Professor Stainier’s Bio:
1984: BA Biology, Brandeis University; 1990: PhD in Biochemistry and Molecular Biology, Harvard University; 1990-1994: Postdoc, Massachusetts General Hospital; 1995, I set up my own lab at the University of California San Francisco (Dept. of Biochemistry and Biophysics); since 2012, Director, Dept. of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Germany.

My lab has mostly been concerned with investigating developmental processes (e.g., cardiovascular development) and tissue regeneration (e.g., adult heart regeneration) using both forward and reverse genetic approaches, and mostly in the zebrafish model. Several years ago, when investigating the phenotypic difference between knockout (mutant) and knockdown (antisense treated) zebrafish embryos, we discovered a cellular process we termed transcriptional adaptation (TA). In this process, mutant mRNA degradation, likely via degradation products or their derivatives, triggers the transcriptional modulation of so-called adapting genes. In some cases, e.g., when one (or more) of the upregulated adapting genes is functionally redundant with the mutated gene, this process compensates for the loss of the mutated gene’s product. Notably, unlike other mechanisms underlying genetic robustness, TA is not triggered by the loss of protein function. This unexpected observation has prompted studies into the machinery of TA and the contexts in which it functions.