Optimal stomatal regulation is important for plant adaptation to changing environmental conditions and for maintaining crop yield. The guard-cell signal GABA is produced from glutamate by Glutamate Decarboxylase (GAD) during a reaction that generates carbon dioxide (CO2) as a by-product. Here, we investigated a putative connection between GABA signalling and the more clearly defined CO2 signalling pathway in guard cells. The GABA-deficient mutant lines gad2-1, gad2-2 and gad1/2/4/5 were examined for stomatal sensitivity to various CO2 concentrations. Our findings show a phenotypical discrepancy between the allelic mutant lines gad2-1 and gad2-2 – a weakened CO2 response in gad2-1 (GABI_474_E05) in contrast to a wild-type response in gad2-2 (SALK_028819) and gad1/2/4/5. Through transcriptomic and genomic investigation, we traced the response of gad2-1 to a deletion of full-length Mitogen-activated protein kinase 12 (MPK12) in the GABI-KAT line, thereafter as renamed gad2-1*. Guard cell-specific complementation of MPK12 restored the gad2-1* CO2 phenotype, which confirms the proposed importance of MPK12 to CO2 sensitivity. Additionally, we found that stomatal opening under low atmospheric CO2 occurs independently of the GABA-modulated opening-channel ALMT9. Our results confirm that GABA has a role in modulating the rate of stomatal opening and closing – but not in response to CO2 per se.

中文翻译：

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GABA 不调节拟南芥气孔 CO2 信号传导

最佳气孔调节对于植物适应不断变化的环境条件和维持作物产量非常重要。保卫细胞信号 GABA 是在反应过程中由谷氨酸脱羧酶 (GAD) 从谷氨酸产生的，该反应会产生副产物二氧化碳 (CO2)。在这里，我们研究了保卫细胞中 GABA 信号传导和更明确定义的 CO2 信号传导途径之间的假定联系。检查 GABA 缺陷突变株系 gad2-1、gad2-2 和 gad1/2/4/5 的气孔对不同 CO2 浓度的敏感性。我们的研究结果表明，等位基因突变系 gad2-1 和 gad2-2 之间存在表型差异——gad2-1 (GABI_474_E05) 中的 CO2 反应减弱，而 gad2-2 (SALK_028819) 和 gad1/2/ 中的野生型反应则相反。 4/5。通过转录组学和基因组研究，我们追踪了 gad2-1 对 GABI-KAT 系中全长丝裂原激活蛋白激酶 12 (MPK12) 缺失的反应，此后更名为 gad2-1*。 MPK12 的保卫细胞特异性互补恢复了 gad2-1* CO2 表型，这证实了 MPK12 对 CO2 敏感性的重要性。此外，我们发现低大气二氧化碳下气孔打开的发生与 GABA 调节的打开通道 ALMT9 无关。我们的结果证实，GABA 在调节气孔打开和关闭的速率方面发挥着作用，但本身并不对二氧化碳做出反应。