Poster
Xander C. L Zuijdgeest (he/him/his)
University of Tuebingen
Tubingen, Baden-Wurttemberg, Germany
Jeffery L. Dangl
University of North Carolina at Chapel Hill
Chapel Hill, North Carolina, United States
Farid El Kasmi
Group Leader
University of Tuebingen
Tuebingen, Baden-Wurttemberg, Germany
Findings from your experiments can essentially do two things: agree or disagree with your current hypothesis. But what if your findings align with your hypothesis, and yet you find out later that your hypothesis was wrong all along? What if your interpretation of your results is leading you to a dead end? We studied helper NLRs (RNLs), which are crucial downstream signaling partners to many sensor NLRs in the perception of pathogen effectors. In Arabidopsis, there are two families of RNLs: the ADR1 family and the NRG1 family. These RNLs are potent cell killing machinery upon activation and therefore must be tightly regulated. In this project, we hypothesized that ADR1 family RNLs may be negatively regulated by a member of the NRG1 family, NRG1.1. This hypothesis originated from a combinatorial RNL mutant (adr1-l1-1 adr1-l2-4 nrg1.1-2) that portrayed all the hallmarks of auto-immunity in Arabidopsis. Further genetic evidence suggested that ADR1 was auto-actively signalling in absence of these three other RNLs. We continued to study this finding through genetic and biochemical approaches to uncover the mechanisms behind inter-familial RNL regulation. However, as we furthered our investigation, the puzzle pieces started to no longer fit together. Ultimately, we uncovered problems that originated from two different sources of material that have led us down to a dead end. ‘Failed’ science is not discussed nearly as often as it should be, so let’s talk about it!