Parasitic plant infestations dramatically reduce the yield of many major food crops of sub-Saharan Africa and pose a serious threat to food security on the continent. The first committed step of a successful infestation is the germination of parasite seeds in response to a group of related small molecule hormones called strigolactones (SLs), which are emitted by host roots. Despite the important role of strigolactones, it is not clear how host-derived strigolactones germinate parasitic plants. In contrast, gibberellin acts as the dominant hormone for stimulating germination in nonparasitic plant species by inhibiting a set of DELLA repressors. By expressing strigolactone receptors from the parasitic plant Striga hermonthica in GA auxotrophic mutants in Arabidopsis and adding strigolactones, we completely restore germination of GA auxotrophs. Striga receptors coopt and enhance signalling through MAX2, a component of the HTL/KAI2 pathway to circumvent the GA requirement for germination. AtHTL/KAI2 negatively controls the SMAX1 protein and we discovered that loss of SMAX1 function allows germination despite the presence of DELLA repressors. Finally, we defined a specific set of strigolactone-induced genes that led to germination in the absence of GA. We propose that Striga has evolved strigolactone receptors to boost a latent nonparasitic signaling pathway, enabling SLs to become the dominant germination signal and bypass GA-dependent germination in these species.
