Tanaka Atsushi, Ohno Naoki, Nakajima Kensuke, Matsuda Yusuke
Research Center for the Development of Intelligent Self-Organized Biomaterials, Research Center for Environmental Bioscience, and Department of Bioscience, Kwansei-Gakuin University, 2-1 Gakuen, Sanda, Hyogo, Japan, 669-1337.
Research Center for the Development of Intelligent Self-Organized Biomaterials, Research Center for Environmental Bioscience, and Department of Bioscience, Kwansei-Gakuin University, 2-1 Gakuen, Sanda, Hyogo, Japan, 669-1337
Plant Physiol. 2016 Feb;170(2):1105-16. doi: 10.1104/pp.15.01738. Epub 2015 Dec 11.
Our previous study showed that three CO2/cAMP-responsive elements (CCRE) CCRE1, CCRE2, and CCRE3 in the promoter of the chloroplastic β-carbonic anhydrase 1 gene in the marine diatom Phaeodactylum tricornutum (Pptca1) were critical for the cAMP-mediated transcriptional response to ambient CO2 concentration. Pptca1 was activated under CO2 limitation, but the absence of light partially disabled this low-CO2-triggered transcriptional activation. This suppression effect disappeared when CCRE2 or two of three CCREs were replaced with a NotI restriction site, strongly suggesting that light signal cross-talks with CO2 on the cAMP-signal transduction pathway that targets CCREs. The paralogous chloroplastic carbonic anhydrase gene, ptca2 was also CO2/cAMP-responsive. The upstream truncation assay of the ptca2 promoter (Pptca2) revealed a short sequence of -367 to -333 relative to the transcription-start site to be a critical regulatory region for the CO2 and light responses. This core-regulatory region comprises one CCRE1 and two CCRE2 sequences. Further detailed analysis of Pptca2 clearly indicates that two CCRE2s are the cis-element governing the CO2/light response of Pptca2. The transcriptional activation of two Pptcas in CO2 limitation was evident under illumination with a photosynthetically active light wavelength, and an artificial electron acceptor from the reduction side of PSI efficiently inhibited Pptcas activation, while neither inhibition of the linear electron transport from PSII to PSI nor inhibition of ATP synthesis showed an effect on the promoter activity, strongly suggesting a specific involvement of the redox level of the stromal side of the PSI in the CO2/light cross talk.
我们之前的研究表明,海洋硅藻三角褐指藻(Phaeodactylum tricornutum)叶绿体β-碳酸酐酶1基因(Pptca1)启动子中的三个CO2/环磷酸腺苷应答元件(CCRE),即CCRE1、CCRE2和CCRE3,对于环磷酸腺苷介导的对环境CO2浓度的转录反应至关重要。Pptca1在CO2限制条件下被激活,但缺乏光照会部分抑制这种低CO2触发的转录激活。当CCRE2或三个CCRE中的两个被NotI限制性酶切位点取代时,这种抑制作用消失,这强烈表明光信号在靶向CCRE的环磷酸腺苷信号转导途径上与CO2发生相互作用。同源的叶绿体碳酸酐酶基因ptca2也对CO2/环磷酸腺苷有应答。ptca2启动子(Pptca2)的上游截短分析表明,相对于转录起始位点,-367至-333的短序列是CO2和光反应的关键调控区域。这个核心调控区域包含一个CCRE1和两个CCRE2序列。对Pptca2的进一步详细分析清楚地表明,两个CCRE2是控制Pptca2的CO2/光反应的顺式元件。在光合有效光波长的光照下,CO2限制条件下两个Pptca的转录激活很明显,并且来自光系统I还原侧的人工电子受体有效抑制了Pptca的激活,而抑制从光系统II到光系统I的线性电子传递以及抑制ATP合成均未对启动子活性产生影响,这强烈表明光系统I基质侧的氧化还原水平在CO2/光相互作用中具有特定作用。