Greater fruit selection following an appearance-based compared with a health-based health promotion poster

Background: This study investigated the impact of an appearance-based compared to a traditional health-based public health message for healthy eating. Methods: 166 British University students (41 male; aged 20.6±1.9 years) were randomized to view either an appearance-based (n=82) or a health-based (n=84) fruit promotion poster. Intentions to consume fruit and immediate fruit selection (laboratory observation) were assessed immediately after poster-viewing and subsequent self-report fruit consumption was assessed 3 days later. Results: Intentions to consume fruit were not predicted by poster type (β=0.03, p=0.74), but were associated with fruit-based liking, past consumption, attitudes, and social norms (smallest β=0.16, p=0.04). Immediate fruit selection was greater following the appearance-based compared to the health-based poster (β=-0.24, p<0.01), and this effect remained when controlling for participant characteristics (β=-0.21, p<0.01). Subsequent fruit consumption was greater following the appearance-based compared to the health-based poster (β=-0.22, p=0.03), but this effect became non-significant on consideration of participant characteristics (β=-0.15, p=0.13), and was instead associated with fruit-based liking and past consumption (smallest β=0.24, p=0.03). Conclusions: These findings demonstrate the clear value of an appearance-based compared to a health-based health promotion poster for increasing fruit selection. A distinction between outcome measures, and the value of a behavioural measure is also demonstrated

Xeroderma Pigmentosum Groups C and A in Algerian Patients with Deregulation of both Transcription and DNA Repair

International audienceXeroderma Pigmentosum (XP) is a rare autosomal recessive disorder characterized by an extreme sensitivity to UV rays from sunlight, a high incidence of skin cancer and occasional neurological symptoms. XP, primarily defined as a DNA repair syndrome, has been found associated with defects in the Nucleotide Excision Repair (NER) pathway, and more recently by transcriptional deregulation. XP results from mutations in eight genes (XPA to XPG and XPV) coding for proteins involved in NER. Abstract We report here two cases of XP patients from Algeria, describe their clinical features, identify the causative mutations, and molecularly define their etiology. We determined that each XP individual bears XPC and XPA mutations respectively. Both mutations disrupt expression of their corresponding genes: while the XPC p.Val548Alafs*25 variant was not expressed, the truncated XPA p.Arg228* variant was detected in the patient's cells. Unscheduled DNA synthesis (UDS) and Recovery of RNA synthesis after DNA damage (RRS) assays, as well as immunofluorescence on Ultraviolet-irradiated patient cells showed deficiency in the NER pathway. Moreover, we also found that the patients' cells were defective in transcription, especially certain Retinoic-acid receptor (RAR)-responsive genes. Altogether our data revealed both DNA repair and transcriptional defaults that defined the molecular etiology for these two XP individuals, and may help to understand some of the patients' clinical features

XPC is an RNA polymerase II cofactor recruiting ATAC to promoters by interacting with E2F1

International audienceThe DNA damage sensor XPC is involved in nucleotide excision repair. Here we show that in the absence of damage, XPC co-localizes with RNA polymerase II (Pol II) and active post-translational histone modifications marks on a subset of class II promoters in human fibroblasts. XPC depletion triggers specific gene down-expression due to a drop in the deposition of histone H3K9 acetylation mark and pre-initiation complex formation. XPC interacts with the histone acetyltransferase KAT2A and specifically triggers the recruitment of the KAT2A-containing ATAC complex to the promoters of down-expressed genes. We show that a strong E2F1 signature characterizes the XPC/KAT2A-bound promoters and that XPC interacts with E2F1 and promotes its binding to its DNA element. Our data reveal that the DNA repair factor XPC is also an RNA polymerase II cofactor recruiting the ATAC coactivator complex to promoters by interacting with the DNA binding transcription factor E2F1