BACKGROUND Proteasomes remove regulatory proteins in eukaryotic cells, and control a variety of plant processes. Proteasomes are localized to the cytosol and nuclear, but their role in plant biology has recently been extended to chloroplasts, where it regulates TOC complex. This is turn controls the import of nuclear-encoded chloroplastic proteins, which remodels the chloroplast proteome and facilitates proper developmental transitions. Proteasomal regulation of the TOC complex also alleviates stressors that generate reactive oxygen species. These recent advances motivated us to determine if proteasome inhibition rapidly alters photosynthetic processes stemming from photoinhibition induced by high light. RESULTS The short-term effects of proteasome inhibition on photosystem II during light stress was measured in Chlamydomonas reinhardtii, which allowed the dual monitoring of both chlorophyll fluorescence and cell viability. After 48 h at low light, proteasome inhibition did not affect viability or photochemistiry, but decreased cell concentration and increased cell volume. Two hours of high light stress impaired the efficiency of photosystem II in proteasome-inhibited cells, as determined by a decrease in Fv/Fm and the electron transport rate. Elevated photoinhibition in proteasome inhibited cells was not caused by a decrease in cell viability or chlorophyll content. Recovery from photoinhibition was attenuated in MG132-treated cells, and suppressed growth of a reestablished culture. Proteasome inhibition decreased de novo protein synthesis, which possibly constrained the ability to remodel the plastid proteome, and thus hampering the ability to adjust to high light stress. CONCLUSION The proteasome is implicated in protecting photosystem II from photoinhibition. In addition to high light stress, other stressors- including metals, drought, and salt- are also known to generate reactive oxygen species localized to the chloroplast. Therefore, proteasome maintenance in plants may help protect photosynthesis during abiotic stress, which could increase crop yield during adverse conditions.

中文翻译：

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蛋白酶体的抑制迅速加剧了莱茵衣藻的高光胁迫期间的光抑制并阻碍了恢复。

背景技术蛋白酶体去除真核细胞中的调节蛋白，并控制多种植物过程。蛋白酶体位于细胞质和核中，但它们在植物生物学中的作用最近已扩展到叶绿体，在叶绿体中它调节TOC复合物。这反过来又控制了核编码的叶绿体蛋白的导入，从而重塑叶绿体蛋白质组并促进适当的发育过渡。蛋白酶体对TOC复合物的调节还缓解了产生活性氧的应激源。这些最新进展促使我们确定蛋白酶体抑制是否能迅速改变强光诱导的光抑制引起的光合作用过程。结果在莱茵衣藻中测定了蛋白酶体抑制对光胁迫下光系统II的短期影响，从而可以同时监测叶绿素荧光和细胞活力。在弱光下48小时后，蛋白酶体抑制作用不会影响生存力或光化学反应，但会降低细​​胞浓度并增加细胞体积。根据Fv / Fm和电子传输速率的降低，两小时的高光胁迫削弱了光系统II在蛋白酶体抑制细胞中的效率。蛋白酶体抑制细胞中光抑制的升高不是由细胞活力或叶绿素含量的降低引起的。在MG132处理的细胞中，光抑制的恢复减弱，并抑制了重建培养物的生长。蛋白酶体的抑制降低了从头蛋白质的合成，这可能限制了质体蛋白质组重塑的能力，从而阻碍了适应高光胁迫的能力。结论蛋白酶体参与保护光系统II免受光抑制作用。除了高光胁迫外，还已知其他胁迫源（包括金属，干旱和盐分）会产生定位于叶绿体的活性氧。因此，植物中的蛋白酶体维持可能有助于保护非生物胁迫期间的光合作用，这可能会在不利条件下提高作物产量。