Session Chair: Gunnhildur Ásta Traustadóttir
14:45-15:00: The role of the autophagy protein ATG7 in blood
15:00-15:15: A region of ATG7 evolved in early vertebrates and might account for a new function
15:15-15:30: Epitranscriptomic regulation of DNA repair genes
15:30-15:45: Does SETDB2 play a part in generating the MITFlow transcriptional cell state in melanoma?
Abstracts in session A-Z
Aðalhöfundur: Valgerður J. Hjaltalín
We have described a region of ATG7 that evolved in early vertebrates and has stabilized in mammals, being overall under strong purifying selection. This suggests that the region might account for a new function of the protein. Interestingly, two cancer related sites reside in this region.
Ramile Dilshat. The MITF-low transcriptional state dictates the highly resistant melanoma cells and displays abundant expression of ECM and focal adhesion genes, negative MITF targets. We showed that SETDB2, a direct MITF target, is the epigenetic repressor of MITF-low state and MITF target genes.
Main author: Karen Kristjánsdóttir
Project focuses on a key protein in the DNA-DSB repair pathway, RNF168 and how it is regulated by two members of the AlkB-family of alkylation damage repair proteins, ALKBH3 and FTO. They do so by removing a methylation mark from the RNF168 mRNA transcript.
Author: Fannar Óli Ólafsson. Autophagy is a conserved recycling process vital for cellular homeostasis. ATG7 is among key autophagy proteins where it facilitates the formation of autophagosomal membranes by lipidating LC3. A shorter isoform of ATG7, unable to bind to LC3, is mainly expressed in blood. Its role will be analyzed.