👤 David E Conroy

Self-determination theory characterizes drinking motives according to level of autonomy and locus of control and aligns with harm reduction approaches to alcohol use. This study used latent profile analysis (LPA) to identify motivational profiles of self-determined behavioral regulations for drinking and to test their associations with sociodemographic variables and alcohol consumption and outcomes. Adults aged 18-57 (N = 630, M A four-profile model fit best. The "Aimless Drinkers" profile (n = 75, 11.9%) had low intrinsic regulation (e.g., enjoyment of drinking) and was disproportionately male (ORs = 2.35-2.65). The "Pleasure Drinker" profile (n = 114, 18.1%) had average intrinsic and low other regulations and was significantly older (OR = 1.07) than the "Externally Controlled Drinker" profile (n = 177, 28.1%), which had high external regulation (e.g., drinking due to social pressure). Externally controlled drinkers reported greater drinking intensity (M Older individuals were more likely to drink due to intrinsic enjoyment, which may reflect a shift toward greater autonomy over alcohol consumption with increasing age. Drinking primarily for enjoyment also facilitated more positive drinking outcomes. Future research should investigate whether motivational profiles of behavioral regulations for drinking predict long-term trajectories of alcohol consumption and alcohol-related risks. Show less

Centrosomes, the principal microtubule-organising centres in animal cells, contain centrins, small, conserved calcium-binding proteins unique to eukaryotes. Centrin2 binds to xeroderma pigmentosum group C protein (XPC), stabilising it, and its presence slightly increases nucleotide excision repair (NER) activity in vitro. In previous work, we deleted all three centrin isoforms present in chicken DT40 cells and observed delayed repair of UV-induced DNA lesions, but no centrosome abnormalities. Here, we explore how centrin2 controls NER. In the centrin null cells, we expressed centrin2 mutants that cannot bind calcium or that lack sites for phosphorylation by regulatory kinases. Expression of any of these mutants restored the UV sensitivity of centrin null cells to normal as effectively as expression of wild-type centrin. However, calcium-binding-deficient and T118A mutants showed greatly compromised localisation to centrosomes. XPC recruitment to laser-induced UV-like lesions was only slightly slower in centrin-deficient cells than in controls, and levels of XPC and its partner HRAD23B were unaffected by centrin deficiency. Interestingly, we found that overexpression of the centrin interactor POC5 leads to the assembly of linear, centrin-dependent structures that recruit other centrosomal proteins such as PCM-1 and NEDD1. Together, these observations suggest that assembly of centrins into complex structures requires calcium binding capacity, but that such assembly is not required for centrin activity in NER. Show less