High light acclimation in the secondary plastids containing diatom Phaeodactylum tricornutum is triggered by the redox state of the plastoquinone pool.

In diatoms the process of energy-dependent chlorophyll fluorescence quenching (qE) has an important role in photoprotection. Three components are essential for qE: 1) the light-dependent generation of a transthylakoidal proton gradient, 2) the de-epoxidation of the xanthophyll diadinoxanthin (Dd) into diatoxanthin (Dt), and 3) specific nuclear-encoded antenna proteins, called LHCX. We used the model diatom Phaeodactylum tricornutum to investigate the concerted light acclimation response of the qE key components LHCX, proton gradient and xanthophyll cycle pigments (Dd+Dt), and to identify the intracellular light responsive trigger. At high light exposure, the up-regulation of three of the LHCX genes and the de novo synthesis of Dd+Dt led to a pronounced rise of qE. By inhibiting either the conversion of Dd to Dt or the translation of LHCX genes, the qE amplification was abolished and the diatom cells suffered from stronger photoinhibition. Artificial modification of the redox state of the plastoquinone (PQ) pool via DCMU and DBMIB resulted in a disturbance of the Dd+Dt synthesis in an opposite way. Moreover, we could increase the transcription of two of the four LHCX genes under low light conditions by reducing the PQ pool using DBMIB. Altogether, our results underline the central role of the redox state of the PQ pool in the light acclimation of diatoms. Additionally, they emphasize strong evidence for the existence of a plastid-to-nucleus retrograde signaling mechanism in an organism with plastids that derived from secondary endosymbiosis.