Moseley Jeffrey L, Chang Chiung-Wen, Grossman Arthur R
Carnegie Institution, Department of Plant Biology, 260 Panama Street, Stanford, California 94305, USA.
Eukaryot Cell. 2006 Jan;5(1):26-44. doi: 10.1128/EC.5.1.26-44.2006.
The Chlamydomonas reinhardtii transcription factor PSR1 is required for the control of activities involved in scavenging phosphate from the environment during periods of phosphorus limitation. Increased scavenging activity reflects the development of high-affinity phosphate transport and the expression of extracellular phosphatases that can cleave phosphate from organic compounds in the environment. A comparison of gene expression patterns using microarray analyses and quantitative PCRs with wild-type and psr1 mutant cells deprived of phosphorus has revealed that PSR1 also controls genes encoding proteins with potential "electron valve" functions--these proteins can serve as alternative electron acceptors that help prevent photodamage caused by overexcitation of the photosynthetic electron transport system. In accordance with this finding, phosphorus-starved psr1 mutants die when subjected to elevated light intensities; at these intensities, the wild-type cells still exhibit rapid growth. Acclimation to phosphorus deprivation also involves a reduction in the levels of transcripts encoding proteins involved in photosynthesis and both cytoplasmic and chloroplast translation as well as an increase in the levels of transcripts encoding stress-associated chaperones and proteases. Surprisingly, phosphorus-deficient psr1 cells (but not wild-type cells) also display expression patterns associated with specific responses to sulfur deprivation, suggesting a hitherto unsuspected link between the signal transduction pathways involved in controlling phosphorus and sulfur starvation responses. Together, these results demonstrate that PSR1 is critical for the survival of cells under conditions of suboptimal phosphorus availability and that it plays a key role in controlling both scavenging responses and the ability of the cell to manage excess absorbed excitation energy.
莱茵衣藻转录因子PSR1在磷限制期间控制从环境中清除磷的相关活动中是必需的。清除活性的增加反映了高亲和力磷转运的发展以及细胞外磷酸酶的表达,这些酶能够从环境中的有机化合物中裂解出磷。通过对野生型和缺乏磷的psr1突变体细胞进行微阵列分析和定量PCR来比较基因表达模式,结果表明PSR1还控制着编码具有潜在“电子阀”功能蛋白质的基因——这些蛋白质可作为替代电子受体,有助于防止光合电子传递系统过度激发所导致的光损伤。根据这一发现,缺磷的psr1突变体在光照强度升高时会死亡;而在这些强度下,野生型细胞仍能快速生长。对磷缺乏的适应还涉及到参与光合作用、细胞质和叶绿体翻译的蛋白质编码转录本水平的降低,以及与应激相关的伴侣蛋白和蛋白酶编码转录本水平的增加。令人惊讶的是,缺磷的psr1细胞(而非野生型细胞)还表现出与对硫缺乏的特定反应相关的表达模式,这表明在控制磷和硫饥饿反应的信号转导途径之间存在着迄今未被怀疑的联系。总之,这些结果表明PSR1对于细胞在次优磷可用性条件下的存活至关重要,并且它在控制清除反应以及细胞管理过量吸收的激发能的能力方面发挥着关键作用。