Gabrielius Jakutis
Human cells accumulate thousands of new lesions in their DNA every day, yet the vast majority of them do not lead to diseases or other observable damage. Throughout evolution, cells have acquired various ways to retain their functions in the presence of deleterious genetic perturbations. This genetic robustness was known to be achieved by various mechanisms, such as protein feedback loops. Recently, genetic compensation via transcriptional upregulation of related genes (also known as transcriptional adaptation) was discovered as an important mechanism conferring robustness independently of the loss of protein function.
In my PhD, I am developing cell line transcriptional adaptation (TA) models that allow a better temporal dissection of the process in order to acquire a more accurate list of direct targets/adapting genes. I seek to distinguish primary from secondary effects on gene expression, i.e. a specific set of genes that gets upregulated directly by TA in contrast to those genes further modulating the transcriptome. Additionally, I utilize human iPS and HEK293T cells to study transcriptional adaptation in humans.
https://orcid.org/0000-0002-1311-5742