Carbonic anhydrases, EPF2 and a novel protease mediate CO2 control of stomatal development.
Carbonic anhydrases, EPF2 and a novel protease mediate CO2 control of stomatal development.
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DOI：
10.1038/nature13452
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发表时间：
2014-09-11
期刊：
影响因子：
64.8
通讯作者：
Schroeder, Julian I.
中科院分区：
文献类型：
--
作者：
Engineer, Cawas B.;Ghassemian, Majid;Anderson, Jeffrey C.;Peck, Scott C.;Hu, Honghong;Schroeder, Julian I.
环境刺激，包括二氧化碳水平升高，调节气孔发育，然而，介导的CO2信号的感知和中继气孔发育机械的关键机制仍然难以捉摸。为了适应CO2的吸收和水分的流失，植物调节气表皮气孔气体交换孔的发育。不同种类的植物表现出气孔密度的下降，以响应大气中CO2的持续上升（参考文献）。迄今为止，一个突变体表现出这种CO2控制的气孔发育反应的失调，hic（这是在细胞壁蜡生物合成缺陷，参考），已经被确认了在这里，我们发现最近分离的拟南芥β-碳酸酐酶双突变体（ca 1 ca 4）表现出对CO2浓度升高的反应逆转，在CO2浓度升高时气孔发育增加。我们的特点是介导这种反应的机制，并确定了一个胞外信号通路参与调节CO2控制的气孔发育的碳酸酐酶。转录物的RNA-seq分析显示，胞外前肽编码基因表皮图案因子2（EPF 2），而不是EPF 1（参考文献），在野生型叶片中诱导，但在升高的CO2水平下不诱导inca 1 ca 4突变体叶片。此外，EPF 2是必不可少的CO2控制气孔发育。利用细胞壁蛋白质组学分析和CO2依赖的转录组学分析，我们确定了一种新的CO2诱导的胞外蛋白酶，CRSP（CO2响应分泌蛋白酶），作为一个调解人的CO2控制气孔发育。我们的研究结果确定机制和基因，在抑制气孔发育的叶片在大气CO2浓度升高，包括碳酸酐酶编码基因CA 1和CA 4和分泌的蛋白酶CRSP，切割前肽EPF 2，反过来抑制气孔发育。这些机制的阐明促进了对植物如何感知和传递升高的CO2信号的理解，并为指导未来研究环境挑战如何调节植物中的气体交换提供了一个框架。
Environmental stimuli, including elevated carbon dioxide levels, regulate stomatal development; however, the key mechanisms mediating the perception and relay of the CO2 signal to the stomatal development machinery remain elusive. To adapt CO2 intake to water loss, plants regulate the development of stomatal gas exchange pores in the aerial epidermis. A diverse range of plant species show a decrease in stomatal density in response to the continuing rise in atmospheric CO2 (ref.). To date, one mutant that exhibits deregulation of this CO2-controlled stomatal development response, hic (which is defective in cell-wall wax biosynthesis, ref.), has been identified. Here we show that recently isolated Arabidopsis thaliana β-carbonic anhydrase double mutants (ca1 ca4) exhibit aninversion in their response to elevated CO2, showing increased stomatal development at elevated CO2 levels. We characterized the mechanisms mediating this response and identified an extracellular signalling pathway involved in the regulation of CO2-controlled stomatal development by carbonic anhydrases. RNA-seq analyses of transcripts show that the extracellular pro-peptide-encoding gene EPIDERMAL PATTERNING FACTOR 2 (EPF2), but not EPF1 (ref.), is induced in wild-type leaves but not inca1 ca4 mutant leaves at elevated CO2 levels. Moreover, EPF2 is essential for CO2 control of stomatal development. Using cell-wall proteomic analyses and CO2-dependent transcriptomic analyses, we identified a novel CO2-induced extracellular protease, CRSP (CO2 RESPONSE SECRETED PROTEASE), as a mediator of CO2-controlled stomatal development. Our results identify mechanisms and genes that function in the repression of stomatal development in leaves during atmospheric CO2 elevation, including the carbonic-anhydrase-encoding genes CA1 and CA4 and the secreted protease CRSP, which cleaves the pro-peptide EPF2, in turn repressing stomatal development. Elucidation of these mechanisms advances the understanding of how plants perceive and relay the elevated CO2 signal and provides a framework to guide future research into how environmental challenges can modulate gas exchange in plants.
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