Molecular genetic and physiological investigations into the acclimation of the cyanobacterial photosynthetic apparatus to nutrient deprivation.

摘要

When the cyanobacterium Synechococcus sp. Strain PCC 7942 (a photoautotrophic, oxygen-evolving prokaryote) is deprived of an essential nutrient, growth stops and the cells appear yellow or yellow-green instead of the normal blue-green. This 'bleaching' of cell pigmentation is mainly due to the degradation of the major light-harvesting pigments of the cells, the phycobiliproteins, which are assembled into water-soluble, macromolecular complexes called phycobilisomes. Phycobilisomes were shown to be degraded in two steps in nitrogen- or sulfur-deprived cells. The size of the phycobilisomes was first reduced by the removal, or trimming, of distal rod components, and the trimmed phycobilisomes were then completely degraded. In contrast, phosphorus-deprived cells exhibited little phycobilisome degradation. Nutrient-deprived cells also exhibited a decline in photosystem II activity. However, photosystem I remained active in all three cases, probably providing energy via cyclic photophosphorylation for the maintenance of basic cellular processes.; To identify genes involved in this acclimation of the photosynthetic apparatus to nutrient deficiency, a mutant (nb11) that did not bleach during sulfur deprivation was isolated. nb11 appeared normal except that it could not degrade its phycobilisomes during either nitrogen or sulfur deprivation. nb11 was complemented by a novel gene, designated nblA (non{dollar}underline{lcub}rm bl{rcub}{dollar}eaching), that was transcriptionally activated in nutrient-deprived cells. Increased expression of nblA was shown to be necessary, and perhaps sufficient, to trigger phycobilisome degradation.; A second novel gene (txlA, thioredoxin-like), a new member of the family of protein disulfide oxidoreductases, was identified just downstream and in the opposite orientation of nblA. txlA was constitutively transcribed, and antisense txlA mRNA, driven from the nblA promoter, was also produced in nutrient-deprived cells. Disruption of txlA at the C-terminus interfered with the efficient conversion of the primary products of photochemistry into growth. This metabolic defect affected the regulation of cellular photosynthetic pigment and reaction center contents, and the effect observed appeared to depend on the interaction of TxlA with a second locus that was polymorphic in the wild-type strain. Further examination of txlA may provide valuable new insights into the regulation of the photosynthetic apparatus.