Interferon (IFN)-like antiviral effect is induced by unspecific cross-linking of cell surface receptors

Photosystem I preparations were irradiated with UV to destroy vitamin K₁ in situ. The depletion of vitamin K₁ resulted in inactivation of NADP⁺ photoreduction and introduction of a 220 ms component in the flash generated P700⁺ re-reduction at room temperature. The photoreduction of the terminal FeS centers FA and FB in control and vitamin K₁-depleted preparations at 7 K were comparable. The data confirm that vitamin K₁ is functionally implicated in primary electron transfer reactions in PS I at physiological temperature, and that the anomalous results at cryogenic temperature may be explicable in terms of a by-pass of the vitamin K₁ acceptor site or heterogeneity introduced into the photosystem by quinone removal.