Dutta Siddhartha, Mohanty Sasmita, Tripathy Baishnab C
School of Life Sciences, Jawaharlal Nehru University, New Delhi 110 067, India.
Plant Physiol. 2009 Jun;150(2):1050-61. doi: 10.1104/pp.109.137265. Epub 2009 Apr 29.
Modulation of photosynthesis and chloroplast biogenesis, by low and high temperatures, was studied in 12-d-old pea (Pisum sativum) plants grown at 25 degrees C and subsequently exposed to 7 degrees C or 40 degrees C up to 48 h. The decline in variable chlorophyll a fluorescence/maximum chlorophyll a fluorescence and estimated electron transport rate in temperature-stressed plants was substantially restored when they were transferred to room temperature. The ATP-driven import of precursor of small subunit of Rubisco (pRSS) into plastids was down-regulated by 67% and 49% in heat-stressed and chill-stressed plants, respectively. Reduction in binding of the pRSS to the chloroplast envelope membranes in heat-stressed plants could be due to the down-regulation of Toc159 gene/protein expression. In addition to impaired binding, reduced protein import into chloroplast in heat-stressed plants was likely due to decreased gene/protein expression of certain components of the TOC complex (Toc75), the TIC complex (Tic20, Tic32, Tic55, and Tic62), stromal Hsp93, and stromal processing peptidase. In chill-stressed plants, the gene/protein expression of most of the components of protein import apparatus other than Tic110 and Tic40 were not affected, suggesting the central role of Tic110 and Tic40 in inhibition of protein import at low temperature. Heating of intact chloroplasts at 35 degrees C for 10 min inhibited protein import, implying a low thermal stability of the protein import apparatus. Results demonstrate that in addition to decreased gene and protein expression, down-regulation of photosynthesis in temperature-stressed plants is caused by reduced posttranslational import of plastidic proteins required for the replacement of impaired proteins coded by nuclear genome.
研究了低温和高温对12日龄豌豆（Pisum sativum）植株光合作用和叶绿体生物发生的调节作用。这些植株在25℃下生长，随后分别暴露于7℃或40℃环境中长达48小时。将温度胁迫处理的植株转移至室温后，其可变叶绿素a荧光/最大叶绿素a荧光比值的下降以及估算的电子传递速率均得到显著恢复。在热胁迫和冷胁迫的植株中，由ATP驱动的核酮糖-1,5-二磷酸羧化酶小亚基前体（pRSS）向质体的导入分别下调了67%和49%。热胁迫植株中pRSS与叶绿体被膜的结合减少，可能是由于Toc159基因/蛋白表达下调所致。除了结合受损外，热胁迫植株中叶绿体蛋白导入减少可能还归因于转运器外膜复合物（TOC复合物，Toc75）、转运器内膜复合物（TIC复合物，Tic20、Tic32、Tic55和Tic62）、基质Hsp93以及基质加工肽酶某些组分的基因/蛋白表达降低。在冷胁迫植株中，除Tic110和Tic40外，大多数蛋白导入装置组分的基因/蛋白表达未受影响，这表明Tic110和Tic40在低温抑制蛋白导入过程中起核心作用。完整叶绿体在35℃下加热10分钟会抑制蛋白导入，这意味着蛋白导入装置的热稳定性较低。结果表明，除基因和蛋白表达降低外，温度胁迫植株光合作用下调还源于用于替换核基因组编码的受损蛋白所需的质体蛋白翻译后导入减少。
