ABSTRACT
AIM: Many individuals play an instrument or sing during childhood, but they often stop later in life. This study surveyed adults representative of the Swedish population about musical activities during childhood. METHODS: We asked 3820 adults (65% women) aged from 27 to 54 from the Swedish Twin Registry, who took extra music lessons to those provided at school, to fill in a web-based questionnaire. Factors analysed were the age they started studying music, the instrument they played, kind of teaching, institution and educational content, number of lessons and perceived characteristics of the lessons, the music environment during their childhood years and their preferred music genre. All variables were dichotomised. RESULTS: Factors strongly associated with continued playing or singing were male sex, young starting age, cultural family background, self-selected instrument, attending music classes and more than once a week, church-related or private education, pop, rock or classical music, playing by ear and improvisation. CONCLUSION: Several significant predictors determined whether a child continued to sing or play an instrument as an adult and many could be externally influenced, such as starting at a young age, taking music classes more than once a week, improvisation and the type of music they played.
Subject(s)
Music/psychology , Recreation/psychology , Singing , Adolescent , Adult , Child , Child, Preschool , Female , Humans , Logistic Models , Male , Middle Aged , Surveys and Questionnaires , SwedenABSTRACT
Neuropeptide Y (NPY) has been implicated in depression, emotional processing and stress response. Part of this evidence originates from human single-nucleotide polymorphism (SNP) studies. In the present study, we report that a SNP in the rat Npy promoter (C/T; rs105431668) affects in vitro transcription and DNA-protein interactions. Genotyping studies showed that the C-allele of rs105431668 is present in a genetic rat model of depression (Flinders sensitive line; FSL), while the SNP's T-allele is present in its controls (Flinders resistant line; FRL). In vivo experiments revealed binding of a transcription factor (CREB2) and a histone acetyltransferase (Ep300) only at the SNP locus of the FRL. Accordingly, the FRL had increased hippocampal levels of Npy mRNA and H3K18 acetylation; a gene-activating histone modification maintained by Ep300. Next, based on previous studies showing antidepressant-like effects of physical activity in the FSL, we hypothesized that physical activity may affect Npy's epigenetic status. In line with this assumption, physical activity was associated with increased levels of Npy mRNA and H3K18 acetylation. Physical activity was also associated with reduced mRNA levels of a histone deacetylase (Hdac5). Conclusively, the rat rs105431668 appears to be a functional Npy SNP that may underlie depression-like characteristics. In addition, the achieved epigenetic reprogramming of Npy provides molecular support for the putative effectiveness of physical activity as a non-pharmacological antidepressant.
Subject(s)
Depression/genetics , Epigenesis, Genetic/physiology , Motor Activity/physiology , Neuropeptide Y/genetics , Polymorphism, Single Nucleotide/genetics , Animals , Deception , Depression/physiopathology , Disease Models, Animal , Gene Expression/genetics , Gene Expression/physiology , Genotype , Hippocampus/chemistry , Hippocampus/physiology , Neuropeptide Y/analysis , Neuropeptide Y/physiology , Polymerase Chain Reaction , Promoter Regions, Genetic/genetics , Promoter Regions, Genetic/physiology , Rats , Transcription Factors/physiologyABSTRACT
Wilms' tumor gene 1 (WT1) is a transcription factor involved in developmental processes. In adult hematopoiesis, only a small portion of early progenitor cells express WT1, whereas most leukemias show persistently high levels, suggesting an oncogenic role. We have previously characterized oncogenic BCR/ABL1 tyrosine kinase signaling pathways for increased WT1 expression. In this study, we show that overexpression of BCR/ABL1 in CD34+ progenitor cells leads to reduced expression of interferon regulatory factor 8 (IRF8), in addition to increased WT1 expression. Interestingly, IRF8 is known as a tumor suppressor in some leukemias and we investigated whether WT1 might repress IRF8 expression. When analyzed in four leukemia mRNA expression data sets, WT1 and IRF8 were anticorrelated. Upon overexpression in CD34+ progenitors, as well as in U937 cells, WT1 strongly downregulated IRF8 expression. All four major WT1 splice variants induced repression, but not the zinc-finger-deleted WT1 mutant, indicating dependence on DNA binding. A reporter construct with the IRF8 promoter was repressed by WT1, dependent on a putative WT1-response element. Binding of WT1 to the IRF8 promoter was demonstrated by chromatin immunoprecipitation. Our results identify IRF8 as a direct target gene for WT1 and provide a possible mechanism for oncogenic effects of WT1 in leukemia.
