Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9882083 | Archives of Biochemistry and Biophysics | 2005 | 12 Pages |
Abstract
A pufX gene deletion in the purple bacterium Rhodobacter capsulatus causes a severe photosynthetic defect and increases core light-harvesting complex (LH1) protein and bacteriochlorophyll a (BChl) levels. It was suggested that PufX interrupts the LH1 α/β ring around the reaction centre, allowing quinone/quinol exchange. However, naturally PufXâ purple bacteria grow photosynthetically with an uninterrupted LH1. We discovered that substitutions of the Rhodobacter-specific LH1 α seryl-2 decrease carotenoid levels in PufXâR. capsulatus. An LH1 αS2F mutation improved the photosynthetic growth of a PufXâ strain lacking the peripheral LH2 antenna, although LH1 BChl absorption remained above wild-type, suggesting that Rhodobacter-specific carotenoid binding is involved in the PufXâ photosynthetic defect and LH1 expansion is not. Furthermore, PufX overexpression increased LH1-like BChl absorption without inhibiting photosynthetic growth. PufX+ LH1 αS2-substituted mutant strains had wild-type carotenoid levels, indicating that PufX modulates LH1 carotenoid binding, inducing a conformational change that favours quinone/quinol exchange.
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Authors
Muktak Aklujkar, J. Thomas Beatty,