From photoprotection to plasticity: transposon activation in the Chlamydomonas det1 mutant.

Transposable elements (TEs) contribute to genomic adaptation but are typically silenced to maintain genome integrity. In this study, we investigated TE activation in a Chlamydomonas reinhardtii mutant deficient in DE-ETIOLATED1 (DET1). This mutant was originally identified for its enhanced high-light tolerance due to constitutive nonphotochemical quenching (NPQ). While NPQ mitigates light-induced stress, its persistent activation compromises growth under low light (LL). Notably, the slow-growing det1 cultures under LL conditions rapidly reverted to a fast-growing phenotype. The recurrent emergence of fast-growing suppressor mutants indicated a previously unrecognized role of DET1 in TE suppression. To explore this possibility, we performed phenotypic, molecular, and genomic analyses, including TE insertion mapping and gene expression studies in det1 and its suppressor mutants. Our analysis uncovered that the phenotypic suppression resulted from the insertion of a specific TE, Bill, into the subunits for a transcription factor for the photoprotective genes LHCSR1/3, CrCO/NF-Ys. These insertions disrupted NPQ, restored efficient light harvesting, and facilitated growth in LL. These results suggest that DET1 integrates NPQ induction for photoprotection and TE mobilization for genomic plasticity, bridging short-term responses with long-term adaptation.