Proteasome inhibition rapidly exacerbates photoinhibition and impedes recovery during high light stress in Chlamydomonas reinhardtii
Proteasome inhibition rapidly exacerbates photoinhibition and impedes recovery during high light stress in Chlamydomonas reinhardtii
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DOI：
10.1186/s12870-020-2236-6
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发表时间：
2020-01-13
影响因子：
5.3
通讯作者：
Van Hoewyk, Doug
中科院分区：
文献类型：
--
作者：
Mendoza, Felipe;Berry, Carson;Van Hoewyk, Doug
背景蛋白酶体在真核细胞中去除调节蛋白，并控制植物的多种过程。蛋白酶体定位于细胞质和细胞核，但其在植物生物学中的作用最近已扩展到叶绿体，在那里它调节TOC复合物。这反过来控制核编码的叶绿体蛋白质的输入，其重塑叶绿体蛋白质组并促进适当的发育转变。TOC复合物的蛋白酶体调节也抑制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会迅速改变强光诱导的光抑制引起的光合过程。结果蛋白酶体抑制对莱茵衣藻光系统II的短期影响在光胁迫下进行了测量，这使得叶绿素荧光和细胞活力的双重监测。在低光下48小时后，蛋白酶体抑制不影响活力或光化学，但降低细胞浓度和增加细胞体积。两个小时的强光胁迫损害了光系统II的效率，在蛋白酶体抑制细胞，确定减少Fv/Fm和电子传递速率。蛋白酶体抑制细胞中的光抑制升高不是由细胞活力或叶绿素含量的降低引起的。在MG 132处理的细胞中，光抑制的恢复减弱，并抑制重建培养物的生长。蛋白酶体抑制降低从头蛋白质合成，这可能限制了重塑质体蛋白质组的能力，从而阻碍了适应高光胁迫的能力。结论蛋白酶体参与了光系统II的光抑制保护作用。除了强光胁迫外，其他胁迫物-包括金属，干旱和盐-也已知会产生定位于叶绿体的活性氧。因此，植物蛋白酶体的维持可能有助于在非生物胁迫期间保护光合作用，从而在不利条件下提高作物产量。
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.