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MYB transcription factors are important regulators of the plant response to abiotic stress. Their participation in the salinity stress of the key forage legume species alfalfa (Medicago sativa) was investigated here by comparing the transcriptomes of the two cultivars Dryland (DL) and Sundory (SD), which differed with respect to their ability to tolerate salinity stress. When challenged by the stress, DL plants were better able than SD ones to scavenge reactive oxygen species. A large number of genes encoding transcription regulators, signal transducers and proteins involved in both primary and secondary metabolism were differentially transcribed in the two cultivars, especially when plants were subjected to salinity stress. The set of induced genes included 17 MYB family of transcription factors, all of which were subsequently isolated. The effect of constitutively expressing these genes on the salinity tolerance expressed by Arabidopsis thaliana was investigated. The introduction of MsMYB4 significantly increased the plants’ salinity tolerance in an abscisic acid-dependent manner. A sub-cellular localization experiment and a transactivation assay indicated that MsMYB4 was deposited in the nucleus and was able to activate transcription in yeast. Based on this information, we propose that the MsMYB4 products is likely directly involved in alfalfa’s response to salinity stress.

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Descending nociceptive modulation from the supraspinal structures plays an important role in cancer-induced bone pain (CIBP). Rostral ventromedial medulla (RVM) is a critical component of descending nociceptive facilitation circuitry, but so far the mechanisms are poorly known. In this study, we investigated the role of RVM glial activation in the descending nociceptive facilitation circuitry in a CIBP rat model. CIBP rats showed significant activation of microglia and astrocytes, and also up-regulation of phosphorylated p38 mitogen-activated protein kinase (p38 MAPK) and pro-inflammatory mediators released by glial cells (IL-1β, IL-6, TNF-α and brain-derived neurotrophic factor) in the RVM. Stereotaxic microinjection of the glial inhibitors (minocycline and fluorocitrate) into CIBP rats' RVM could reverse the glial activation and significantly attenuate mechanical allodynia in a time-dependent manner. RVM microinjection of p38 MAPK inhibitor (SB203580) abolished the activation of microglia, reversed the associated up-regulation of pro-inflammatory mediators and significantly attenuated mechanical allodynia. Taken together, these results suggest that RVM glial activation is involved in the pathogenesis of CIBP. RVM microglial p38 MAPK signaling pathway is activated and leads to the release of downstream pro-inflammatory mediators, which contribute to the descending facilitation of CIBP.

β-arrestin 2, a regulatory molecule of G protein-coupled receptor, has been proved to play an important role in regulating functions of mu opioid receptor. Changes of β-arrestin 2 expression might affect the function of mu opioid receptors and the effect of its agonists. In this study, antigene RNAs (agRNAs), which could selectively target gene transcription start sites and potently inhibit gene expression, were used to downregulate the expression of β-arrestin 2 to investigate its effects on morphine analgesia and tolerance in mice. After intracerebroventricular administration of recombinant lentivirus encoding β-arrestin 2 agRNAs to the mice, β-arrestin 2 expression was significantly decreased for more than 3 weeks. Mice treated with β-arrestin 2 agRNAs showed enhanced analgesic effects in response to morphine and failed to develop antinociceptive tolerance. These results suggest that inhibition of β-arrestin 2 in the brain with specific agRNAs can improve morphine efficacy, and consequently provide us a useful strategy for treatment of chronic intractable pain and morphine tolerance in vivo.

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