Pantaleno Rosario, Scuffi Denise, Schiel Paula, Schwarzländer Markus, Costa Alex, García-Mata Carlos
Instituto de Investigaciones Biológicas, Consejo Nacional de Investigaciones Científicas y Técnicas, Universidad Nacional de Mar del Plata, Mar del Plata, Argentina.
Institute of Plant Biology and Biotechnology (IBBP), University of Münster, Münster, Germany.
Plant Cell Environ. 2025 Jan;48(1):537-552. doi: 10.1111/pce.15155. Epub 2024 Sep 17.
Plants regulate gas exchange with the environment and modulate transpirational water flow through guard cells, which set the aperture of the stomatal pores. External and internal stimuli are detected by guard cells and integrated into a signalling network that modulate turgor pressure and, hence, pore size. Pathogen-associated molecular patterns are among the stimuli that induce stomatal closure, to prevent pathogen entry through the pores, and this response, also referred to as stomatal immunity, is one of the hallmarks of PAMP-triggered immunity. While reactive oxygen species (ROS)-mediated signalling plays a key role in stomatal immunity, also the gasotransmitter hydrogen sulphide (HS) interacts with key components of the guard cell signalling network to induce stomatal closure. While the role of HS, produced by the main cytosolic source L-cysteine desulfhydrase 1, has been already investigated, there are additional enzymatic sources that synthesize HS in different subcellular compartments. Their function has remained enigmatic, however. In this work, we elucidate the involvement of the mitochondrial HS source, β-cyanoalanine synthase CAS-C1, on stomatal immunity induced by the bacterial PAMP flagellin (flg22). We show that cas-c1 plants are impaired to induce flg22-triggered stomatal closure and apoplastic ROS production, while they are more susceptible to bacterial surface inoculation. Moreover, mitochondrial HS donor AP39 induced stomatal closure in an RBOHD-dependent manner, while depletion of endogenous HS, impaired RBOHD-mediated apoplastic ROS production. In addition, pharmacological disruption of mitochondrial electron transport chain activity, affected stomatal closure produced by flg22, indicating its participation in the stomatal immunity response. Our findings add evidence to the emerging realization that intracellular organelles play a decisive role in orchestrating stomatal signalling and immune responses and suggest that mitochondrial-derived HS is an important player of the stomatal immunity signalling network.
植物通过保卫细胞调节与环境的气体交换，并调节蒸腾水流，保卫细胞决定气孔的孔径。外部和内部刺激被保卫细胞检测到，并整合到一个信号网络中，该网络调节膨压，进而调节孔径大小。病原体相关分子模式是诱导气孔关闭的刺激因素之一，以防止病原体通过气孔进入，这种反应也被称为气孔免疫，是病原体相关分子模式触发的免疫的标志之一。虽然活性氧（ROS）介导的信号传导在气孔免疫中起关键作用，但气体信号分子硫化氢（HS）也与保卫细胞信号网络的关键成分相互作用，诱导气孔关闭。虽然由主要的胞质来源L-半胱氨酸脱硫酶1产生的HS的作用已经得到研究，但还有其他酶来源在不同的亚细胞区室中合成HS。然而，它们的功能仍然是个谜。在这项工作中，我们阐明了线粒体HS来源β-氰基丙氨酸合酶CAS-C1在细菌病原体相关分子模式鞭毛蛋白（flg22）诱导的气孔免疫中的作用。我们表明，cas-c1植物在诱导flg22触发的气孔关闭和质外体ROS产生方面受损，而它们对细菌表面接种更敏感。此外，线粒体HS供体AP39以依赖于RBOHD的方式诱导气孔关闭，而内源性HS的消耗损害了RBOHD介导的质外体ROS产生。此外，线粒体电子传递链活性的药理学破坏影响了flg22产生的气孔关闭，表明其参与了气孔免疫反应。我们的发现为细胞内细胞器在协调气孔信号传导和免疫反应中起决定性作用这一逐渐形成的认识增加了证据，并表明线粒体衍生的HS是气孔免疫信号网络的重要参与者。
