Depletion of Vipp1 in Synechocystis sp PCC 6803 affects photosynthetic activity before the loss of thylakoid membranes

Depletion of Vipp1 in Synechocystis sp PCC 6803 affects photosynthetic activity before the loss of thylakoid membranes
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DOI:
10.1111/j.1574-6968.2008.01470.x
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发表时间:
2009-03-01
影响因子:
2.1
通讯作者:
Xu, Xudong
Xu, Xudong
中科院分区:
生物学4区
文献类型:
--
作者:
Gao, Hong;Xu, Xudong

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Synechocystis sp. PCC 6803的vipp1突变体在混合营养和异养条件下都不能完全分离。一个具有铜调控启动子的vipp1基因(P-petE-vipp1)被整合到merodiploid突变体基因组的中性平台中。铜诱导P-petE-vipp1的表达,使vipp1突变体完全分离,并观察了胞囊胞菌6803在质体1 (vipp1)中具有不同水平的囊泡诱导蛋白的表型。当P-petE-vipp1因铜剥夺而关闭时,聚囊藻几乎同时失去Vipp1和光合活性,并在后期失去类囊体膜和细胞活力。光系统II (PSII)介导的电子转移比PSII介导的电子转移减少得快得多。通过一系列浓度测试,我们发现在0.025 μ M Cu2+培养基中生长的P-petE-vipp1细胞类囊体膜没有减少,但光合活性和活力大大降低。这些结果表明,与之前的报道相反,光合活性的丧失可能不是由于类囊体膜的丧失,而可能是由Synechocystis 6803中Vipp1的丧失更直接地引起的。
A vipp1 mutant of Synechocystis sp. PCC 6803 could not be completely segregated under either mixotrophic or heterotrophic conditions. A vipp1 gene with a copper-regulated promoter (P-petE-vipp1) was integrated into a neutral platform in the genome of the merodiploid mutant. The copper-induced expression of P-petE-vipp1 allowed a complete segregation of the vipp1 mutant and observation of the phenotype of Synechocystis 6803 with different levels of vesicle-inducing protein in plastids 1 (Vipp1). When P-petE-vipp1 was turned off by copper deprivation, Synechocystis lost Vipp1 and photosynthetic activity almost simultaneously, and at a later stage, thylakoid membranes and cell viability. The photosystem II (PSII)-mediated electron transfer was much more rapidly reduced than the PSI-mediated electron transfer. By testing a series of concentrations, we found that P-petE-vipp1 cells grown in medium with 0.025 mu M Cu2+ showed no reduction of thylakoid membranes, but greatly reduced photosynthetic activity and viability. These results suggested that in contrast to a previous report, the loss of photosynthetic activity may not have been due to the loss of thylakoid membranes, but may have been caused more directly by the loss of Vipp1 in Synechocystis 6803.