Feedback mechanisms are important for keeping signaling pathways in check and able to respond dynamically to changes in signal intensity. We have found that a gene that has increased expression after karrikin treatment, KARRIKIN UPREGULATED F-BOX1 (KUF1), is likely to have a role in feedback regulation of karrikin and KAI2 ligand (KL) metabolism. Plants that lack a functional KUF1 gene are hypersensitive to KAR1, and also show developmental and transcriptional phenotypes consistent with increased KL abundance.
Because KUF1 is an F-box protein, like MAX2, the many phenotypes of the kuf1 mutant are likely due to overaccumulation of the protein targets of KUF1. In collaboration with Prof. Josh Gendron’s lab at Yale, we have been searching for the protein targets of KUF1. We are characterizing candidate targets through reverse genetic and biochemical approaches. We anticipate that these targets will give us important clues about how karrikin and KL are metabolized, and bring us one step closer to identifying KL.
For further reading, see
Sepulveda C, Guzmán MA, Li Q, Villaécija-Aguilar JA, UGMartinez SE, Kamran M, Khosla A, Liu W, Gendron JM, Gutjahr C, Waters MT, Nelson DC. (2022) “KARRIKIN UP-REGULATED F-BOX 1 (KUF1) imposes negative feedback regulation of karrikin and KAI2 ligand metabolism in Arabidopsis thaliana.” PNAS USA, 119(11).