Kobayashi Mari, Okada Katsuhiko, Ikeuchi Masahiko
Department of Life Sciences (Biology), The University of Tokyo, Komaba 3-8-1, Meguro, Tokyo, 153-8902 Japan.
Plant Cell Physiol. 2005 Sep;46(9):1561-7. doi: 10.1093/pcp/pci169. Epub 2005 Jul 20.
psbK encodes a small transmembrane component of PSII. Here we report that the psbK-disruptant of Synechocystis sp. PCC 6803 cannot survive under photomixotrophic conditions of light and glucose after transient growth, while the wild type is able to grow. A spontaneous yellow-green mutant that recovered the sustained growth under the same conditions was isolated from the psbK-disruptant. Instead of recovery, the mutant largely lost photoautotrophic growth. By phenotype complementation, the mutation was identified in cpcA as a sequence replacement with a close downstream segment, generating an inverted repeat of 23 bp. The mutant phenotype was characterized by (i) the complete loss of alpha- and beta-phycocyanin; (ii) increased accumulation of PSII; and (iii) greatly reduced transcripts harboring cpcA in abundance and in size. The inverted repeat generated in cpcA probably led to the early termination of transcription. A possible mechanism for such a mutation is discussed.
psbK编码光系统II的一个小跨膜组分。在此我们报道,集胞藻PCC 6803的psbK缺失突变体在短暂生长后,无法在光照和葡萄糖的光混合营养条件下存活,而野生型能够生长。从psbK缺失突变体中分离出一个在相同条件下恢复持续生长的自发黄绿突变体。该突变体并非恢复,而是在很大程度上丧失了光合自养生长能力。通过表型互补,在cpcA中鉴定出该突变是与紧邻下游片段的序列置换,产生了一个23 bp的反向重复序列。该突变体的表型特征为:(i)α-和β-藻蓝蛋白完全丧失;(ii)光系统II积累增加;(iii)含有cpcA的转录本在丰度和大小上大幅减少。cpcA中产生的反向重复序列可能导致转录提前终止。讨论了这种突变的一种可能机制。