 Hello, my name is Guido Blotz and I am one of the authors of the paper Mood-YH gene expression and alternative splicing in controls and polyposis patients, recently published in Human Mutation. The Mood-YH gene encodes a DNA repair glycosylase and approximately 10 years ago it has been found that loss of this gene in the germline predisposes to colorectal polyposis and cancer. Just like in other diseases-orated genes, in a fraction of alterations that have been identified in patients, it is difficult to assess if they are causative for the disease. And in case of the Mood-YH gene, this is additionally complicated by the fact that the gene is strongly alternatively spliced. For example it contains three alternative first axons which are shown in colours in the diagram below. So when an alteration is located in one of the alternatively spliced areas, it may affect only one or a few transcript types. So for understanding the effect that such an alteration has, it is certainly essential to know how relevant the affected transcript types are. However, even if an alteration is located outside the alternatively spliced gene regions, knowledge of the relevant transcripts is also very important if a functional analysis on the protein level is to be performed. And for these reasons, we systematically determined the relevant transcripts of the Mood-YH gene. We detected a tissue-specific regulation of the overall expression and also of the composition of different transcript types. Additionally, we tested the stability of the protein products that the major transcripts encode. And based on all this information, we proposed a panel of the most relevant Mood-YH gene products. We finally analysed a comparatively frequent splice site alteration which is located in one of the alternative first accents and we found that carriers of this alteration have significantly reduced expression of the affected transcript. In the paper, we have included a discussion which deals with the question in how far this functional defect may translate to an increase of polyposis and cancer risk for carriers. With this work, we think we could get a much clearer picture of the expression of the Mood-YH gene and we hope that this will give a much more solid basis for estimation or for functional assessment of unclear genetic alterations found in humans in Mood-YH. So I hope you may now be interested in reading the paper. If you have any questions about this work, you are certainly welcome to contact me. Thank you very much for your interest.