Director, Dept. of Developmental Genetics, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany since 2012, and prior to that he was a Professor at the University of California San Francisco (Dept. of Biochemistry and Biophysics).

His lab has been investigating developmental processes and tissue regeneration using both forward and reverse genetic approaches, and mostly in the zebrafish model. Several years ago, when investigating the phenotypic differences between knockout (mutant) and knockdown (antisense treated) zebrafish embryos, his lab discovered a cellular process they 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 as well as potential therapeutic avenues based on TA.