COACHES, CLIMATES, “FIELD” GOALS, AND EFFICACY: A “DE-CONSTRUCTION” OF THE MASTERY-APPROACH TO COACHING AND EXAMINATION OF RELATIONSHIPS TO PSYCHOSOCIAL OUTCOMES IN A YOUTH FOOTBALL PLAYER DEVELOPMENT PROGRAM.

In support of the achievement goal theory (AGT), empirical research has demonstrated psychosocial benefits of the mastery-oriented learning climate. In this study, we examined the effects of perceived coaching behaviors on various indicators of psychosocial well-being (competitive anxiety, self-esteem, perceived competence, enjoyment, and future intentions for participation), as mediated by perceptions of the coach-initiated motivational climate, achievement goal orientations and perceptions of sport-specific skills efficacy. Using a pre-post test design, 1,464 boys, ages 10-15 (M = 12.84 years, SD = 1.44), who participated in a series of 12 football skills clinics were surveyed from various locations across the United States. Using structural equation modeling (SEM) path analysis and hierarchical regression analysis, the cumulative direct and indirect effects of the perceived coaching behaviors on the psychosocial variables at post-test were parsed out to determine what types of coaching behaviors are more conducive to the positive psychosocial development of youth athletes. The study demonstrated that how coaching behaviors are perceived impacts the athletes’ perceptions of the motivational climate and achievement goal orientations, as well as self-efficacy beliefs. These effects in turn affect the athletes’ self-esteem, general competence, sport-specific competence, competitive anxiety, enjoyment, and intentions to remain involved in the sport. The findings also clarify how young boys internalize and interpret coaches’ messages through modification of achievement goal orientations and sport-specific efficacy beliefs.

MECHANISM OF UPREGULATION OF PHOSPHATIDYLCHOLINE SYNTHESIS DURING PICORNAVIRUS INFECTION AND ITS ROLE IN THE DEVELOPMENT OF VIRAL REPLICATION ORGANELLES

Picornaviruses are a group of human and animal pathogens capable of inflicting serious public health diseases and economic burdens. Treatments options through vaccines for prevention or antivirals to cure infection are not available for the vast majority of these viruses. These shortcomings, in the development of vaccines or antivirals therapeutic, are linked to the genetic diversity and to an incomplete understanding of the biology of these viruses. Despite the diverse host range, this group of positive-strand RNA viruses shares the same replication mechanisms, including the development of membranous structures (replication organelles) in the cytoplasm of infected cells. The development of these membranous structures, which serve as sites for the replication of the viral RNA genome, has been linked to the hijacking of elements of the cellular membrane metabolism pathways. Here we show that upon picornavirus infection, there is a specific activation of acyl-CoA synthetase enzymes resulting in strong import and accumulation of long chain fatty acids in the cytoplasm of infected cells. We show that the newly imported fatty acids serve as a substrate for the upregulation of phosphatidylcholine synthesis required for the structural development of replication organelles. In this work, we identified that acyl-CoA synthetase long chain 3 (ACSL3) is required for the upregulation of lipids syntheses and the replication of poliovirus. We have shown that the poliovirus protein 2A was required but not sufficient for the activation of import of long chain fatty acids in infected cells. We demonstrated that the fatty acid import is upregulated upon infection by diverse picornaviruses and that such upregulation is not dependent on activation of ER stress response or the autophagy pathways. In this work, we have demonstrated that phosphatidylcholine was required for the structural development of replication organelles. Phosphatidylcholine synthesis was dispensable for the production of infectious particles at high MOI but required at a low MOI for the protection of the replication complexes from the cellular innate immunity mechanisms.