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  • In addition JMJ proteins respond to


    In addition, JMJ proteins respond to biotic stress and abiotic stress in plants. Rice genes OsJMJ704 and OsJMJ705, which have demethylase activities of H3K27me2/3 and H3K4me2/3, respectively, regulate defense-related genes and affect the defense ability of rice against bacterial pathogen Xoo (Li et al., 2013; Hou et al., 2015). Abiotic stresses such as heat, salt and drought significantly influence the growth and development of plants, especially crops. The JMJ genes take part in the process of tolerance to abiotic stress. Arabidopsis gene JMJ15 has H3K4 demethylase activity. Over-expression of JMJ15 in plants enhances the tolerance to salt stress, and loss-of-function mutants are sensitive to salt stress (Yang et al., 2012a; Shen et al., 2014). However, research on the function of JMJ protein in response to abiotic stress in rice is to date very limited. OsJMJ703 has been shown to specifically remove histone H3K4 mono-, di-, and trimethylation (Chen et al., 2013; Cui et al., 2013). OsJMJ703 affects the level of H3K4 trimethylation in the promoter region of cytokinin oxidase gene and affects the activity of the retrotransposons Karma and LINE1 (Chen et al., 2013). In this study, we observed the growth and development of rice plants over-expressing OsJMJ703 and RNA interference OsJMJ703, along with tissue FK228 patterns. We found that OsJMJ703 is involved in rice growth and development and influences the flowering time of rice. In addition, OsJMJ703 responds to PEG stress and overexpressing the expression of OsJMJ703 is sensitive to drought stress in rice. This study provides a theoretical basis for the biological function of JmjC protein and improves the study of drought resistance in rice.
    Materials and methods
    Conflicts of interest
    Acknowledgements We thank Dr. Kang Chong of the Institute of Botany, Chinese Academy of Science, for providing the pTCK303 vector. Thank the Rice Genome Resource Center for providing the plasmid (AK121381) to obtain the full length of OsJMJ703.
    Introduction Neuropathic pain is the pain arising directly from a lesion or disease that affects the somatosensory system. Globally, neuropathic pain is a common clinical problem and typically causes patients intense distress [1]. This kind of disease affects 7–10% of the general population worldwide. Accumulating evidence demonstrates that the burden of chronic neuropathic pain is related to the complexity of neuropathic symptoms, poor outcomes and challenging treatment decisions [2]. Neuropathic pain can develop after nerve injury, when deleterious changes occur in injured neurons and along nociceptive and descending modulatory pathways in the central nervous system [3]. Upon nerve injury, inflammatory cells are activated in the peripheral nerve ending and synaptic junctions in the dorsal horn of the spinal cord. These cells include microglia, mast cells, and astrocytes [3]. The activated inflammatory cells secrete inflammatory cytokines or mediators, which act on neurons and regulate the development of neuropathic pain [3], [4]. For instance, activated mast cells secrete inflammatory mediators such as 5-hydroxytryptamine (5-HT) and prostaglandin E2 (PGE2), which stimulate neurons through their receptors [3], [4]. Other inflammatory cytokines include interleukins (IL-1β, IL-2β, IL-6, and IL-8), tumor necrosis factor alpha (TNF-α), C-C motif chemokine ligand 2 (CCL2) and so on [3]. These inflammatory factors cooperate to regulate the activation of neurons and development of neuropathic pain [2], [3]. Neurotrophins such as nerve growth factor, brain-derived neurotrophic factor (BDNF) and neurotrophin 3 (NT-3) have been studied extensively in different animal models of neuropathic pain [5]. For example, the BDNF signaling plays a well-established function in modulating the excitation of the mesolimbic reward system in psychiatric disorders [6]. Importantly, BNDF is a driving force behind neuroplasticity in neuropathic and central sensitization pain [7]. Chronic constrictive injury (CCI) of the sciatic nerve increased the expression of BDNF, which in turn contributed to the nociceptive in CCI mice [6], supporting the notion that BDNF may be a promising target for treatment of neuropathic pain. However, the mechanism by which BDNF is regulated during neuropathic pain remains largely unknown.