om92, a glp-1 enhancer mutation, is an allele of ekl-1

Germline stem cell proliferation in C. elegans requires activation of the GLP-1/Notch receptor, which is located on the germline plasma membrane and encoded by the glp-1 gene. We previously identified several genes whose products directly or indirectly promote activity of the GLP-1 signaling pathway by finding mutations that enhance the germline phenotype of a glp-1(ts) allele, glp-1(bn18) . Here, we report phenotypic and molecular analysis of a new ekl-1 allele, ekl-1(om92) , that enhances the glp-1(bn18) phenotype. ekl-1(om92) is a 244 bp deletion predicted to generate a frameshift and premature termination codon, yielding a severely truncated protein, suggesting it is a null allele

The Future of American Sentencing: A National Roundtable on Blakely

In the wake of the dramatic Supreme Court decision in Blakely v. Washington, Stanford Law School convened an assembly of the most eminent academic and professional sentencing experts in the country to jointly assess the meaning of the decision and its implications for federal and state sentencing reform. The event took place on October 8 and 9, just a few months after Blakely came down and the very week that the Supreme Court heard the arguments in United States v. Booker and United States v. Fanfan, the cases that will test Blakely\u27s application to the Federal Sentencing Guidelines. Thus the Roundtable offered these experts an intellectual breathing space at a crucial point in American criminal law. The event was built around six sessions, with shifting panels of participants doing brief presentations on the subject of the session, and with others then joining in the discussion. We are pleased that FSR is able to publish this version of the proceedings of the event-a condensed and edited transcript of the sessions

Videogame-Related Illness and Injury: A Review of the Literature and Predictions for Pokemon GO!

OBJECTIVE: Reports of videogame-related illness and injury soon emerged in the literature with the inception of videogame systems and subsequent development of novel gaming platforms and technologies. In an effort to better detail the impacts of these phenomena and provide recommendations for injury prevention as it relates to Pokemon Go and the larger world of augmented reality games, we conducted an extensive systems-based review of past trends in videogame-related illness and injury from the literature. MATERIALS AND METHODS: A literature review using PubMed, Medline, and PsycInfo databases with search terms Pokemon GO, videogame injuries, augmented reality injuries, and Nintendo Injury was performed. The search was limited to the English language, and the Boolean were used to combine the search terms. RESULTS: The literature search yielded 359 peer-reviewed articles, 44 of which met the study criteria and included in the review. Seventeen additional popular press reports detailing injuries related to Pokémon Go were also incorporated. Videogame-related injuries and illness include both physical trauma as well as psychological and behavioral disorder with unique patterns of injury and illness linked to specific gaming platforms. CONCLUSIONS: As videogames become increasingly advanced and immersive, they expose players to unique and often more serious injury and illness. Augmented reality games, such as Pokemon GO, are the next step in the evolution of this trend and likely portend a future in which many pathologic processes may become increasingly common

Protein Phosphatase 2A-SUR-6/B55 Regulates Centriole Duplication in C. elegans by Controlling the Levels of Centriole Assembly Factors

Centrioles play a crucial role in mitotic spindle assembly and duplicate precisely once per cell cycle. In worms, flies, and humans, centriole assembly is dependent upon a key regulatory kinase (ZYG-1/Sak/Plk4) and its downstream effectors SAS-5 and SAS-6. Here we report a role for protein phosphatase 2A (PP2A) in centriole duplication. We find that the PP2A catalytic subunit LET-92, the scaffolding subunit PAA-1, and the B55 regulatory subunit SUR-6 function together to positively regulate centriole assembly. In PP2A-SUR-6-depleted embryos, the levels of ZYG-1 and SAS-5 are reduced and the ZYG-1- and SAS-5-dependent recruitment of SAS-6 to the nascent centriole fails. We show that PP2A physically associates with SAS-5 in vivo and that inhibiting proteolysis can rescue SAS-5 levels and the centriole duplication defect of PP2A-depleted embryos. Together, our findings indicate that PP2A-SUR-6 promotes centriole assembly by protecting ZYG-1 and SAS-5 from degradation. © 2011 Elsevier Inc