissues during development, but hardly detectable in adult mice. We are now performing immunohistochemical and behavior analysis to further evaluate reported DISC1 functions. Conclusions: DISC1 may not be required for normal mouse embryogenesis or behavior. Novelty: The biological role of DISC1 and commercial antibodies used to evaluate its expression may need to be reevaluated. Title: 17-AAG, an Hsp90 inhibitor, ameliorates polyglutamine-mediated motor neuron degeneration. Background: Heat-shock protein 90 (Hsp90) functions as a multichaperone complex that folds, assembles and regulates homeostasis of its client proteins. Androgen receptor (AR), a pathogenic gene product in spinal and …