The proteasome is an essential protein-degradation machinery in eukaryotic cells that controls protein turnover and thereby the biogenesis and function of cell organelles. Chloroplasts import thousands of nuclear-encoded precursor proteins from the cytosol, suggesting that the bulk of plastid proteins is transiently exposed to the cytosolic proteasome complex. Therefore, there is a cytosolic equilibrium between chloroplast precursor protein import and proteasomal degradation. We show here that a shift in this equilibrium, induced by mild genetic proteasome impairment, results in elevated precursor protein abundance in the cytosol and significantly increased accumulation of functional photosynthetic complexes in protein import-deficient chloroplasts. Importantly, a proteasome lid mutant shows improved photosynthetic performance, even in the absence of an import defect, signifying that functional precursors are continuously degraded. Hence, turnover of plastid precursors in the cytosol represents a mechanism to constrain thylakoid membrane assembly and photosynthetic electron transport.

蛋白酶体是真核细胞中重要的蛋白质降解机制，它控制蛋白质周转，从而控制细胞器的生物发生和功能。叶绿体从细胞质中输入数千个核编码的前体蛋白，这表明大部分质体蛋白短暂地暴露于细胞质蛋白酶体复合物中。因此，叶绿体前体蛋白输入和蛋白酶体降解之间存在细胞质平衡。我们在这里表明，由轻度遗传蛋白酶体损伤引起的这种平衡的转变，导致细胞质中前体蛋白丰度升高，并显着增加蛋白质输入缺陷的叶绿体中功能性光合复合物的积累。重要的是，即使没有输入缺陷，蛋白酶体盖突变体也显示出改善的光合作用性能，这表明功能前体不断降解。因此，细胞质中质体前体的周转代表了一种限制类囊体膜组装和光合电子传递的机制。