Bound by Fate: The Role of Reactive Oxygen Species in Receptor-Like Kinase Signaling[OPEN]
نویسندگان
چکیده
In plants, receptor-like kinases (RLKs) and extracellular reactive oxygen species (ROS) contribute to the communication between the environment and the interior of the cell. Apoplastic ROS production is a frequent result of RLK signaling in a multitude of cellular processes; thus, by their nature, these two signaling components are inherently linked. However, it is as yet unclear how ROS signaling downstream of receptor activation is executed. In this review, we provide a broad view of the intricate connections between RLKs and ROS signaling and describe the regulatory events that control and coordinate extracellular ROS production. We propose that concurrent initiation of ROS-dependent and -independent signaling linked to RLKs might be a critical element in establishing cellular responses. Furthermore, we discuss the possible ROS sensing mechanisms in the context of the biochemical environment in the apoplast. We suggest that RLK-dependent modulation of apoplastic and intracellular conditions facilitates ROS perception and signaling. Based on data from plant and animal models, we argue that specific RLKs could be components of the ROS sensing machinery or ROS sensors. The importance of the crosstalk between RLK and ROS signaling is discussed in the context of stomatal immunity. Finally, we highlight challenges in the understanding of these signaling processes and provide perspectives for future research.
منابع مشابه
Reactive Oxygen Species and p38MAPK Have a Role in the Smad2 Linker Region Phosphorylation Induced by TGF-β
Background: Transforming growth factor-β (TGF-β) in addition to the C-terminal region can phosphorylate receptor-regulated Smads (R-Smads) in their linker region. The aim of the present study was to evaluate the role of signaling mediators such as NAD(P)H oxidases (reactive oxygen species [ROS] generators), ROS, and ROS-sensitive p38 mitogen-activated protein kinase (p38MAPK) in this signaling ...
متن کاملInterplay of Phosphorylated Apoptosis Repressor with CARD, Casein Kinase-2 and Reactive Oxygen Species in Regulating Endothelin-1–Induced Cardiomyocyte Hypertrophy
Objective(s): The role of the Apoptosis repressor with caspase recruitment domain (ARC) in apoptosis and in certain hypertrophic responses has been previously investigated, but its regulation of Endothelin-1 induced cardiac hypertrophy remains unknown. The present study discusses the inhibitory role of ARC against endothelin–induced hypertrophy. Results:In present study Endothelin treated car...
متن کاملBiochemical Aspects of Protein Changes in Seed Physiology and Germination
Seed storage proteins are synthesized as sources of carbon, nitrogen and sulfur for the next generation of plants. Reactive oxygen species serve as second messengers for signal transduction; however, molecular targets of oxidant signaling have not been defined. Here, many researchers showes that ligand–receptor mediated signaling promotes reactive oxygen species– dependent protein carbonylation...
متن کاملBiochemical Aspects of Protein Changes in Seed Physiology and Germination
Seed storage proteins are synthesized as sources of carbon, nitrogen and sulfur for the next generation of plants. Reactive oxygen species serve as second messengers for signal transduction; however, molecular targets of oxidant signaling have not been defined. Here, many researchers showes that ligand–receptor mediated signaling promotes reactive oxygen species– dependent protein carbonylation...
متن کاملP22: The Association between TrkB Signaling Pathway and NMDARs in LTP Induction
Long-term potentiation (LTP) is a biological process of learning and memory after a high-frequency train of electrical stimulations. By binding of brain-derived neurotrophic factor (BDNF) to Tropomyosin receptor kinase B (TrKB) receptors in postsynaptic neurons, tyrosine kinase Fyn is bound to these receptors and hereby plays a mediating role to binding and activation of N-methyl-D-aspartic aci...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
عنوان ژورنال:
دوره شماره
صفحات -
تاریخ انتشار 2017