Wow! surprised I am incredibly happy for the "Special Prize of the Editor" of "Wissenschaft kommuniziert":

Thanks a lot! This really motiviates me to blog more regularly again in the near future... embarassed

picture modified from Goldstein Lab via flickr

Whoever read the newspaper lately, probably came across this story: the BBC has written about it, but also The Guardian and the Washington Post: there might be life now on the moon! The questions: since when? from where? and what kind? are easy to answer: since April 2019, from Earth and it's water bears or tardigrades. I still remember my biology undergrad classes: tardigrades were a highlight in them! Unfortunately, since my specialization in molecular medicine, developmental biology and genetics I had nothing to do with these maximally cute microscopic creatures. That's why I was all the happier to find more articles on tardigrades within the last couple of years. Above all, their incredible resistance to radiation was of interest. And this superpower is bestowed on tardigrades by this week's gene Dsup, damage suppressor protein. Attention: the dsup gene should not be confused with the sup gene. Because sup encoded the SUPERMAN Protein of the thale cress, or arabidopsis thaliana, probably the most important plant model organism (more on that perhaps in another article).

Virus: CowpeaMosaicVirus3D by Thomas Splettstoesser for, CC-BY-SA-3.0

The year 2018 is about to end and it was yet another extremely eventful year for molecular biology and biomedicine. CRISPR has captured the headlines around the globe. But not every piece of research that has caused a sensation and astonishment this year has been directly related to CRISPR. As early as January 2018, two articles were published in the same issue of the journal Cell, which was jaw-dropping for several members of our working group, including myself. Back then - due to an acute lack of time - I did not manage to explain why these two articles had such an effect. Anyway, here finally is the long overdue article on the ARC gene and the question about whether an evolutionarily ancient virus(!), could be responsible for us being able to remember things so well.

We have reached a stage where the amount of studies that describe the function of a particular gene in a particular model organism and under particular conditions has become unmanageable. At the same time, articles that describe a completely new cellular mechanism that may occur in all animal and plant cells, but has remained hidden so far, became extremely rare. That's why the two articles that appeared in the journal Nature last week are so special. And to understand what makes them special, we need to have a closer look on a paradoxical observation in the field of genetics that has become more prevalent over the last few years.

Genetic engineering methods such as CRISPR nowadays allow the targeted mutation of a gene, so that the function of the encoded protein is completely lost. This is called a genetic knock-out. Other methods, such as the use of RNA interference, allow the downregulation of gene function by blocking the mRNA transcript of the corresponding gene or initiate their degradation. As a result, the translation of these mRNA molecules is disturbed, so that much less of the corresponding protein is formed. However, a few functional molecules remain, which is why we call those methods knock-down procedures. Absurdly, however, it was repeatedly observed that these knock-down approaches lead to a stronger effect than the previously mentioned knock-out approaches, which nevertheless lead to a complete loss of the protein under investigation. How is that possible? This remained a mystery for quite some time…

When in 1979 six research groups independently described a 53 kDa protein, none of the participants suspected to which genetic superstar this protein would develop. This protein, which due to its molecular weight was given the not-so-impressive name p53, is perhaps the most important policeman in our cells; but only as long as it works properly. If p53 loses its functionality, it’s getting pretty dangerous. In fact, no other gene is mutated more frequently in tumor cells than p53. So how does normal p53 manage to keep all of our body cells in check and what does it all have to do with CRISPR?